The AGA Trainee and Early Career Committee was formed in 2013 to address the needs of those at the beginning of their careers in gastroenterology. The committee is composed of 12 trainee and early career members, whose mission is to develop and support programs relevant to the needs of young clinicians and researchers in the field of GI. In an initial needs assessment, a survey of GI fellows/trainees was undertaken, which revealed a gap in preparation for the transition from fellowship to practice. In particular, respondents expressed a desire to better understand issues related to practice skills, including health care economics, billing/coding, contract negotiation, and health policy. In addition, some trainees felt uncomfortable bringing questions about their private practice job search to academic faculty, who in turn may not have the necessary experience to provide answers regarding various private practice models and opportunities. Furthermore, fellows have little time and opportunity to learn about the rapidly shifting health care environment that will directly affect their future GI practice. To address these unmet needs, the AGA Trainee and Early Career Committee (in partnership with the Practice Management and Economics Committee as well as the Education and Training Committee) developed a workshop to educate fellows and early career GIs about practice and employment models, contracts and negotiations, compliance, health care policy, and other pertinent topics.

These workshops were designed with a half-day curriculum and based regionally to facilitate attendance as well as to capture the local practice patterns in different regions. They were launched during the 2014-2015 academic year in three cities – Boston, Los Angeles, and Chicago – and received extremely positive feedback from participants.

Since then, 16 additional workshops have been held in the following locations: Columbus, Ohio; Philadelphia; Houston; San Diego; New York; Stanford, Calif.; Pinehurst, N.C.; and Iowa City, Iowa (simulcast). At various times, workshops were held in partnership with local societies such as the New York Society of Gastrointestinal Endoscopy, the North Carolina Society of Gastroenterology, and the Texas Society of Gastrointestinal Endoscopy, which offered additional opportunities for networking. Overall, the 19 regional practice skills workshops held over the last 4 years have reached 420 fellows and early career GIs.

Dr. Ketwaroo is assistant professor, Baylor College of Medicine, and therapeutic endoscopist, Michael E DeBakey VA Medical Center, Houston. Dr. Liang is instructor of medicine, division of gastroenterology, NYU Langone Health, and staff physician, VA New York Harbor Health Care System. Ms. Brown is senior manager of constituency programs, AGA. Ms. NuQuay is senior director, member relations and constituency programs, AGA.

The AGA Trainee and Early Career Committee was formed in 2013 to address the needs of those at the beginning of their careers in gastroenterology. The committee is composed of 12 trainee and early career members, whose mission is to develop and support programs relevant to the needs of young clinicians and researchers in the field of GI. In an initial needs assessment, a survey of GI fellows/trainees was undertaken, which revealed a gap in preparation for the transition from fellowship to practice. In particular, respondents expressed a desire to better understand issues related to practice skills, including health care economics, billing/coding, contract negotiation, and health policy. In addition, some trainees felt uncomfortable bringing questions about their private practice job search to academic faculty, who in turn may not have the necessary experience to provide answers regarding various private practice models and opportunities. Furthermore, fellows have little time and opportunity to learn about the rapidly shifting health care environment that will directly affect their future GI practice. To address these unmet needs, the AGA Trainee and Early Career Committee (in partnership with the Practice Management and Economics Committee as well as the Education and Training Committee) developed a workshop to educate fellows and early career GIs about practice and employment models, contracts and negotiations, compliance, health care policy, and other pertinent topics.

These workshops were designed with a half-day curriculum and based regionally to facilitate attendance as well as to capture the local practice patterns in different regions. They were launched during the 2014-2015 academic year in three cities – Boston, Los Angeles, and Chicago – and received extremely positive feedback from participants.

Since then, 16 additional workshops have been held in the following locations: Columbus, Ohio; Philadelphia; Houston; San Diego; New York; Stanford, Calif.; Pinehurst, N.C.; and Iowa City, Iowa (simulcast). At various times, workshops were held in partnership with local societies such as the New York Society of Gastrointestinal Endoscopy, the North Carolina Society of Gastroenterology, and the Texas Society of Gastrointestinal Endoscopy, which offered additional opportunities for networking. Overall, the 19 regional practice skills workshops held over the last 4 years have reached 420 fellows and early career GIs.

Dr. Ketwaroo is assistant professor, Baylor College of Medicine, and therapeutic endoscopist, Michael E DeBakey VA Medical Center, Houston. Dr. Liang is instructor of medicine, division of gastroenterology, NYU Langone Health, and staff physician, VA New York Harbor Health Care System. Ms. Brown is senior manager of constituency programs, AGA. Ms. NuQuay is senior director, member relations and constituency programs, AGA.

The AGA Trainee and Early Career Committee was formed in 2013 to address the needs of those at the beginning of their careers in gastroenterology. The committee is composed of 12 trainee and early career members, whose mission is to develop and support programs relevant to the needs of young clinicians and researchers in the field of GI. In an initial needs assessment, a survey of GI fellows/trainees was undertaken, which revealed a gap in preparation for the transition from fellowship to practice. In particular, respondents expressed a desire to better understand issues related to practice skills, including health care economics, billing/coding, contract negotiation, and health policy. In addition, some trainees felt uncomfortable bringing questions about their private practice job search to academic faculty, who in turn may not have the necessary experience to provide answers regarding various private practice models and opportunities. Furthermore, fellows have little time and opportunity to learn about the rapidly shifting health care environment that will directly affect their future GI practice. To address these unmet needs, the AGA Trainee and Early Career Committee (in partnership with the Practice Management and Economics Committee as well as the Education and Training Committee) developed a workshop to educate fellows and early career GIs about practice and employment models, contracts and negotiations, compliance, health care policy, and other pertinent topics.

These workshops were designed with a half-day curriculum and based regionally to facilitate attendance as well as to capture the local practice patterns in different regions. They were launched during the 2014-2015 academic year in three cities – Boston, Los Angeles, and Chicago – and received extremely positive feedback from participants.

Since then, 16 additional workshops have been held in the following locations: Columbus, Ohio; Philadelphia; Houston; San Diego; New York; Stanford, Calif.; Pinehurst, N.C.; and Iowa City, Iowa (simulcast). At various times, workshops were held in partnership with local societies such as the New York Society of Gastrointestinal Endoscopy, the North Carolina Society of Gastroenterology, and the Texas Society of Gastrointestinal Endoscopy, which offered additional opportunities for networking. Overall, the 19 regional practice skills workshops held over the last 4 years have reached 420 fellows and early career GIs.

Dr. Ketwaroo is assistant professor, Baylor College of Medicine, and therapeutic endoscopist, Michael E DeBakey VA Medical Center, Houston. Dr. Liang is instructor of medicine, division of gastroenterology, NYU Langone Health, and staff physician, VA New York Harbor Health Care System. Ms. Brown is senior manager of constituency programs, AGA. Ms. NuQuay is senior director, member relations and constituency programs, AGA.

Soluble amyloid-beta in cerebrospinal fluid (CSF) decreased when subjects with obstructive sleep apnea used a positive airway pressure device with good adherence, suggesting that improving sleep could reduce the risk of Alzheimer’s disease in this population.

yelo34/ThinkStock

The small decrease in cerebrospinal amyloid-beta 40 (Ab40) and Ab42 hints at decreased neuronal release of the neurotoxic protein, wrote Yo-El S. Ju, MD, and her colleagues. The report was published online in Annals of Neurology.

Alzheimer’s disease (AD) biomarker studies typically find decreased CSF levels associated with increased Ab brain plaques. But before plaques form, increased soluble Ab in CSF is a risk factor for aggregation. Thus, higher soluble Ab levels in mid-life may suggest a risk of later Ab pathology, wrote Dr. Ju of Washington University, St. Louis.

“We tested individuals without any AD pathology as assessed by Ab42 [in CSF], a highly sensitive biomarker of amyloid plaques,” Dr. Ju and her coauthors wrote. “This means our study findings can be extrapolated to the large population of people with OSA [obstructive sleep apnea], many of whom are middle-aged or younger, and have many years to accrue benefit from AD risk reduction ... The effect of OSA on SWA [slow wave activity], Ab, and possibly tau, is a probable proximal step in a cascade whereby OSA increases the risk of AD.”

The researchers recruited 35 subjects with mild to severe OSA and without abnormal Ab levels in CSF. Subjects used auto-titrating positive airway pressure (PAP) for 1-4 months; 18 were sufficiently compliant to be included in the analysis (more than 4 hours on more than 70% of 30 preceding nights as recorded by the machine). CSF was obtained after a baseline polysomnogram and after the treatment period lasting 1-4 months.

Of the 18 analyzed patients, 7 had mild OSA and 11 had moderate to severe OSA. They were an average of nearly 57 years old with a mean body mass index of 30.4 kg/m²; 7 patients had hypertension.

PAP treatment was effective, indicated by a normalized apnea-hypopnea index and decreased time in hypoxemia. Total sleep time and sleep efficiency were unchanged, but slow-wave activity did increase. As expected, hourly arousals and time in hypoxemia decreased, and hypoxic nadir shifted from an oxygen saturation of 82.5% to 91%.

“As a group, there was no significant change in Ab with treatment,” the researchers wrote. But a correlational analysis found that “greater improvement in OSA was associated with greater decrease in Ab40 and Ab42. Additionally, we found that change in tau negatively correlated with OSA improvement.”

The team suggested a two-factor model to explain the relationship between OSA and Ab levels. “Due to decreased SWA, there would be relatively increased release of Ab into the [interstitial fluid]. However, as OSA severity worsens, pressure effects of obstructive respiratory events impede the clearance of Ab and tau out of the interstitial space, resulting in lower levels in the CSF and an inverse U-shaped curve. In this model, a small improvement in OSA may result in an increase in Ab or tau, whereas a larger improvement in OSA – that ameliorates both SWA and clearance mechanisms – will result in a decrease in Ab and tau.”

The project was funded in part by Philips-Respironics, which provided the devices, and by the National Institutes of Health. Philips-Respironics had no input or role in any other part of the study. The authors had no financial disclosures.

msullivan@mdedge.com

SOURCE: Ju YS et al. Ann Neurol. 2018 Dec 31. doi: 10.1002/ana.25408.

Soluble amyloid-beta in cerebrospinal fluid (CSF) decreased when subjects with obstructive sleep apnea used a positive airway pressure device with good adherence, suggesting that improving sleep could reduce the risk of Alzheimer’s disease in this population.

yelo34/ThinkStock

The small decrease in cerebrospinal amyloid-beta 40 (Ab40) and Ab42 hints at decreased neuronal release of the neurotoxic protein, wrote Yo-El S. Ju, MD, and her colleagues. The report was published online in Annals of Neurology.

Alzheimer’s disease (AD) biomarker studies typically find decreased CSF levels associated with increased Ab brain plaques. But before plaques form, increased soluble Ab in CSF is a risk factor for aggregation. Thus, higher soluble Ab levels in mid-life may suggest a risk of later Ab pathology, wrote Dr. Ju of Washington University, St. Louis.

“We tested individuals without any AD pathology as assessed by Ab42 [in CSF], a highly sensitive biomarker of amyloid plaques,” Dr. Ju and her coauthors wrote. “This means our study findings can be extrapolated to the large population of people with OSA [obstructive sleep apnea], many of whom are middle-aged or younger, and have many years to accrue benefit from AD risk reduction ... The effect of OSA on SWA [slow wave activity], Ab, and possibly tau, is a probable proximal step in a cascade whereby OSA increases the risk of AD.”

The researchers recruited 35 subjects with mild to severe OSA and without abnormal Ab levels in CSF. Subjects used auto-titrating positive airway pressure (PAP) for 1-4 months; 18 were sufficiently compliant to be included in the analysis (more than 4 hours on more than 70% of 30 preceding nights as recorded by the machine). CSF was obtained after a baseline polysomnogram and after the treatment period lasting 1-4 months.

Of the 18 analyzed patients, 7 had mild OSA and 11 had moderate to severe OSA. They were an average of nearly 57 years old with a mean body mass index of 30.4 kg/m²; 7 patients had hypertension.

PAP treatment was effective, indicated by a normalized apnea-hypopnea index and decreased time in hypoxemia. Total sleep time and sleep efficiency were unchanged, but slow-wave activity did increase. As expected, hourly arousals and time in hypoxemia decreased, and hypoxic nadir shifted from an oxygen saturation of 82.5% to 91%.

“As a group, there was no significant change in Ab with treatment,” the researchers wrote. But a correlational analysis found that “greater improvement in OSA was associated with greater decrease in Ab40 and Ab42. Additionally, we found that change in tau negatively correlated with OSA improvement.”

The team suggested a two-factor model to explain the relationship between OSA and Ab levels. “Due to decreased SWA, there would be relatively increased release of Ab into the [interstitial fluid]. However, as OSA severity worsens, pressure effects of obstructive respiratory events impede the clearance of Ab and tau out of the interstitial space, resulting in lower levels in the CSF and an inverse U-shaped curve. In this model, a small improvement in OSA may result in an increase in Ab or tau, whereas a larger improvement in OSA – that ameliorates both SWA and clearance mechanisms – will result in a decrease in Ab and tau.”

The project was funded in part by Philips-Respironics, which provided the devices, and by the National Institutes of Health. Philips-Respironics had no input or role in any other part of the study. The authors had no financial disclosures.

msullivan@mdedge.com

SOURCE: Ju YS et al. Ann Neurol. 2018 Dec 31. doi: 10.1002/ana.25408.

Soluble amyloid-beta in cerebrospinal fluid (CSF) decreased when subjects with obstructive sleep apnea used a positive airway pressure device with good adherence, suggesting that improving sleep could reduce the risk of Alzheimer’s disease in this population.

yelo34/ThinkStock

The small decrease in cerebrospinal amyloid-beta 40 (Ab40) and Ab42 hints at decreased neuronal release of the neurotoxic protein, wrote Yo-El S. Ju, MD, and her colleagues. The report was published online in Annals of Neurology.

Alzheimer’s disease (AD) biomarker studies typically find decreased CSF levels associated with increased Ab brain plaques. But before plaques form, increased soluble Ab in CSF is a risk factor for aggregation. Thus, higher soluble Ab levels in mid-life may suggest a risk of later Ab pathology, wrote Dr. Ju of Washington University, St. Louis.

“We tested individuals without any AD pathology as assessed by Ab42 [in CSF], a highly sensitive biomarker of amyloid plaques,” Dr. Ju and her coauthors wrote. “This means our study findings can be extrapolated to the large population of people with OSA [obstructive sleep apnea], many of whom are middle-aged or younger, and have many years to accrue benefit from AD risk reduction ... The effect of OSA on SWA [slow wave activity], Ab, and possibly tau, is a probable proximal step in a cascade whereby OSA increases the risk of AD.”

The researchers recruited 35 subjects with mild to severe OSA and without abnormal Ab levels in CSF. Subjects used auto-titrating positive airway pressure (PAP) for 1-4 months; 18 were sufficiently compliant to be included in the analysis (more than 4 hours on more than 70% of 30 preceding nights as recorded by the machine). CSF was obtained after a baseline polysomnogram and after the treatment period lasting 1-4 months.

Of the 18 analyzed patients, 7 had mild OSA and 11 had moderate to severe OSA. They were an average of nearly 57 years old with a mean body mass index of 30.4 kg/m²; 7 patients had hypertension.

PAP treatment was effective, indicated by a normalized apnea-hypopnea index and decreased time in hypoxemia. Total sleep time and sleep efficiency were unchanged, but slow-wave activity did increase. As expected, hourly arousals and time in hypoxemia decreased, and hypoxic nadir shifted from an oxygen saturation of 82.5% to 91%.

“As a group, there was no significant change in Ab with treatment,” the researchers wrote. But a correlational analysis found that “greater improvement in OSA was associated with greater decrease in Ab40 and Ab42. Additionally, we found that change in tau negatively correlated with OSA improvement.”

The team suggested a two-factor model to explain the relationship between OSA and Ab levels. “Due to decreased SWA, there would be relatively increased release of Ab into the [interstitial fluid]. However, as OSA severity worsens, pressure effects of obstructive respiratory events impede the clearance of Ab and tau out of the interstitial space, resulting in lower levels in the CSF and an inverse U-shaped curve. In this model, a small improvement in OSA may result in an increase in Ab or tau, whereas a larger improvement in OSA – that ameliorates both SWA and clearance mechanisms – will result in a decrease in Ab and tau.”

The project was funded in part by Philips-Respironics, which provided the devices, and by the National Institutes of Health. Philips-Respironics had no input or role in any other part of the study. The authors had no financial disclosures.

msullivan@mdedge.com

SOURCE: Ju YS et al. Ann Neurol. 2018 Dec 31. doi: 10.1002/ana.25408.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.¹ The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.² Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.^3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

 

 

Discussion

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.⁶ Females lay more than 200 eggs that hatch in approximately 6 to 10 days.⁷ Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.⁶

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.^3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.³ Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.⁴ Additionally, they frequently move around to find a suitable host.⁵ As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.⁸ Other presentations include purpuric macules, bullae, and papular urticaria.^8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.¹¹

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.¹² The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.⁴ It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.¹²

Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.⁸ Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.⁸ The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.² Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.¹ The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.² Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.^3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

 

 

Discussion

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.⁶ Females lay more than 200 eggs that hatch in approximately 6 to 10 days.⁷ Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.⁶

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.^3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.³ Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.⁴ Additionally, they frequently move around to find a suitable host.⁵ As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.⁸ Other presentations include purpuric macules, bullae, and papular urticaria.^8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.¹¹

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.¹² The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.⁴ It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.¹²

Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.⁸ Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.⁸ The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.² Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

Bedbugs are common pests causing several health and economic consequences. With increased travel, pesticide resistance, and a lack of awareness about prevention, bedbugs have become even more difficult to control, especially within large population centers.¹ The US Environmental Protection Agency considers bedbugs to be a considerable public health issue.² Typically, they are found in private residences; however, there have been more reports of bedbugs discovered in the workplace within the last 20 years.^3-5 Herein, we present a case of bedbugs presenting in this unusual environment.

Case Report

A 42-year-old man presented to our dermatology clinic with intensely itchy bumps over the bilateral posterior arms of 3 months’ duration. He had no other skin, hair, or nail concerns. Over the last 3 months prior to dermatologic evaluation, he was treated by an outside physician with topical steroids, systemic antibiotics, topical antifungals, and even systemic steroids with no improvement of the lesions or symptoms. On clinical examination at the current presentation, 8 to 10 pink dermal papules coalescing into 10-cm round patches were noted on the bilateral posterior arms (Figure 1). A punch biopsy of the posterior right arm was performed, and histologic analysis showed a dense superficial and deep infiltrate and a perivascular infiltrate of lymphocytes and eosinophils (Figure 2). No notable epidermal changes were observed.

At this time, the patient was counseled that the most likely cause was some unknown arthropod exposure. Given the chronicity of the patient’s disease course, bedbugs were favored; however, an extensive search of the patient’s home failed to uncover any arthropods, let alone bedbugs. A few weeks later, the patient discovered insects emanating from the mesh backing of his office chair while at work (Figure 3). The location of the intruders corresponded exactly with the lesions on the posterior arms. The occupational health office at his workplace collected samples of the arthropods and confirmed they were bedbugs. The patient’s lesions resolved with topical clobetasol once eradication of the workplace was complete.

 

 

Discussion

Morphology and Epidemiology
Bedbugs are wingless arthropods that have flat, oval-shaped, reddish brown bodies. They are approximately 4.5-mm long and 2.5-mm wide (Figure 4). The 2 most common species of bedbugs that infect humans are Cimex lectularius and Cimex hemipterus. Bedbugs are most commonly found in hotels, apartments, and residential households near sleep locations. They reside in crevices, cracks, mattresses, cushions, dressers, and other structures proximal to the bed. During the day they remain hidden, but at night they emerge for a blood meal. The average lifespan of a bedbug is 6 to 12 months.⁶ Females lay more than 200 eggs that hatch in approximately 6 to 10 days.⁷ Bedbugs progress through 5 nymph stages before becoming adults; several blood meals are required to advance each stage.⁶

Although commonly attributed to the home, bedbugs are being increasingly seen in the office setting.^3-5 In a survey given to pest management professionals in 2015, more than 45% reported that they were contracted by corporations for bedbug infestations in office settings, an increase from 18% in 2010 and 36% in 2013.³ Bedbugs are brought into offices through clothing, luggage, books, and other personal items. Unable to find hosts at night, bedbugs adapt to daytime hours and spread to more unpredictable locations, including chairs, office equipment, desks, and computers.⁴ Additionally, they frequently move around to find a suitable host.⁵ As a result, the growth rate of bedbugs in an office setting is much slower than in the home, with fewer insects. Our patient did not have bedbugs at home, but it is possible that other employees transported them to the office over time.

Clinical Manifestations
Bedbugs cause pruritic and nonpruritic skin rashes, often of the arms, legs, neck, and face. A common reaction is an erythematous papule with a hemorrhagic punctum caused by one bite.⁸ Other presentations include purpuric macules, bullae, and papular urticaria.^8-10 Although bedbugs are suspected to transmit infectious diseases, no reports have substantiated that claim.¹¹

Our patient had several coalescing dermal papules on the arms indicating multiple bites around the same area. Due to the stationary aspect of his job—with the arms resting on his chair while typing at his desk—our patient was an easy target for consistent blood meals.

Detection
Due to an overall smaller population of insects in an office setting, detection of bedbugs in the workplace can be difficult. Infestations can be primarily identified on visual inspection by pest control.¹² The mesh backing on our patient’s chair was one site where bedbugs resided. It is important to check areas where employees congregate, such as lounges, lunch areas, conference rooms, and printers.⁴ It also is essential to examine coatracks and locker rooms, as employees may leave personal items that can serve as a source of transmission of the bugs from home. Additional detection tools provided by pest management professionals include canines, as well as devices that emit pheromones, carbon dioxide, or heat to ensnare the insects.¹²

Treatment
Treatment of bedbug bites is quite variable. For some patients, lesions may resolve on their own. Pruritic maculopapular eruptions can be treated with topical pramoxine or doxepin.⁸ Patients who develop allergic urticaria can use oral antihistamines. Systemic reactions such as anaphylaxis can be treated with a combination of intramuscular epinephrine, antihistamines, and corticosteroids.⁸ The etiology of our patient’s condition initially was unknown, and thus he was given unnecessary systemic steroids and antifungals until the source of the rash was identified and eradicated. Topical clobetasol was subsequently administered and was sufficient to resolve his symptoms.

Final Thoughts

Bedbugs continue to remain a nuisance in the home. This case provides an example of bedbugs in the office, a location that is not commonly associated with bedbug infestations. Bedbugs pose numerous psychological, economic, and health consequences.² Productivity can be reduced, as patients with symptomatic lesions will be unable to work effectively, and those who are unaffected may be unwilling to work knowing their office environment poses a health risk. In addition, employees may worry about bringing the bedbugs home. It is important that employees be educated on the signs of a bedbug infestation and take preventive measures to stop spreading or introducing them to the office space. Due to the scattered habitation of bedbugs in offices, pest control managers need to be vigilant to identify sources of infestation and eradicate accordingly. Clinical manifestations can be nonspecific, resembling autoimmune disorders, fungal infections, or bites from other various arthropods; thus, treatment is highly dependent on the patient’s history and occupational exposure.

Bedbugs have successfully adapted to a new environment in the office space. Dermatologists and other health care professionals can no longer exclusively associate bedbugs with the home. When the clinical and histological presentation suggests an arthropod assault, we must counsel our patients to surveil their homes and work settings alike. If necessary, they should seek the assistance of occupational health professionals.

Editor’s Note: This is the second installment of the Private Practice Perspectives column, which is a collaboration between the AGA’s The New Gastroenterologist and the Digestive Health Physicians Association (DHPA). In this issue’s column, David Ramsay (Winston Salem, N.C.) provides valuable advice on the very important topic of picking the right practice.
Bryson W. Katona, MD, PhD
Editor in Chief, The New Gastroenterologist

Just 7 years ago, I faced the same difficult decisions many new gastroenterologists have. Like many physicians coming out of a residency and fellowship program, I had loans to repay and family to consider when evaluating the choices about where I would practice.

Looking back, there were several essential questions that helped guide my decision-making process. If you are early in your career as a GI, here are some questions to ask yourself and tips that I’ve learned along the way that may help make the decision about which practice is right for you.

What do you want to do with your training and skills? This may sound obvious, but it’s important to align your interests with the right practice. Did you receive extra training in endoscopic procedures, such as endoscopic ultrasonography and endoscopic retrograde cholangiopancreatography? Do you want to specialize in inflammatory bowel disease? Have a passion for hepatology? Look for a practice that has those specific opportunities available to match your interests.

In addition, some GI docs want to pursue their interest in research. Keep in mind that many independent practices have research arms and offer physicians the opportunity to continue on this path.

Lastly, consider whether you want to be involved in the business of medicine or take on a leadership role. Many practices offer (and even encourage) those opportunities, and you can winnow down your list of practices based on whether they allow you to take on those roles.

Where do you want to live? My wife and I completed our residencies and fellowships in Washington, but when it came time to find a place to practice medicine, we knew we wanted to be near family. We narrowed our search to Tennessee, Florida, and North Carolina, where we eventually ended up.

Of course, wherever you decide to go is a personal choice. Some people prefer living on the coasts or want to reside in a major city. This might come as a surprise to some, but very often you will command a higher salary in rural areas or smaller cities, which are traditionally underserved by our profession. That starts to matter when you think about paying off your student loan debt.

What is the long-term potential of each position? This is perhaps the most important question to ask. Does your new practice offer ownership potential? Are there opportunities to share in the various (ancillary) revenue streams, such as an ambulatory surgery center, anesthesia, or pathology? How soon might you have the opportunity to buy in and what is the buy in structure and cost? What are the practice rules around offering partnerships?

These are all questions that you should ask up front. Remember that the lifestyle you start out with may change over the course of your career. Find a practice that offers opportunities for growth because your long-term income potential is much more important than your starting salary or size of any sign-on bonus.

Once you’ve decided the answers to some of these questions, here are a few tips to help you land a job at the right medical practice.

Talk to your mentors and tap into your connections: Most GI physicians completing a fellowship will have mentors who have connections to practices. Speak with them about where to look. In addition, most medical societies and state-specific GI societies post classified job listings. Use these professional memberships.

Don’t be afraid of the cold call: If you know where you might want to live, you should consider cold calls to practices in the area to see what opportunities are available. That’s how I found my job. I started calling practices in North Carolina. Those that didn’t have openings knew of, and shared names of, practices in the state that did.

Call the local hospitals and ask to speak to the charge nurse in endoscopy: This is one the best tips I got to help narrow the field. These nurses are a great source of information with honest feedback about the reputation of the local GI practices.

Look for collegiality: This can be harder to spot, but it’s a good sign when the CEOs or practice administrators are engaging and take the time to answer questions.

Look for groups that don’t have a lot of turnover: This is another important sign. We call it the churn and burn: We all know of fellows who have joined a practice where they work long hours but never have the opportunity to make partner. You might ask the question directly: How many physicians have come here and left within the first 5 years of employment? A high turnover rate is a red flag. No matter what type of practice you choose, the key is to look at your long-term prospects, not just at short-term rewards. After all, that’s what will give you the greatest opportunities – and likely make you happiest in your career.
 

David Ramsay, MD, is treasurer of the Digestive Health Physicians Association. He is President of Digestive Health Specialists in Winston Salem, N.C., which he joined in 2012 after working in the Washington area.

Editor’s Note: This is the second installment of the Private Practice Perspectives column, which is a collaboration between the AGA’s The New Gastroenterologist and the Digestive Health Physicians Association (DHPA). In this issue’s column, David Ramsay (Winston Salem, N.C.) provides valuable advice on the very important topic of picking the right practice.
Bryson W. Katona, MD, PhD
Editor in Chief, The New Gastroenterologist

Just 7 years ago, I faced the same difficult decisions many new gastroenterologists have. Like many physicians coming out of a residency and fellowship program, I had loans to repay and family to consider when evaluating the choices about where I would practice.

Looking back, there were several essential questions that helped guide my decision-making process. If you are early in your career as a GI, here are some questions to ask yourself and tips that I’ve learned along the way that may help make the decision about which practice is right for you.

What do you want to do with your training and skills? This may sound obvious, but it’s important to align your interests with the right practice. Did you receive extra training in endoscopic procedures, such as endoscopic ultrasonography and endoscopic retrograde cholangiopancreatography? Do you want to specialize in inflammatory bowel disease? Have a passion for hepatology? Look for a practice that has those specific opportunities available to match your interests.

In addition, some GI docs want to pursue their interest in research. Keep in mind that many independent practices have research arms and offer physicians the opportunity to continue on this path.

Lastly, consider whether you want to be involved in the business of medicine or take on a leadership role. Many practices offer (and even encourage) those opportunities, and you can winnow down your list of practices based on whether they allow you to take on those roles.

Where do you want to live? My wife and I completed our residencies and fellowships in Washington, but when it came time to find a place to practice medicine, we knew we wanted to be near family. We narrowed our search to Tennessee, Florida, and North Carolina, where we eventually ended up.

Of course, wherever you decide to go is a personal choice. Some people prefer living on the coasts or want to reside in a major city. This might come as a surprise to some, but very often you will command a higher salary in rural areas or smaller cities, which are traditionally underserved by our profession. That starts to matter when you think about paying off your student loan debt.

What is the long-term potential of each position? This is perhaps the most important question to ask. Does your new practice offer ownership potential? Are there opportunities to share in the various (ancillary) revenue streams, such as an ambulatory surgery center, anesthesia, or pathology? How soon might you have the opportunity to buy in and what is the buy in structure and cost? What are the practice rules around offering partnerships?

These are all questions that you should ask up front. Remember that the lifestyle you start out with may change over the course of your career. Find a practice that offers opportunities for growth because your long-term income potential is much more important than your starting salary or size of any sign-on bonus.

Once you’ve decided the answers to some of these questions, here are a few tips to help you land a job at the right medical practice.

Talk to your mentors and tap into your connections: Most GI physicians completing a fellowship will have mentors who have connections to practices. Speak with them about where to look. In addition, most medical societies and state-specific GI societies post classified job listings. Use these professional memberships.

Don’t be afraid of the cold call: If you know where you might want to live, you should consider cold calls to practices in the area to see what opportunities are available. That’s how I found my job. I started calling practices in North Carolina. Those that didn’t have openings knew of, and shared names of, practices in the state that did.

Call the local hospitals and ask to speak to the charge nurse in endoscopy: This is one the best tips I got to help narrow the field. These nurses are a great source of information with honest feedback about the reputation of the local GI practices.

Look for collegiality: This can be harder to spot, but it’s a good sign when the CEOs or practice administrators are engaging and take the time to answer questions.

Look for groups that don’t have a lot of turnover: This is another important sign. We call it the churn and burn: We all know of fellows who have joined a practice where they work long hours but never have the opportunity to make partner. You might ask the question directly: How many physicians have come here and left within the first 5 years of employment? A high turnover rate is a red flag. No matter what type of practice you choose, the key is to look at your long-term prospects, not just at short-term rewards. After all, that’s what will give you the greatest opportunities – and likely make you happiest in your career.
 

David Ramsay, MD, is treasurer of the Digestive Health Physicians Association. He is President of Digestive Health Specialists in Winston Salem, N.C., which he joined in 2012 after working in the Washington area.

Editor’s Note: This is the second installment of the Private Practice Perspectives column, which is a collaboration between the AGA’s The New Gastroenterologist and the Digestive Health Physicians Association (DHPA). In this issue’s column, David Ramsay (Winston Salem, N.C.) provides valuable advice on the very important topic of picking the right practice.
Bryson W. Katona, MD, PhD
Editor in Chief, The New Gastroenterologist

Just 7 years ago, I faced the same difficult decisions many new gastroenterologists have. Like many physicians coming out of a residency and fellowship program, I had loans to repay and family to consider when evaluating the choices about where I would practice.

Looking back, there were several essential questions that helped guide my decision-making process. If you are early in your career as a GI, here are some questions to ask yourself and tips that I’ve learned along the way that may help make the decision about which practice is right for you.

What do you want to do with your training and skills? This may sound obvious, but it’s important to align your interests with the right practice. Did you receive extra training in endoscopic procedures, such as endoscopic ultrasonography and endoscopic retrograde cholangiopancreatography? Do you want to specialize in inflammatory bowel disease? Have a passion for hepatology? Look for a practice that has those specific opportunities available to match your interests.

In addition, some GI docs want to pursue their interest in research. Keep in mind that many independent practices have research arms and offer physicians the opportunity to continue on this path.

Lastly, consider whether you want to be involved in the business of medicine or take on a leadership role. Many practices offer (and even encourage) those opportunities, and you can winnow down your list of practices based on whether they allow you to take on those roles.

Where do you want to live? My wife and I completed our residencies and fellowships in Washington, but when it came time to find a place to practice medicine, we knew we wanted to be near family. We narrowed our search to Tennessee, Florida, and North Carolina, where we eventually ended up.

Of course, wherever you decide to go is a personal choice. Some people prefer living on the coasts or want to reside in a major city. This might come as a surprise to some, but very often you will command a higher salary in rural areas or smaller cities, which are traditionally underserved by our profession. That starts to matter when you think about paying off your student loan debt.

What is the long-term potential of each position? This is perhaps the most important question to ask. Does your new practice offer ownership potential? Are there opportunities to share in the various (ancillary) revenue streams, such as an ambulatory surgery center, anesthesia, or pathology? How soon might you have the opportunity to buy in and what is the buy in structure and cost? What are the practice rules around offering partnerships?

These are all questions that you should ask up front. Remember that the lifestyle you start out with may change over the course of your career. Find a practice that offers opportunities for growth because your long-term income potential is much more important than your starting salary or size of any sign-on bonus.

Once you’ve decided the answers to some of these questions, here are a few tips to help you land a job at the right medical practice.

Talk to your mentors and tap into your connections: Most GI physicians completing a fellowship will have mentors who have connections to practices. Speak with them about where to look. In addition, most medical societies and state-specific GI societies post classified job listings. Use these professional memberships.

Don’t be afraid of the cold call: If you know where you might want to live, you should consider cold calls to practices in the area to see what opportunities are available. That’s how I found my job. I started calling practices in North Carolina. Those that didn’t have openings knew of, and shared names of, practices in the state that did.

Call the local hospitals and ask to speak to the charge nurse in endoscopy: This is one the best tips I got to help narrow the field. These nurses are a great source of information with honest feedback about the reputation of the local GI practices.

Look for collegiality: This can be harder to spot, but it’s a good sign when the CEOs or practice administrators are engaging and take the time to answer questions.

Look for groups that don’t have a lot of turnover: This is another important sign. We call it the churn and burn: We all know of fellows who have joined a practice where they work long hours but never have the opportunity to make partner. You might ask the question directly: How many physicians have come here and left within the first 5 years of employment? A high turnover rate is a red flag. No matter what type of practice you choose, the key is to look at your long-term prospects, not just at short-term rewards. After all, that’s what will give you the greatest opportunities – and likely make you happiest in your career.
 

David Ramsay, MD, is treasurer of the Digestive Health Physicians Association. He is President of Digestive Health Specialists in Winston Salem, N.C., which he joined in 2012 after working in the Washington area.

In a position statement published online ahead of print Jan. 2 in Neurology, the American Academy of Neurology urges uniformity in the laws, policies, and practices related to brain death. Such uniformity would reduce uncertainty and improve patient care, according to the authors. The statement, which was drafted by the AAN’s Brain Death Working Group, also supports the development of uniform policies regarding brain death and its determination within American medical institutions. Finally, the document provides neurologists with guidance for responding to requests for accommodation, including objections to the determination of brain death and to the withdrawal of organ-sustaining technology.

The AAN defines brain death as death resulting from irreversible loss of function of the entire brain. The Uniform Determination of Death Act of 1981 held that brain death and circulatory death (that is, death resulting from irreversible loss of function of the circulatory system) are equivalent, and the AAN acknowledges this equivalence.

The two current medical standards for brain death are the AAN’s 2010 Evidence-Based Guideline Update: Determining Brain Death in Adults and the 2011 Guidelines for the Determination of Brain Death in Infants and Children, which was published by the pediatric section of the Society of Critical Care Medicine, the sections of neurology and critical care of the American Academy of Pediatrics, and the Child Neurology Society. “The AAN is unaware of any cases in which compliant application of the brain death guidelines led to inaccurate determination of death with return of any brain function, including consciousness, brainstem reflexes, or ventilatory effort,” according to their 2019 statement.

The only jurisdiction with laws that specifically defer to these standards, however, is Nevada. The vagueness of most states’ laws has contributed to divergent legal interpretations and idiosyncratic standards for determining brain death, according to the statement.

“The AAN believes that a specific, uniform standard for the determination of brain death is critically important to provide the highest quality patient-centered neurologic and end-of-life care,” said James Russell, DO, MS, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., and lead author of the position statement. “The AAN supports the development of legislation in every state modeled after the Nevada statute, which specifically defers to these current adult and pediatric brain death guidelines and any future updates.”

In addition to uniform institutional policies for determining brain death within U.S. medical facilities, the AAN calls for the development of training programs and credentialing mechanisms for physicians who determine brain death, regardless of their specialties. The association also supports research that enhances understanding of brain death and enhanced professional and public education.

While expressing respect and sympathy for requests for limited accommodation, the AAN asserts that these requests “must be based on the values of the patient, and not those of loved ones or other surrogate decision makers.” The association further observes that physicians have no ethical obligation to provide medical treatment to a deceased patient. New Jersey is the only state that legally obliges physicians to provide indefinite accommodation and continued application of organ-sustaining technology.

“The AAN believes that its members have both the moral authority and professional responsibility, when lawful, to perform a brain death evaluation, including apnea testing, after informing a patient’s loved ones or lawful surrogates of that intention, but without obligation to obtain informed consent,” according to the statement. “This position is analogous to the authority and responsibility historically granted to the medical profession to determine circulatory death without the requirement for additional informed consent.”

If a dispute about indefinite accommodation cannot be resolved, it is acceptable for a physician to withdraw organ-sustaining technology unilaterally over the objection of loved ones when legally permitted, according to the AAN. Such unilateral action is a measure of last resort and does not apply when the patient is a pregnant woman, said the authors. In the latter case, the ethical analysis should focus mainly on the welfare of the fetus.

The AAN provided financial support for the Brain Death Working Group’s efforts. The statement’s authors reported no relevant disclosures. The American Neurological Association and the Child Neurology Society have endorsed the AAN’s position statement.

egreb@mdedge.com

SOURCE: Russell JA et al. Neurology. 2018 Jan 2. doi: 10.1212/WNL.0000000000006750.
 

In a position statement published online ahead of print Jan. 2 in Neurology, the American Academy of Neurology urges uniformity in the laws, policies, and practices related to brain death. Such uniformity would reduce uncertainty and improve patient care, according to the authors. The statement, which was drafted by the AAN’s Brain Death Working Group, also supports the development of uniform policies regarding brain death and its determination within American medical institutions. Finally, the document provides neurologists with guidance for responding to requests for accommodation, including objections to the determination of brain death and to the withdrawal of organ-sustaining technology.

The AAN defines brain death as death resulting from irreversible loss of function of the entire brain. The Uniform Determination of Death Act of 1981 held that brain death and circulatory death (that is, death resulting from irreversible loss of function of the circulatory system) are equivalent, and the AAN acknowledges this equivalence.

The two current medical standards for brain death are the AAN’s 2010 Evidence-Based Guideline Update: Determining Brain Death in Adults and the 2011 Guidelines for the Determination of Brain Death in Infants and Children, which was published by the pediatric section of the Society of Critical Care Medicine, the sections of neurology and critical care of the American Academy of Pediatrics, and the Child Neurology Society. “The AAN is unaware of any cases in which compliant application of the brain death guidelines led to inaccurate determination of death with return of any brain function, including consciousness, brainstem reflexes, or ventilatory effort,” according to their 2019 statement.

The only jurisdiction with laws that specifically defer to these standards, however, is Nevada. The vagueness of most states’ laws has contributed to divergent legal interpretations and idiosyncratic standards for determining brain death, according to the statement.

“The AAN believes that a specific, uniform standard for the determination of brain death is critically important to provide the highest quality patient-centered neurologic and end-of-life care,” said James Russell, DO, MS, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., and lead author of the position statement. “The AAN supports the development of legislation in every state modeled after the Nevada statute, which specifically defers to these current adult and pediatric brain death guidelines and any future updates.”

In addition to uniform institutional policies for determining brain death within U.S. medical facilities, the AAN calls for the development of training programs and credentialing mechanisms for physicians who determine brain death, regardless of their specialties. The association also supports research that enhances understanding of brain death and enhanced professional and public education.

While expressing respect and sympathy for requests for limited accommodation, the AAN asserts that these requests “must be based on the values of the patient, and not those of loved ones or other surrogate decision makers.” The association further observes that physicians have no ethical obligation to provide medical treatment to a deceased patient. New Jersey is the only state that legally obliges physicians to provide indefinite accommodation and continued application of organ-sustaining technology.

“The AAN believes that its members have both the moral authority and professional responsibility, when lawful, to perform a brain death evaluation, including apnea testing, after informing a patient’s loved ones or lawful surrogates of that intention, but without obligation to obtain informed consent,” according to the statement. “This position is analogous to the authority and responsibility historically granted to the medical profession to determine circulatory death without the requirement for additional informed consent.”

If a dispute about indefinite accommodation cannot be resolved, it is acceptable for a physician to withdraw organ-sustaining technology unilaterally over the objection of loved ones when legally permitted, according to the AAN. Such unilateral action is a measure of last resort and does not apply when the patient is a pregnant woman, said the authors. In the latter case, the ethical analysis should focus mainly on the welfare of the fetus.

The AAN provided financial support for the Brain Death Working Group’s efforts. The statement’s authors reported no relevant disclosures. The American Neurological Association and the Child Neurology Society have endorsed the AAN’s position statement.

egreb@mdedge.com

SOURCE: Russell JA et al. Neurology. 2018 Jan 2. doi: 10.1212/WNL.0000000000006750.
 

In a position statement published online ahead of print Jan. 2 in Neurology, the American Academy of Neurology urges uniformity in the laws, policies, and practices related to brain death. Such uniformity would reduce uncertainty and improve patient care, according to the authors. The statement, which was drafted by the AAN’s Brain Death Working Group, also supports the development of uniform policies regarding brain death and its determination within American medical institutions. Finally, the document provides neurologists with guidance for responding to requests for accommodation, including objections to the determination of brain death and to the withdrawal of organ-sustaining technology.

The AAN defines brain death as death resulting from irreversible loss of function of the entire brain. The Uniform Determination of Death Act of 1981 held that brain death and circulatory death (that is, death resulting from irreversible loss of function of the circulatory system) are equivalent, and the AAN acknowledges this equivalence.

The two current medical standards for brain death are the AAN’s 2010 Evidence-Based Guideline Update: Determining Brain Death in Adults and the 2011 Guidelines for the Determination of Brain Death in Infants and Children, which was published by the pediatric section of the Society of Critical Care Medicine, the sections of neurology and critical care of the American Academy of Pediatrics, and the Child Neurology Society. “The AAN is unaware of any cases in which compliant application of the brain death guidelines led to inaccurate determination of death with return of any brain function, including consciousness, brainstem reflexes, or ventilatory effort,” according to their 2019 statement.

The only jurisdiction with laws that specifically defer to these standards, however, is Nevada. The vagueness of most states’ laws has contributed to divergent legal interpretations and idiosyncratic standards for determining brain death, according to the statement.

“The AAN believes that a specific, uniform standard for the determination of brain death is critically important to provide the highest quality patient-centered neurologic and end-of-life care,” said James Russell, DO, MS, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., and lead author of the position statement. “The AAN supports the development of legislation in every state modeled after the Nevada statute, which specifically defers to these current adult and pediatric brain death guidelines and any future updates.”

In addition to uniform institutional policies for determining brain death within U.S. medical facilities, the AAN calls for the development of training programs and credentialing mechanisms for physicians who determine brain death, regardless of their specialties. The association also supports research that enhances understanding of brain death and enhanced professional and public education.

While expressing respect and sympathy for requests for limited accommodation, the AAN asserts that these requests “must be based on the values of the patient, and not those of loved ones or other surrogate decision makers.” The association further observes that physicians have no ethical obligation to provide medical treatment to a deceased patient. New Jersey is the only state that legally obliges physicians to provide indefinite accommodation and continued application of organ-sustaining technology.

“The AAN believes that its members have both the moral authority and professional responsibility, when lawful, to perform a brain death evaluation, including apnea testing, after informing a patient’s loved ones or lawful surrogates of that intention, but without obligation to obtain informed consent,” according to the statement. “This position is analogous to the authority and responsibility historically granted to the medical profession to determine circulatory death without the requirement for additional informed consent.”

If a dispute about indefinite accommodation cannot be resolved, it is acceptable for a physician to withdraw organ-sustaining technology unilaterally over the objection of loved ones when legally permitted, according to the AAN. Such unilateral action is a measure of last resort and does not apply when the patient is a pregnant woman, said the authors. In the latter case, the ethical analysis should focus mainly on the welfare of the fetus.

The AAN provided financial support for the Brain Death Working Group’s efforts. The statement’s authors reported no relevant disclosures. The American Neurological Association and the Child Neurology Society have endorsed the AAN’s position statement.

egreb@mdedge.com

SOURCE: Russell JA et al. Neurology. 2018 Jan 2. doi: 10.1212/WNL.0000000000006750.
 

Total spending on medical marketing in the United States increased from $17.7 billion in 1997 to $29.9 billion in 2016, according to an analysis of direct-to-consumer (DTC) and professional marketing for prescription drugs, disease awareness campaigns, health services, and laboratory tests.

“Increased medical marketing reflects a convergence of scientific, economic, legal, and social forces,” wrote Lisa M. Schwartz, MD, and her coauthor, adding that “although marketing expanded over 20 years, regulatory oversight remains relatively limited.” Dr. Schwartz, then codirector of the Center for Medicine and Media at The Dartmouth Institute in Lebanon, N.H., died in November of 2018, after her work was accepted for publication in JAMA.

Dr. Schwartz and her coauthor, David Woloshin, MD, also of Dartmouth, reviewed consumer advertising and professional marketing data, along with searches of medical literature and business journals, to ascertain the quantity and impact of spending. The most money was spent on marketing to medical professionals, which increased from $15.6 billion in 1997 to $20.3 billion in 2016. In terms of percentages, the biggest increase was seen in DTC advertising: $2.1 billion in 1997 (11.9% of total spending) ballooned to $9.6 billion (32.1% of total spending).

These increases were not accompanied by corresponding regulatory efforts to limit influence or protect patients and consumers. In 2016, the Food and Drug Administration’s Office of Prescription Drug Promotion received 97,252 promotional materials that drug companies submitted for review, compared with 34,182 in 1997, but violation letters for prescription drug advertising decreased from 156 to 11. In the same year, the FDA reviewed 41% of core materials – such as risk disclosures and key messages – for new drugs or indications prior to launch, a performance measure the coauthors called “critically important.”

In regard to disease awareness campaigns, 2004 guidance from the FDA on awareness advertising – including standards for unbranded campaigns and recommendations to avoid encouraging self-diagnosis and self-treatment – was withdrawn in 2015 and never replaced. The Federal Trade Commission, which has jurisdiction over unbranded advertising, has not taken regulatory action of its own; any FDA requests for investigation are unknown. In addition, these 2 decades have not seen state attorneys general initiate any action against deceptive consumer advertising, nor has the FTC acted against misleading laboratory test promotion.

“The FDA and FTC should establish and enforce standards for responsible disease awareness campaigns,” the coauthors wrote, “including criteria to validate symptom quizzes (or banning them) and evidence-based strategies to minimize misconceptions that a drug can treat all symptoms of disease.”

Overall, spending on medical marketing actually increased faster than did spending on health services overall. Marketing saw a remarkable 430% increase ($542 million to $2.9 billion) over the 2 decades, while health services spending increased by 90% ($1.2 trillion to $2.2 trillion).

One of the rare similarities from 1997 to 2016 was spending on marketing prescription drugs to physicians, typically through face-to-face meetings and hospital visits; this held steady at approximately $5 billion. However, spending on drug samples increased from $8.9 billion to $13.5 billion, while medical journal advertising declined drastically from $744 million to $119 million.

Spending on DTC marketing of prescription drugs increased across all therapeutic categories but three: cholesterol, allergy, and osteoporosis, each of which saw top-selling drugs either become over-the-counter or lose patent protection. Spending on drugs for diabetes/endocrine disease went from $27 million in 1997 to a whopping $725 million in 2016, followed by dermatology drugs ($67 million to $605 million) and pain/central nervous system drugs ($56 million to $542 million).

The coauthors shared potential limitations of their study, including the likelihood that they underestimated how much is actually spent on medical marketing. “Data on professional marketing (e.g., detailing) of laboratory tests, health services or devices, and pharmaceutical company spending on coupons or rebates, online promotion, and meetings and events could not be obtained,” they noted. In addition, company marketing budgets often do not include additional expenses that should count toward this total, and any published literature on medical marketing’s return on investment is largely based on observational data and cannot be fully relied upon.

The two coauthors previously served as medical experts in testosterone litigation and were cofounders of a company that provided data about the benefits and harms of prescription drugs, which ceased operations in December 2016. No other conflicts of interest were reported.


SOURCE: Schwartz LM et al. JAMA. 2019 Jan 8. doi: 10.1001/jama.2018.19320.

Total spending on medical marketing in the United States increased from $17.7 billion in 1997 to $29.9 billion in 2016, according to an analysis of direct-to-consumer (DTC) and professional marketing for prescription drugs, disease awareness campaigns, health services, and laboratory tests.

“Increased medical marketing reflects a convergence of scientific, economic, legal, and social forces,” wrote Lisa M. Schwartz, MD, and her coauthor, adding that “although marketing expanded over 20 years, regulatory oversight remains relatively limited.” Dr. Schwartz, then codirector of the Center for Medicine and Media at The Dartmouth Institute in Lebanon, N.H., died in November of 2018, after her work was accepted for publication in JAMA.

Dr. Schwartz and her coauthor, David Woloshin, MD, also of Dartmouth, reviewed consumer advertising and professional marketing data, along with searches of medical literature and business journals, to ascertain the quantity and impact of spending. The most money was spent on marketing to medical professionals, which increased from $15.6 billion in 1997 to $20.3 billion in 2016. In terms of percentages, the biggest increase was seen in DTC advertising: $2.1 billion in 1997 (11.9% of total spending) ballooned to $9.6 billion (32.1% of total spending).

These increases were not accompanied by corresponding regulatory efforts to limit influence or protect patients and consumers. In 2016, the Food and Drug Administration’s Office of Prescription Drug Promotion received 97,252 promotional materials that drug companies submitted for review, compared with 34,182 in 1997, but violation letters for prescription drug advertising decreased from 156 to 11. In the same year, the FDA reviewed 41% of core materials – such as risk disclosures and key messages – for new drugs or indications prior to launch, a performance measure the coauthors called “critically important.”

In regard to disease awareness campaigns, 2004 guidance from the FDA on awareness advertising – including standards for unbranded campaigns and recommendations to avoid encouraging self-diagnosis and self-treatment – was withdrawn in 2015 and never replaced. The Federal Trade Commission, which has jurisdiction over unbranded advertising, has not taken regulatory action of its own; any FDA requests for investigation are unknown. In addition, these 2 decades have not seen state attorneys general initiate any action against deceptive consumer advertising, nor has the FTC acted against misleading laboratory test promotion.

“The FDA and FTC should establish and enforce standards for responsible disease awareness campaigns,” the coauthors wrote, “including criteria to validate symptom quizzes (or banning them) and evidence-based strategies to minimize misconceptions that a drug can treat all symptoms of disease.”

Overall, spending on medical marketing actually increased faster than did spending on health services overall. Marketing saw a remarkable 430% increase ($542 million to $2.9 billion) over the 2 decades, while health services spending increased by 90% ($1.2 trillion to $2.2 trillion).

One of the rare similarities from 1997 to 2016 was spending on marketing prescription drugs to physicians, typically through face-to-face meetings and hospital visits; this held steady at approximately $5 billion. However, spending on drug samples increased from $8.9 billion to $13.5 billion, while medical journal advertising declined drastically from $744 million to $119 million.

Spending on DTC marketing of prescription drugs increased across all therapeutic categories but three: cholesterol, allergy, and osteoporosis, each of which saw top-selling drugs either become over-the-counter or lose patent protection. Spending on drugs for diabetes/endocrine disease went from $27 million in 1997 to a whopping $725 million in 2016, followed by dermatology drugs ($67 million to $605 million) and pain/central nervous system drugs ($56 million to $542 million).

The coauthors shared potential limitations of their study, including the likelihood that they underestimated how much is actually spent on medical marketing. “Data on professional marketing (e.g., detailing) of laboratory tests, health services or devices, and pharmaceutical company spending on coupons or rebates, online promotion, and meetings and events could not be obtained,” they noted. In addition, company marketing budgets often do not include additional expenses that should count toward this total, and any published literature on medical marketing’s return on investment is largely based on observational data and cannot be fully relied upon.

The two coauthors previously served as medical experts in testosterone litigation and were cofounders of a company that provided data about the benefits and harms of prescription drugs, which ceased operations in December 2016. No other conflicts of interest were reported.


SOURCE: Schwartz LM et al. JAMA. 2019 Jan 8. doi: 10.1001/jama.2018.19320.

Total spending on medical marketing in the United States increased from $17.7 billion in 1997 to $29.9 billion in 2016, according to an analysis of direct-to-consumer (DTC) and professional marketing for prescription drugs, disease awareness campaigns, health services, and laboratory tests.

“Increased medical marketing reflects a convergence of scientific, economic, legal, and social forces,” wrote Lisa M. Schwartz, MD, and her coauthor, adding that “although marketing expanded over 20 years, regulatory oversight remains relatively limited.” Dr. Schwartz, then codirector of the Center for Medicine and Media at The Dartmouth Institute in Lebanon, N.H., died in November of 2018, after her work was accepted for publication in JAMA.

Dr. Schwartz and her coauthor, David Woloshin, MD, also of Dartmouth, reviewed consumer advertising and professional marketing data, along with searches of medical literature and business journals, to ascertain the quantity and impact of spending. The most money was spent on marketing to medical professionals, which increased from $15.6 billion in 1997 to $20.3 billion in 2016. In terms of percentages, the biggest increase was seen in DTC advertising: $2.1 billion in 1997 (11.9% of total spending) ballooned to $9.6 billion (32.1% of total spending).

These increases were not accompanied by corresponding regulatory efforts to limit influence or protect patients and consumers. In 2016, the Food and Drug Administration’s Office of Prescription Drug Promotion received 97,252 promotional materials that drug companies submitted for review, compared with 34,182 in 1997, but violation letters for prescription drug advertising decreased from 156 to 11. In the same year, the FDA reviewed 41% of core materials – such as risk disclosures and key messages – for new drugs or indications prior to launch, a performance measure the coauthors called “critically important.”

In regard to disease awareness campaigns, 2004 guidance from the FDA on awareness advertising – including standards for unbranded campaigns and recommendations to avoid encouraging self-diagnosis and self-treatment – was withdrawn in 2015 and never replaced. The Federal Trade Commission, which has jurisdiction over unbranded advertising, has not taken regulatory action of its own; any FDA requests for investigation are unknown. In addition, these 2 decades have not seen state attorneys general initiate any action against deceptive consumer advertising, nor has the FTC acted against misleading laboratory test promotion.

“The FDA and FTC should establish and enforce standards for responsible disease awareness campaigns,” the coauthors wrote, “including criteria to validate symptom quizzes (or banning them) and evidence-based strategies to minimize misconceptions that a drug can treat all symptoms of disease.”

Overall, spending on medical marketing actually increased faster than did spending on health services overall. Marketing saw a remarkable 430% increase ($542 million to $2.9 billion) over the 2 decades, while health services spending increased by 90% ($1.2 trillion to $2.2 trillion).

One of the rare similarities from 1997 to 2016 was spending on marketing prescription drugs to physicians, typically through face-to-face meetings and hospital visits; this held steady at approximately $5 billion. However, spending on drug samples increased from $8.9 billion to $13.5 billion, while medical journal advertising declined drastically from $744 million to $119 million.

Spending on DTC marketing of prescription drugs increased across all therapeutic categories but three: cholesterol, allergy, and osteoporosis, each of which saw top-selling drugs either become over-the-counter or lose patent protection. Spending on drugs for diabetes/endocrine disease went from $27 million in 1997 to a whopping $725 million in 2016, followed by dermatology drugs ($67 million to $605 million) and pain/central nervous system drugs ($56 million to $542 million).

The coauthors shared potential limitations of their study, including the likelihood that they underestimated how much is actually spent on medical marketing. “Data on professional marketing (e.g., detailing) of laboratory tests, health services or devices, and pharmaceutical company spending on coupons or rebates, online promotion, and meetings and events could not be obtained,” they noted. In addition, company marketing budgets often do not include additional expenses that should count toward this total, and any published literature on medical marketing’s return on investment is largely based on observational data and cannot be fully relied upon.

The two coauthors previously served as medical experts in testosterone litigation and were cofounders of a company that provided data about the benefits and harms of prescription drugs, which ceased operations in December 2016. No other conflicts of interest were reported.


SOURCE: Schwartz LM et al. JAMA. 2019 Jan 8. doi: 10.1001/jama.2018.19320.

The definition of warts is variable, largely reflecting their manifold appearance, biologic potential, and public health concerns. One vernacular dictionary defines warts as:

Small, benign growths caused by a vital infection of the skin or mucous membrane. The virus infects the surface layer. The viruses that cause warts are members of the human papilloma virus (HPV) family. Warts are not cancerous but some strains of HPV, usually not associated with warts, have been linked with cancer formation. Warts are contagious from person to person and from one area of the body to another on the same person.¹

The World Health Organization defines warts by their structural components as:

Human papillomavirus (HPV) is a small, non-enveloped deoxyribonucleic acid (DNA) virus that infects skin or mucosal cells. The circular, double-stranded viral genome is approximately 8-kb in length. The genome encodes for 6 early proteins responsible for virus replication and 2 late proteins, L1 and L2, which are the viral structural proteins.²

In pediatric and adolescent dermatology, warts often are defined by their location and morphology; for example, facial warts typically are flat, minimally hyperkeratotic, or filiform, wherein the base is narrow and the lesion is tall, growing at a 90° angle to the surface of the skin. On the arms and legs, warts usually present as round to oval papules with overlying thick hyperkeratosis and/or callosity.^3,4 Common warts usually are flesh colored or lighter, and heavily pigmented lesions should be evaluated dermoscopically for a pigment network and biopsied when pigment is present.⁵

In this article, a successful paradigm for management of pediatric warts is provided with enhanced outcomes based on further insight into the disease course and patient selection.

Epidemiology of Pediatric Warts

There are more than 200 types of human papillomaviruses (HPV), with more than 100 oncogenic types. There is quite a bit of homology by species and genus that contributes to cross-immunity and similar behavior between certain types of HPV. The lifetime incidence of warts is very high. Approximately 30% of children develop a wart.⁶ A review of the 2007 National Health Interview Survey of 9417 children demonstrated a steady increase in prevalence of warts from 1 to 2 years of age to 7 to 8 years of age, with a peak at 9 to 10 years of age and a plateau at 11 to 17 years of age. Warts were most common in non-Hispanic white children and less common in black children.⁷ In an in-person survey of 12,370 individuals aged 18 to 74 years from 5 European countries, warts were the most common physician-diagnosed (27.3%) and self-reported (41.0%) dermatologic condition. Warts are more common in Northern countries (eg, Netherlands, Germany).⁸ Children with atopic dermatitis have a higher risk of developing warts and extracutaneous infections. In one study, children with warts and atopic dermatitis had a higher number of infections and food allergies and higher incidence of asthma and hay fever than either condition alone.⁹

Clinical Presentation of Warts

Warts usually present as common, palmoplantar, flat, or filiform in childhood, but variations by age are common (eFigure). The common and palmoplantar variants often are caused by HPV types 1 and 2.^4,5 In infancy, vertically transmitted HPV infections can cause juvenile-onset respiratory papillomatosis or vertically transmitted condyloma. Juvenile-onset respiratory papillomatosis refers to upper respiratory papillomas that are difficult to eliminate and has been associated with exfoliated cervical cell testing with 18.1% (13/72) typed HPV-positive, which allows neonates to be exposed to HPV in the upper respiratory tract in utero.¹⁰

Vertically transmitted condyloma is a difficult topic. Much data supports the vertical transmission of condyloma as the leading cause of condyloma in small children; however, a reasonable amount of caution is needed in this patient population. In cases suspicious for sexual abuse as well as those presenting in children 4 years and older, formal household evaluation by a sexual abuse clinic and mandatory reporting is needed. Anywhere from 2.6% to 32% of cases of genital warts in children have been reported to be caused by sexual abuse.^11-13 Therefore, most investigators have recommended careful review of the patient’s history and socioeconomic circumstances as well as a thorough physical examination. Mandatory reporting of suspected child sexual abuse is required in suspicious cases. Because HPV type 16 has been found in vertically transmitted cases, concern for long-term oncogenesis exists.^11-13

Adolescents generally present with lesions on the hands and feet. Plantar warts often are caused by HPV types from the alpha genus. Subtypes noted in plantar warts include HPV types 1a, 2, 27, 57, and 65.¹⁴ By 15 years of age, genital HPV becomes a common adolescent infection, persisting into adulthood.¹⁵ When studied, genital HPV often is subclinical or latent and often is preventable through vaccination. High-risk oncogenic alpha-genus HPV types can immortalize human keratinocytes. When HPV types 11, 16, 18, and 31 are compared, HPV-18 has the highest oncogenic potential based on colony-stimulating potential.¹⁶ Vaccination with the 9-valent HPV vaccine is recommended in adolescence due to the concern for exposures to both low-potential (HPV types 6 and 11) and high-potential (HPV types 16 and 18) oncogenic HPV types. Data strongly support the benefit of 9-valent HPV vaccination in the prevention of sexually transmitted HPV in both males and females.¹⁷

Contagion of HPV is easy due to its excellent survival of fomites on surfaces, which generally is how warts are transferred in gym or pool settings where individuals who walk barefoot in changing rooms are almost twice as likely to contract plantar warts (odds ratio, 1.97 [95% CI, 1.39%-2.79%]).¹⁸ In another case series, walking barefoot, using a swimming pool, and having a household contact with warts were the leading risk factors for contraction of warts in children younger than 13 years.¹⁹ Children often transfer warts from site to site as well as to siblings and other close contacts. Skin-to-skin contact is responsible for sexual transmission of warts, and surface transmission occurs via fomites. Entry of the virus often occurs through small breaks in the skin. Other modes of transmission include orogenital.²⁰

Therapeutic Options

Although the nuances of each available treatment for pediatric warts are beyond the scope of this article, the main core of therapy is 1 of 3 approaches: (1) observation, (2) over-the-counter salicylic acid therapy, and (3) in-office cryotherapy. Observation is an affirmed style of therapy for warts, as it is expected that two-thirds of warts will spontaneously resolve in 2 years and three-quarters will resolve in 3 years.^4,5 Condyloma in children has been responsive to therapies such as cryotherapy and imiquimod,¹³ but spontaneous clearance in 5 years has been noted in 76% of children,²¹ which is linked to development of spontaneous immune response in most individuals.

Therapies for pediatric warts are characterized according to 6 major categories: destructive; immune stimulating; immune modulating, including normalization of epithelial growth; irritant; vascular destructive; and nitric oxide releasing (eTable).

Immune-Stimulating Therapies                                                                                                                                                                                                                         
Immune stimulants often are used to treat warts in children and adolescents who have many lesions, a prolonged disease course, disfigurement, and/or subungual localizations, as well as in those who have been treated with multiple destructive methods without success. Topical imiquimod and oral cimetidine are readily available, while squaric acid (at-home or in-office therapy) and intralesional candida antigen can be used in offices that carry these agents. Topical imiquimod has been reported to achieve success in genital warts in children,¹³ with good efficacy in recalcitrant, periungual, and subungual warts when used for up to 16 weeks.³¹ In one randomized clinical trial, imiquimod cream 5% combined with salicylic acid 15% was applied to warts for 6 to 10 hours for 5 consecutive days per week versus cryotherapy with liquid nitrogen every 2 weeks for a maximum of 3 months. At the end of the study period, 81.1% (30/37) of participants treated with imiquimod and salicylic acid showed clearance of their warts versus 67.3% (33/49) of those treated with cryotherapy.³²

Oral cimetidine has been reported to be successful in treating recalcitrant warts in more than 80% of children when dosed at 30 to 40 mg/kg 3 times daily, requiring 6 to 12 weeks to achieve clearance. Side effects of oral cimetidine include many cytochrome P450 interactions; gynecomastia, which limits usage in teenaged males; and stomach upset.³⁰

Treatment of recalcitrant pediatric warts with intralesional candida antigen has been associated with side effects consistent with delayed-type hypersensitivity reactions. Injections should be administered once monthly, with a minimum of 3 cycles if not effective and up to 6 cycles where partial efficacy is noted. In a retrospective review of 220 cases, 70.9% of children showed complete clearance and 16.8% had partial response.³³ However, the treatment may be limited in children by fear of needles.

Squaric acid dibutyl ester is a universal allergen that is not mutagenic on Ames testing and causes milder allergy symptoms than the mutagenic dinitrochlorobenzene and less erythema and pruritus than diphencyclopropenone. Squaric acid dibutyl ester home therapy was evaluated in 61 children with at least one nonfacial wart.³⁴ Application began with squaric acid dibutyl ester in acetone (SADBE) 2% sensitization on the arm followed by at-home application of SADBE 0.2% three to seven times weekly for a minimum of 2 months to determine benefit and for 3 to 4 months as needed; however, average response was 7 weeks. The average complete clearance was 58% and partial clearance was 18%. Side effects included erythema and mild itching as well as urticaria in one case.³⁴ In-office SADBE also has been evaluated in children. In a case series that included 29 children sensitized with SADBE 1% to 2% under occlusion followed by once monthly application of SADBE 0.5% to 5.0% to their warts, 69% clearance and 10% partial clearance was noted after a little more than 4 months of treatment.³⁵ One retrospective review compared combination SADBE, trichloroacetic acid (TCA), and cantharidin both alone and in combination as duos (eg, SADBE and TCA) or trios (SADBE, TCA, and cantharidin).²³ Of the 74 children whose medical charts were reviewed, the addition of pretreatment of warts with TCA 50% prior to in-office sensitization and monthly in-office application of SADBE increased treatment response to 100% with an average 2.45 months of therapy, whereas no enhancement was noted with cantharidin. Therefore, it appears that there may be enhanced immune reactivity when TCA pretreatment of warts is performed.²³

Immune-Modulating Therapies (Including Normalization of Epithelial Growth)
The most novel immunologic therapy for warts is plerixafor, an agent used to treat WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome, which has been linked to heterozygous gain of function mutations in the chemokine receptor CXCR4 (located on 2q22). In WHIM syndrome, the mutated CXCR4 is more sensitive to CXCL12 activation. Plerixafor is a selective reversible antagonist that blocks the capacity of the chemokine CXCL12 to sustain the permanent activation of CXCR4.³⁷ Combination therapy with plerixafor and topical imiquimod has resulted in wart improvement in WHIM syndrome patients in a small series.³⁸

Oral isotretinoin has been described to be efficacious over placebo at a dosage of 30 mg daily for 12 weeks and can be used in teenagers but requires standard monitoring.³⁶

Nitric Oxide–Releasing Therapies                                                                                                                                                                                                                         
Nitric oxide release may increase local blood flow, thereby increasing immune response, or may have a primary mechanism of antimicrobial activity, which is why these agents have been investigated for wart treatment. Topical garlic has been described anecdotally as a therapy for thin childhood warts with the putative mechanism being nitric oxide release.⁴² A new investigational drug recently has had phase 2 data published. Berdazimer sodium plus carboxymethyl cellulose hydrogel has demonstrated benefit in adult warts, but data in children is lacking.⁴¹

Therapeutic Ladder for Childhood Warts

The therapeutic ladder (Table) for childhood warts starts with first doing no harm. Although many parents are disturbed by their child’s condition, the natural history of resolution is spontaneous and therefore no therapy is required in many cases. The child and his/her caregivers should be engaged to determine if he/she is emotionally disturbed or uncomfortable with their lesions and to address any fears and concerns that some children may experience (eg, contagion risk, pain with ambulation, ostracism). For example, children with hand warts may report that other children will not hold their hand while in line at school. Prominent facial lesions can be particularly problematic for children due to teasing and bullying.

Conclusion

Warts are a common infection in childhood caused by the ubiquitous HPV virus. Therapeutic options abound, but most cases are either ignored or treated with over-the-counter salicylic acid or in-office cryotherapy. The decision to employ alternative therapeutic options requires agreement by the child, his/her caregiver, and the treating physician and can be tailored to suit the desires and needs of the child. Whether or not therapy is offered, spontaneous clearance is frequently seen in common warts. On the other hand, genital warts are associated with later conversion to malignancies of the genital tract; therefore, encouragement of HPV vaccination is needed in the adolescent population to best ensure long-term genital health.

The definition of warts is variable, largely reflecting their manifold appearance, biologic potential, and public health concerns. One vernacular dictionary defines warts as:

Small, benign growths caused by a vital infection of the skin or mucous membrane. The virus infects the surface layer. The viruses that cause warts are members of the human papilloma virus (HPV) family. Warts are not cancerous but some strains of HPV, usually not associated with warts, have been linked with cancer formation. Warts are contagious from person to person and from one area of the body to another on the same person.¹

The World Health Organization defines warts by their structural components as:

Human papillomavirus (HPV) is a small, non-enveloped deoxyribonucleic acid (DNA) virus that infects skin or mucosal cells. The circular, double-stranded viral genome is approximately 8-kb in length. The genome encodes for 6 early proteins responsible for virus replication and 2 late proteins, L1 and L2, which are the viral structural proteins.²

In pediatric and adolescent dermatology, warts often are defined by their location and morphology; for example, facial warts typically are flat, minimally hyperkeratotic, or filiform, wherein the base is narrow and the lesion is tall, growing at a 90° angle to the surface of the skin. On the arms and legs, warts usually present as round to oval papules with overlying thick hyperkeratosis and/or callosity.^3,4 Common warts usually are flesh colored or lighter, and heavily pigmented lesions should be evaluated dermoscopically for a pigment network and biopsied when pigment is present.⁵

In this article, a successful paradigm for management of pediatric warts is provided with enhanced outcomes based on further insight into the disease course and patient selection.

Epidemiology of Pediatric Warts

There are more than 200 types of human papillomaviruses (HPV), with more than 100 oncogenic types. There is quite a bit of homology by species and genus that contributes to cross-immunity and similar behavior between certain types of HPV. The lifetime incidence of warts is very high. Approximately 30% of children develop a wart.⁶ A review of the 2007 National Health Interview Survey of 9417 children demonstrated a steady increase in prevalence of warts from 1 to 2 years of age to 7 to 8 years of age, with a peak at 9 to 10 years of age and a plateau at 11 to 17 years of age. Warts were most common in non-Hispanic white children and less common in black children.⁷ In an in-person survey of 12,370 individuals aged 18 to 74 years from 5 European countries, warts were the most common physician-diagnosed (27.3%) and self-reported (41.0%) dermatologic condition. Warts are more common in Northern countries (eg, Netherlands, Germany).⁸ Children with atopic dermatitis have a higher risk of developing warts and extracutaneous infections. In one study, children with warts and atopic dermatitis had a higher number of infections and food allergies and higher incidence of asthma and hay fever than either condition alone.⁹

Clinical Presentation of Warts

Warts usually present as common, palmoplantar, flat, or filiform in childhood, but variations by age are common (eFigure). The common and palmoplantar variants often are caused by HPV types 1 and 2.^4,5 In infancy, vertically transmitted HPV infections can cause juvenile-onset respiratory papillomatosis or vertically transmitted condyloma. Juvenile-onset respiratory papillomatosis refers to upper respiratory papillomas that are difficult to eliminate and has been associated with exfoliated cervical cell testing with 18.1% (13/72) typed HPV-positive, which allows neonates to be exposed to HPV in the upper respiratory tract in utero.¹⁰

Vertically transmitted condyloma is a difficult topic. Much data supports the vertical transmission of condyloma as the leading cause of condyloma in small children; however, a reasonable amount of caution is needed in this patient population. In cases suspicious for sexual abuse as well as those presenting in children 4 years and older, formal household evaluation by a sexual abuse clinic and mandatory reporting is needed. Anywhere from 2.6% to 32% of cases of genital warts in children have been reported to be caused by sexual abuse.^11-13 Therefore, most investigators have recommended careful review of the patient’s history and socioeconomic circumstances as well as a thorough physical examination. Mandatory reporting of suspected child sexual abuse is required in suspicious cases. Because HPV type 16 has been found in vertically transmitted cases, concern for long-term oncogenesis exists.^11-13

Adolescents generally present with lesions on the hands and feet. Plantar warts often are caused by HPV types from the alpha genus. Subtypes noted in plantar warts include HPV types 1a, 2, 27, 57, and 65.¹⁴ By 15 years of age, genital HPV becomes a common adolescent infection, persisting into adulthood.¹⁵ When studied, genital HPV often is subclinical or latent and often is preventable through vaccination. High-risk oncogenic alpha-genus HPV types can immortalize human keratinocytes. When HPV types 11, 16, 18, and 31 are compared, HPV-18 has the highest oncogenic potential based on colony-stimulating potential.¹⁶ Vaccination with the 9-valent HPV vaccine is recommended in adolescence due to the concern for exposures to both low-potential (HPV types 6 and 11) and high-potential (HPV types 16 and 18) oncogenic HPV types. Data strongly support the benefit of 9-valent HPV vaccination in the prevention of sexually transmitted HPV in both males and females.¹⁷

Contagion of HPV is easy due to its excellent survival of fomites on surfaces, which generally is how warts are transferred in gym or pool settings where individuals who walk barefoot in changing rooms are almost twice as likely to contract plantar warts (odds ratio, 1.97 [95% CI, 1.39%-2.79%]).¹⁸ In another case series, walking barefoot, using a swimming pool, and having a household contact with warts were the leading risk factors for contraction of warts in children younger than 13 years.¹⁹ Children often transfer warts from site to site as well as to siblings and other close contacts. Skin-to-skin contact is responsible for sexual transmission of warts, and surface transmission occurs via fomites. Entry of the virus often occurs through small breaks in the skin. Other modes of transmission include orogenital.²⁰

Therapeutic Options

Although the nuances of each available treatment for pediatric warts are beyond the scope of this article, the main core of therapy is 1 of 3 approaches: (1) observation, (2) over-the-counter salicylic acid therapy, and (3) in-office cryotherapy. Observation is an affirmed style of therapy for warts, as it is expected that two-thirds of warts will spontaneously resolve in 2 years and three-quarters will resolve in 3 years.^4,5 Condyloma in children has been responsive to therapies such as cryotherapy and imiquimod,¹³ but spontaneous clearance in 5 years has been noted in 76% of children,²¹ which is linked to development of spontaneous immune response in most individuals.

Therapies for pediatric warts are characterized according to 6 major categories: destructive; immune stimulating; immune modulating, including normalization of epithelial growth; irritant; vascular destructive; and nitric oxide releasing (eTable).

Immune-Stimulating Therapies                                                                                                                                                                                                                         
Immune stimulants often are used to treat warts in children and adolescents who have many lesions, a prolonged disease course, disfigurement, and/or subungual localizations, as well as in those who have been treated with multiple destructive methods without success. Topical imiquimod and oral cimetidine are readily available, while squaric acid (at-home or in-office therapy) and intralesional candida antigen can be used in offices that carry these agents. Topical imiquimod has been reported to achieve success in genital warts in children,¹³ with good efficacy in recalcitrant, periungual, and subungual warts when used for up to 16 weeks.³¹ In one randomized clinical trial, imiquimod cream 5% combined with salicylic acid 15% was applied to warts for 6 to 10 hours for 5 consecutive days per week versus cryotherapy with liquid nitrogen every 2 weeks for a maximum of 3 months. At the end of the study period, 81.1% (30/37) of participants treated with imiquimod and salicylic acid showed clearance of their warts versus 67.3% (33/49) of those treated with cryotherapy.³²

Oral cimetidine has been reported to be successful in treating recalcitrant warts in more than 80% of children when dosed at 30 to 40 mg/kg 3 times daily, requiring 6 to 12 weeks to achieve clearance. Side effects of oral cimetidine include many cytochrome P450 interactions; gynecomastia, which limits usage in teenaged males; and stomach upset.³⁰

Treatment of recalcitrant pediatric warts with intralesional candida antigen has been associated with side effects consistent with delayed-type hypersensitivity reactions. Injections should be administered once monthly, with a minimum of 3 cycles if not effective and up to 6 cycles where partial efficacy is noted. In a retrospective review of 220 cases, 70.9% of children showed complete clearance and 16.8% had partial response.³³ However, the treatment may be limited in children by fear of needles.

Squaric acid dibutyl ester is a universal allergen that is not mutagenic on Ames testing and causes milder allergy symptoms than the mutagenic dinitrochlorobenzene and less erythema and pruritus than diphencyclopropenone. Squaric acid dibutyl ester home therapy was evaluated in 61 children with at least one nonfacial wart.³⁴ Application began with squaric acid dibutyl ester in acetone (SADBE) 2% sensitization on the arm followed by at-home application of SADBE 0.2% three to seven times weekly for a minimum of 2 months to determine benefit and for 3 to 4 months as needed; however, average response was 7 weeks. The average complete clearance was 58% and partial clearance was 18%. Side effects included erythema and mild itching as well as urticaria in one case.³⁴ In-office SADBE also has been evaluated in children. In a case series that included 29 children sensitized with SADBE 1% to 2% under occlusion followed by once monthly application of SADBE 0.5% to 5.0% to their warts, 69% clearance and 10% partial clearance was noted after a little more than 4 months of treatment.³⁵ One retrospective review compared combination SADBE, trichloroacetic acid (TCA), and cantharidin both alone and in combination as duos (eg, SADBE and TCA) or trios (SADBE, TCA, and cantharidin).²³ Of the 74 children whose medical charts were reviewed, the addition of pretreatment of warts with TCA 50% prior to in-office sensitization and monthly in-office application of SADBE increased treatment response to 100% with an average 2.45 months of therapy, whereas no enhancement was noted with cantharidin. Therefore, it appears that there may be enhanced immune reactivity when TCA pretreatment of warts is performed.²³

Immune-Modulating Therapies (Including Normalization of Epithelial Growth)
The most novel immunologic therapy for warts is plerixafor, an agent used to treat WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome, which has been linked to heterozygous gain of function mutations in the chemokine receptor CXCR4 (located on 2q22). In WHIM syndrome, the mutated CXCR4 is more sensitive to CXCL12 activation. Plerixafor is a selective reversible antagonist that blocks the capacity of the chemokine CXCL12 to sustain the permanent activation of CXCR4.³⁷ Combination therapy with plerixafor and topical imiquimod has resulted in wart improvement in WHIM syndrome patients in a small series.³⁸

Oral isotretinoin has been described to be efficacious over placebo at a dosage of 30 mg daily for 12 weeks and can be used in teenagers but requires standard monitoring.³⁶

Nitric Oxide–Releasing Therapies                                                                                                                                                                                                                         
Nitric oxide release may increase local blood flow, thereby increasing immune response, or may have a primary mechanism of antimicrobial activity, which is why these agents have been investigated for wart treatment. Topical garlic has been described anecdotally as a therapy for thin childhood warts with the putative mechanism being nitric oxide release.⁴² A new investigational drug recently has had phase 2 data published. Berdazimer sodium plus carboxymethyl cellulose hydrogel has demonstrated benefit in adult warts, but data in children is lacking.⁴¹

Therapeutic Ladder for Childhood Warts

The therapeutic ladder (Table) for childhood warts starts with first doing no harm. Although many parents are disturbed by their child’s condition, the natural history of resolution is spontaneous and therefore no therapy is required in many cases. The child and his/her caregivers should be engaged to determine if he/she is emotionally disturbed or uncomfortable with their lesions and to address any fears and concerns that some children may experience (eg, contagion risk, pain with ambulation, ostracism). For example, children with hand warts may report that other children will not hold their hand while in line at school. Prominent facial lesions can be particularly problematic for children due to teasing and bullying.

Conclusion

Warts are a common infection in childhood caused by the ubiquitous HPV virus. Therapeutic options abound, but most cases are either ignored or treated with over-the-counter salicylic acid or in-office cryotherapy. The decision to employ alternative therapeutic options requires agreement by the child, his/her caregiver, and the treating physician and can be tailored to suit the desires and needs of the child. Whether or not therapy is offered, spontaneous clearance is frequently seen in common warts. On the other hand, genital warts are associated with later conversion to malignancies of the genital tract; therefore, encouragement of HPV vaccination is needed in the adolescent population to best ensure long-term genital health.

The definition of warts is variable, largely reflecting their manifold appearance, biologic potential, and public health concerns. One vernacular dictionary defines warts as:

Small, benign growths caused by a vital infection of the skin or mucous membrane. The virus infects the surface layer. The viruses that cause warts are members of the human papilloma virus (HPV) family. Warts are not cancerous but some strains of HPV, usually not associated with warts, have been linked with cancer formation. Warts are contagious from person to person and from one area of the body to another on the same person.¹

The World Health Organization defines warts by their structural components as:

Human papillomavirus (HPV) is a small, non-enveloped deoxyribonucleic acid (DNA) virus that infects skin or mucosal cells. The circular, double-stranded viral genome is approximately 8-kb in length. The genome encodes for 6 early proteins responsible for virus replication and 2 late proteins, L1 and L2, which are the viral structural proteins.²

In pediatric and adolescent dermatology, warts often are defined by their location and morphology; for example, facial warts typically are flat, minimally hyperkeratotic, or filiform, wherein the base is narrow and the lesion is tall, growing at a 90° angle to the surface of the skin. On the arms and legs, warts usually present as round to oval papules with overlying thick hyperkeratosis and/or callosity.^3,4 Common warts usually are flesh colored or lighter, and heavily pigmented lesions should be evaluated dermoscopically for a pigment network and biopsied when pigment is present.⁵

In this article, a successful paradigm for management of pediatric warts is provided with enhanced outcomes based on further insight into the disease course and patient selection.

Epidemiology of Pediatric Warts

There are more than 200 types of human papillomaviruses (HPV), with more than 100 oncogenic types. There is quite a bit of homology by species and genus that contributes to cross-immunity and similar behavior between certain types of HPV. The lifetime incidence of warts is very high. Approximately 30% of children develop a wart.⁶ A review of the 2007 National Health Interview Survey of 9417 children demonstrated a steady increase in prevalence of warts from 1 to 2 years of age to 7 to 8 years of age, with a peak at 9 to 10 years of age and a plateau at 11 to 17 years of age. Warts were most common in non-Hispanic white children and less common in black children.⁷ In an in-person survey of 12,370 individuals aged 18 to 74 years from 5 European countries, warts were the most common physician-diagnosed (27.3%) and self-reported (41.0%) dermatologic condition. Warts are more common in Northern countries (eg, Netherlands, Germany).⁸ Children with atopic dermatitis have a higher risk of developing warts and extracutaneous infections. In one study, children with warts and atopic dermatitis had a higher number of infections and food allergies and higher incidence of asthma and hay fever than either condition alone.⁹

Clinical Presentation of Warts

Warts usually present as common, palmoplantar, flat, or filiform in childhood, but variations by age are common (eFigure). The common and palmoplantar variants often are caused by HPV types 1 and 2.^4,5 In infancy, vertically transmitted HPV infections can cause juvenile-onset respiratory papillomatosis or vertically transmitted condyloma. Juvenile-onset respiratory papillomatosis refers to upper respiratory papillomas that are difficult to eliminate and has been associated with exfoliated cervical cell testing with 18.1% (13/72) typed HPV-positive, which allows neonates to be exposed to HPV in the upper respiratory tract in utero.¹⁰

Vertically transmitted condyloma is a difficult topic. Much data supports the vertical transmission of condyloma as the leading cause of condyloma in small children; however, a reasonable amount of caution is needed in this patient population. In cases suspicious for sexual abuse as well as those presenting in children 4 years and older, formal household evaluation by a sexual abuse clinic and mandatory reporting is needed. Anywhere from 2.6% to 32% of cases of genital warts in children have been reported to be caused by sexual abuse.^11-13 Therefore, most investigators have recommended careful review of the patient’s history and socioeconomic circumstances as well as a thorough physical examination. Mandatory reporting of suspected child sexual abuse is required in suspicious cases. Because HPV type 16 has been found in vertically transmitted cases, concern for long-term oncogenesis exists.^11-13

Adolescents generally present with lesions on the hands and feet. Plantar warts often are caused by HPV types from the alpha genus. Subtypes noted in plantar warts include HPV types 1a, 2, 27, 57, and 65.¹⁴ By 15 years of age, genital HPV becomes a common adolescent infection, persisting into adulthood.¹⁵ When studied, genital HPV often is subclinical or latent and often is preventable through vaccination. High-risk oncogenic alpha-genus HPV types can immortalize human keratinocytes. When HPV types 11, 16, 18, and 31 are compared, HPV-18 has the highest oncogenic potential based on colony-stimulating potential.¹⁶ Vaccination with the 9-valent HPV vaccine is recommended in adolescence due to the concern for exposures to both low-potential (HPV types 6 and 11) and high-potential (HPV types 16 and 18) oncogenic HPV types. Data strongly support the benefit of 9-valent HPV vaccination in the prevention of sexually transmitted HPV in both males and females.¹⁷

Contagion of HPV is easy due to its excellent survival of fomites on surfaces, which generally is how warts are transferred in gym or pool settings where individuals who walk barefoot in changing rooms are almost twice as likely to contract plantar warts (odds ratio, 1.97 [95% CI, 1.39%-2.79%]).¹⁸ In another case series, walking barefoot, using a swimming pool, and having a household contact with warts were the leading risk factors for contraction of warts in children younger than 13 years.¹⁹ Children often transfer warts from site to site as well as to siblings and other close contacts. Skin-to-skin contact is responsible for sexual transmission of warts, and surface transmission occurs via fomites. Entry of the virus often occurs through small breaks in the skin. Other modes of transmission include orogenital.²⁰

Therapeutic Options

Although the nuances of each available treatment for pediatric warts are beyond the scope of this article, the main core of therapy is 1 of 3 approaches: (1) observation, (2) over-the-counter salicylic acid therapy, and (3) in-office cryotherapy. Observation is an affirmed style of therapy for warts, as it is expected that two-thirds of warts will spontaneously resolve in 2 years and three-quarters will resolve in 3 years.^4,5 Condyloma in children has been responsive to therapies such as cryotherapy and imiquimod,¹³ but spontaneous clearance in 5 years has been noted in 76% of children,²¹ which is linked to development of spontaneous immune response in most individuals.

Therapies for pediatric warts are characterized according to 6 major categories: destructive; immune stimulating; immune modulating, including normalization of epithelial growth; irritant; vascular destructive; and nitric oxide releasing (eTable).

Immune-Stimulating Therapies                                                                                                                                                                                                                         
Immune stimulants often are used to treat warts in children and adolescents who have many lesions, a prolonged disease course, disfigurement, and/or subungual localizations, as well as in those who have been treated with multiple destructive methods without success. Topical imiquimod and oral cimetidine are readily available, while squaric acid (at-home or in-office therapy) and intralesional candida antigen can be used in offices that carry these agents. Topical imiquimod has been reported to achieve success in genital warts in children,¹³ with good efficacy in recalcitrant, periungual, and subungual warts when used for up to 16 weeks.³¹ In one randomized clinical trial, imiquimod cream 5% combined with salicylic acid 15% was applied to warts for 6 to 10 hours for 5 consecutive days per week versus cryotherapy with liquid nitrogen every 2 weeks for a maximum of 3 months. At the end of the study period, 81.1% (30/37) of participants treated with imiquimod and salicylic acid showed clearance of their warts versus 67.3% (33/49) of those treated with cryotherapy.³²

Oral cimetidine has been reported to be successful in treating recalcitrant warts in more than 80% of children when dosed at 30 to 40 mg/kg 3 times daily, requiring 6 to 12 weeks to achieve clearance. Side effects of oral cimetidine include many cytochrome P450 interactions; gynecomastia, which limits usage in teenaged males; and stomach upset.³⁰

Treatment of recalcitrant pediatric warts with intralesional candida antigen has been associated with side effects consistent with delayed-type hypersensitivity reactions. Injections should be administered once monthly, with a minimum of 3 cycles if not effective and up to 6 cycles where partial efficacy is noted. In a retrospective review of 220 cases, 70.9% of children showed complete clearance and 16.8% had partial response.³³ However, the treatment may be limited in children by fear of needles.

Squaric acid dibutyl ester is a universal allergen that is not mutagenic on Ames testing and causes milder allergy symptoms than the mutagenic dinitrochlorobenzene and less erythema and pruritus than diphencyclopropenone. Squaric acid dibutyl ester home therapy was evaluated in 61 children with at least one nonfacial wart.³⁴ Application began with squaric acid dibutyl ester in acetone (SADBE) 2% sensitization on the arm followed by at-home application of SADBE 0.2% three to seven times weekly for a minimum of 2 months to determine benefit and for 3 to 4 months as needed; however, average response was 7 weeks. The average complete clearance was 58% and partial clearance was 18%. Side effects included erythema and mild itching as well as urticaria in one case.³⁴ In-office SADBE also has been evaluated in children. In a case series that included 29 children sensitized with SADBE 1% to 2% under occlusion followed by once monthly application of SADBE 0.5% to 5.0% to their warts, 69% clearance and 10% partial clearance was noted after a little more than 4 months of treatment.³⁵ One retrospective review compared combination SADBE, trichloroacetic acid (TCA), and cantharidin both alone and in combination as duos (eg, SADBE and TCA) or trios (SADBE, TCA, and cantharidin).²³ Of the 74 children whose medical charts were reviewed, the addition of pretreatment of warts with TCA 50% prior to in-office sensitization and monthly in-office application of SADBE increased treatment response to 100% with an average 2.45 months of therapy, whereas no enhancement was noted with cantharidin. Therefore, it appears that there may be enhanced immune reactivity when TCA pretreatment of warts is performed.²³

Immune-Modulating Therapies (Including Normalization of Epithelial Growth)
The most novel immunologic therapy for warts is plerixafor, an agent used to treat WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome, which has been linked to heterozygous gain of function mutations in the chemokine receptor CXCR4 (located on 2q22). In WHIM syndrome, the mutated CXCR4 is more sensitive to CXCL12 activation. Plerixafor is a selective reversible antagonist that blocks the capacity of the chemokine CXCL12 to sustain the permanent activation of CXCR4.³⁷ Combination therapy with plerixafor and topical imiquimod has resulted in wart improvement in WHIM syndrome patients in a small series.³⁸

Oral isotretinoin has been described to be efficacious over placebo at a dosage of 30 mg daily for 12 weeks and can be used in teenagers but requires standard monitoring.³⁶

Nitric Oxide–Releasing Therapies                                                                                                                                                                                                                         
Nitric oxide release may increase local blood flow, thereby increasing immune response, or may have a primary mechanism of antimicrobial activity, which is why these agents have been investigated for wart treatment. Topical garlic has been described anecdotally as a therapy for thin childhood warts with the putative mechanism being nitric oxide release.⁴² A new investigational drug recently has had phase 2 data published. Berdazimer sodium plus carboxymethyl cellulose hydrogel has demonstrated benefit in adult warts, but data in children is lacking.⁴¹

Therapeutic Ladder for Childhood Warts

The therapeutic ladder (Table) for childhood warts starts with first doing no harm. Although many parents are disturbed by their child’s condition, the natural history of resolution is spontaneous and therefore no therapy is required in many cases. The child and his/her caregivers should be engaged to determine if he/she is emotionally disturbed or uncomfortable with their lesions and to address any fears and concerns that some children may experience (eg, contagion risk, pain with ambulation, ostracism). For example, children with hand warts may report that other children will not hold their hand while in line at school. Prominent facial lesions can be particularly problematic for children due to teasing and bullying.

Conclusion

Warts are a common infection in childhood caused by the ubiquitous HPV virus. Therapeutic options abound, but most cases are either ignored or treated with over-the-counter salicylic acid or in-office cryotherapy. The decision to employ alternative therapeutic options requires agreement by the child, his/her caregiver, and the treating physician and can be tailored to suit the desires and needs of the child. Whether or not therapy is offered, spontaneous clearance is frequently seen in common warts. On the other hand, genital warts are associated with later conversion to malignancies of the genital tract; therefore, encouragement of HPV vaccination is needed in the adolescent population to best ensure long-term genital health.

In a national health care environment undergoing unprecedented transformation, the specialty of hospital medicine appears to be an island of relative stability, a conclusion that is supported by the principal findings from SHM’s 2018 State of Hospital Medicine (SoHM) report.

The report of hospitalist group practice characteristics, as well as other key data defining the field’s current status, that the Society of Hospital Medicine puts out every 2 years reveals that overall salaries for hospitalist physicians are up by 3.8% since 2016. Although productivity, as measured by work relative value units (RVUs), remained largely flat over the same period, financial support per full-time equivalent (FTE) physician position to hospitalist groups from their hospitals and health systems is up significantly.

Total support per FTE averaged $176,657 in 2018, 12% higher than in 2016, noted Leslie Flores, MHA, SFHM, of Nelson Flores Hospital Medicine Consultants, and a member of SHM’s Practice Analysis Committee, which oversees the biennial survey. Compensation and productivity data were collected by the Medical Group Management Association and licensed by SHM for inclusion in its report.

How do hospitalists use the SoHM report?

Dr. White called the 2018 SoHM report the “most representative and balanced sample to date” of hospitalist group practices, with some of the highest quality data, thanks to more robust participation in the survey by pediatric groups and improved distribution among hospitalist management companies and academic programs.

“Not that past reports had major flaws, but this version is more authoritative, reflecting an intentional effort by our Practice Analysis Committee to bring in more participants from key groups,” he said.

The biennial report has been around long enough to achieve brand recognition in the field as the most authoritative source of information regarding hospitalist practice, he added. “We worked hard this year to balance the participants, with more of our responses than in the past coming from multi-hospital groups, whether 4 to 5 sites, or 20 to 30.”

Surveys were conducted online in January and February of 2018 in response to invitations mailed and emailed to targeted hospital medicine group leaders. A total of 569 groups completed the survey, representing 8,889 hospitalist FTEs, approximately 16% of the total hospitalist workforce. Responses were presented in several categories, including by size of program, region and employment model. Groups that care for adults only represented 87.9% of the surveys, while groups that care for children only were 6.7% and groups that care for both adults and children were 5.4%.

Calls for more productivity

Roberta Himebaugh, MBA, SFHM, senior vice president of acute care services for the national hospitalist management company TeamHealth, and cochair of the SHM Practice Administrators Special Interest Group, said her company’s clients have traditionally asked for greater productivity from their hospitalist contracts as a way to decrease overall costs. Some markets are starting to see a change in that approach, she noted.

“Recently there’s been an increased focus on paying hospitalists to focus on quality rather than just productivity. Some of our clients are willing to pay for that, and we are trying to assign value to this non-billable time or adjust our productivity standards appropriately. I think hospitals definitely understand the value of non-billable services from hospitalists, but still will push us on the productivity targets,” Ms. Himebaugh said.

How is hospitalist practice evolving?

In addition to payment and productivity data, the SoHM report provides a current picture of the evolving state of hospitalist group practices. A key thread is how the work hospitalists are doing, and the way they do it, is changing, with new information about comanagement roles, dedicated admitters, night coverage, geographic rounding, and the like.

Making greater use of nurse practitioners and physician assistants (NPs/PAs), may be one way to change the flat productivity trends, Dr. Brown said. With a cost per RVU that’s roughly half that of a doctor’s, NPs/PAs could contribute to the bottom line. But he sees surprisingly large variation in how hospitalist groups are using them. Typically, they are deployed at a ratio of four doctors to one NP/PA, but that ratio could be two to one or even one to one, he said.

The predominant scheduling model of hospital medicine, 7 days on duty followed by 7 days off, has diminished somewhat in recent years. There appears to be some fluctuation and a gradual move away from 7 on/7 off toward some kind of variable approach, since the former may not be physically sustainable for the doctor over the long haul, Dr. Brown said. Some groups are experimenting with a combined approach.

“I think balancing workload with manpower has always been a challenge for our field. Maybe we should be working shorter shifts or fewer days and making sure our hospitalists aren’t ever sitting around idle,” he said. “And could we come in on nonclinical days to do administrative tasks? I think the solution is out there, but we haven’t created the algorithms to define that yet. If you could somehow use the data for volume, number of beds, nurse staffing, etc., by year and seasonally, you might be able to reliably predict census. This is about applying data hospitals already have in their electronic health records, but utilizing the data in ways that are more helpful.”

Dr. McIlraith added that a big driver of the future of hospital medicine will be the evolution of the EHR and the digitalization of health care, as hospitals learn how to leverage more of what’s in their EHRs. “The impact will grow for hospitalists through the creation and maturation of big data systems – and the learning that can be extracted from what’s contained in the electronic health record.”

Another important question for hospitalist groups is their model of backup scheduling, to make sure there is a replacement available if a scheduled doctor calls in sick or if demand is unexpectedly high.

“In today’s world, this is how we have traditionally managed unpredictability,” Dr. Brown said. “You don’t know when you will need it, but if you need it, you want it immediately. So how do you pay for it – only when the doctor comes in, or also an amount just for being on call?” Some groups pay for both, he said, others for neither.

“We are a group of 70 hospitalists, and if someone is sick you can’t just shut down the service,” said Dr. Chadha. “We are one of the few to use incentives for both, which could include a 1-week decrease in clinical shifts in exchange for 2 weeks of backup. We have times with 25% usage of backup number 1, and 10% usage of backup number 2,” he noted. “But the goal is for our hospitalists to have assurances that there is a backup system and that it works.”

The presence of nocturnists in hospitals continues to rise, with 76.1% of adults-only groups having nocturnists, 27.6% of children-only groups, and 68.2% of adults and children groups. Geographic or unit-based hospital assignments have grown to 36.4% of adult-only groups.

What are hospitalists’ other new roles?

“We have a large group of 50 doctors, with about 40 FTEs, and we are evolving from the traditional generalist role toward more subspecialty comanagement,” said Bryan Huang, MD, physician adviser and associate clinical professor in the division of hospital medicine at the University of California–San Diego. “Our hospitalists are asking what it means to be an academic hospitalist as our teaching roles have shrunk.”

Dr. Huang recently took on a new role as physician adviser for his hospital in such areas as utilization review, patient flow, and length of stay. “I’m spearheading a work group to address quality issues – all of which involve collaboration with other professionals. We also developed an admitting role here for a hospitalist whose sole role for the day is to admit patients.” Nationally up to 51.2% of hospitalist groups utilize a dedicated daytime admitter.

The report found that hospital services for which hospitalists are more likely to be attendings than consultants include GI/liver, 78.4%; palliative care, 77.3%; neurology/stroke, 73.6%; oncology, 67.8%; cardiology, 56.9%; and critical care, 50.7%. Conditions where hospitalists are more likely to consult rather than admit and attend include neurosurgery, orthopedics, general surgery, cardiovascular surgery, and other surgical subspecialties.

Other hospital services routinely provided by adult-only hospitalists include care of patients in an ICU setting (62.7%); primary responsibility for observation units (54.6%); primary clinical responsibility for rapid response teams (48.8%); primary responsibility for code blue or cardiac arrest teams (43.8%); nighttime admissions or tuck-in services (33.9%); and medical procedures (31.5%). For pediatric hospital medicine groups, care of healthy newborns and medical procedures were among the most common services provided, while for hospitalists serving adults and children, rapid response teams, ICUs, and specialty units were most common.

New models of payment for health care

As the larger health care system is being transformed by new payment models and benefit structures, including accountable care organizations (ACOs), value-based purchasing, bundled payments, and other forms of population-based coverage – which is described as a volume-to-value shift in health care – how are these new models affecting hospitalists?

Observers say penetration of these new models varies widely by locality but they haven’t had much direct impact on hospitalists’ practices – at least not yet. However, as hospitals and health systems find themselves needing to learn new ways to invest their resources differently in response to these trends, what matters to the hospital should be of great importance to the hospitalist group.

“I haven’t seen a lot of dramatic changes in how hospitalists engage with value-based purchasing,” Dr. White said. “If we know that someone is part of an ACO, the instinctual – and right – response is to treat them like any other patient. But we still need to be committed to not waste resources.”

Hospitalists are the best people to understand the intricacies of how the health care system works under value-based approaches, Dr. Huang said. “That’s why so many hospitalists have taken leadership positions in their hospitals. I think all of this translates to the practical, day-to-day work of hospitalists, reflected in our focus on readmissions and length of stay.”

Dr. Williams said the health care system still hasn’t turned the corner from fee-for-service to value-based purchasing. “It still represents a tiny fraction of the income of hospitalists. Hospitals still have to focus on the bottom line, as fee-for-service reimbursement for hospitalized patients continues to get squeezed, and ACOs aren’t exactly paying premium rates either. Ask almost any hospital CEO what drives their bottom line today and the answer is volume – along with optimizing productivity. Pretty much every place I look, the future does not look terribly rosy for hospitals.”

Ms. Himebaugh said she is bullish on hospital medicine, in the sense that it’s unlikely to go away anytime soon. “Hospitalists are needed and provide value. But I don’t think we have devised the right model yet. I’m not sure our current model is sustainable. We need to find new models we can afford that don’t require squeezing our providers.”

For more information about the 2018 State of Hospital Medicine Report, contact SHM’s Practice Management Department at: survey@hospitalmedicine.org or call 800-843-3360. See also: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/.

In a national health care environment undergoing unprecedented transformation, the specialty of hospital medicine appears to be an island of relative stability, a conclusion that is supported by the principal findings from SHM’s 2018 State of Hospital Medicine (SoHM) report.

The report of hospitalist group practice characteristics, as well as other key data defining the field’s current status, that the Society of Hospital Medicine puts out every 2 years reveals that overall salaries for hospitalist physicians are up by 3.8% since 2016. Although productivity, as measured by work relative value units (RVUs), remained largely flat over the same period, financial support per full-time equivalent (FTE) physician position to hospitalist groups from their hospitals and health systems is up significantly.

Total support per FTE averaged $176,657 in 2018, 12% higher than in 2016, noted Leslie Flores, MHA, SFHM, of Nelson Flores Hospital Medicine Consultants, and a member of SHM’s Practice Analysis Committee, which oversees the biennial survey. Compensation and productivity data were collected by the Medical Group Management Association and licensed by SHM for inclusion in its report.

How do hospitalists use the SoHM report?

Dr. White called the 2018 SoHM report the “most representative and balanced sample to date” of hospitalist group practices, with some of the highest quality data, thanks to more robust participation in the survey by pediatric groups and improved distribution among hospitalist management companies and academic programs.

“Not that past reports had major flaws, but this version is more authoritative, reflecting an intentional effort by our Practice Analysis Committee to bring in more participants from key groups,” he said.

The biennial report has been around long enough to achieve brand recognition in the field as the most authoritative source of information regarding hospitalist practice, he added. “We worked hard this year to balance the participants, with more of our responses than in the past coming from multi-hospital groups, whether 4 to 5 sites, or 20 to 30.”

Surveys were conducted online in January and February of 2018 in response to invitations mailed and emailed to targeted hospital medicine group leaders. A total of 569 groups completed the survey, representing 8,889 hospitalist FTEs, approximately 16% of the total hospitalist workforce. Responses were presented in several categories, including by size of program, region and employment model. Groups that care for adults only represented 87.9% of the surveys, while groups that care for children only were 6.7% and groups that care for both adults and children were 5.4%.

Calls for more productivity

Roberta Himebaugh, MBA, SFHM, senior vice president of acute care services for the national hospitalist management company TeamHealth, and cochair of the SHM Practice Administrators Special Interest Group, said her company’s clients have traditionally asked for greater productivity from their hospitalist contracts as a way to decrease overall costs. Some markets are starting to see a change in that approach, she noted.

“Recently there’s been an increased focus on paying hospitalists to focus on quality rather than just productivity. Some of our clients are willing to pay for that, and we are trying to assign value to this non-billable time or adjust our productivity standards appropriately. I think hospitals definitely understand the value of non-billable services from hospitalists, but still will push us on the productivity targets,” Ms. Himebaugh said.

How is hospitalist practice evolving?

In addition to payment and productivity data, the SoHM report provides a current picture of the evolving state of hospitalist group practices. A key thread is how the work hospitalists are doing, and the way they do it, is changing, with new information about comanagement roles, dedicated admitters, night coverage, geographic rounding, and the like.

Making greater use of nurse practitioners and physician assistants (NPs/PAs), may be one way to change the flat productivity trends, Dr. Brown said. With a cost per RVU that’s roughly half that of a doctor’s, NPs/PAs could contribute to the bottom line. But he sees surprisingly large variation in how hospitalist groups are using them. Typically, they are deployed at a ratio of four doctors to one NP/PA, but that ratio could be two to one or even one to one, he said.

The predominant scheduling model of hospital medicine, 7 days on duty followed by 7 days off, has diminished somewhat in recent years. There appears to be some fluctuation and a gradual move away from 7 on/7 off toward some kind of variable approach, since the former may not be physically sustainable for the doctor over the long haul, Dr. Brown said. Some groups are experimenting with a combined approach.

“I think balancing workload with manpower has always been a challenge for our field. Maybe we should be working shorter shifts or fewer days and making sure our hospitalists aren’t ever sitting around idle,” he said. “And could we come in on nonclinical days to do administrative tasks? I think the solution is out there, but we haven’t created the algorithms to define that yet. If you could somehow use the data for volume, number of beds, nurse staffing, etc., by year and seasonally, you might be able to reliably predict census. This is about applying data hospitals already have in their electronic health records, but utilizing the data in ways that are more helpful.”

Dr. McIlraith added that a big driver of the future of hospital medicine will be the evolution of the EHR and the digitalization of health care, as hospitals learn how to leverage more of what’s in their EHRs. “The impact will grow for hospitalists through the creation and maturation of big data systems – and the learning that can be extracted from what’s contained in the electronic health record.”

Another important question for hospitalist groups is their model of backup scheduling, to make sure there is a replacement available if a scheduled doctor calls in sick or if demand is unexpectedly high.

“In today’s world, this is how we have traditionally managed unpredictability,” Dr. Brown said. “You don’t know when you will need it, but if you need it, you want it immediately. So how do you pay for it – only when the doctor comes in, or also an amount just for being on call?” Some groups pay for both, he said, others for neither.

“We are a group of 70 hospitalists, and if someone is sick you can’t just shut down the service,” said Dr. Chadha. “We are one of the few to use incentives for both, which could include a 1-week decrease in clinical shifts in exchange for 2 weeks of backup. We have times with 25% usage of backup number 1, and 10% usage of backup number 2,” he noted. “But the goal is for our hospitalists to have assurances that there is a backup system and that it works.”

The presence of nocturnists in hospitals continues to rise, with 76.1% of adults-only groups having nocturnists, 27.6% of children-only groups, and 68.2% of adults and children groups. Geographic or unit-based hospital assignments have grown to 36.4% of adult-only groups.

What are hospitalists’ other new roles?

“We have a large group of 50 doctors, with about 40 FTEs, and we are evolving from the traditional generalist role toward more subspecialty comanagement,” said Bryan Huang, MD, physician adviser and associate clinical professor in the division of hospital medicine at the University of California–San Diego. “Our hospitalists are asking what it means to be an academic hospitalist as our teaching roles have shrunk.”

Dr. Huang recently took on a new role as physician adviser for his hospital in such areas as utilization review, patient flow, and length of stay. “I’m spearheading a work group to address quality issues – all of which involve collaboration with other professionals. We also developed an admitting role here for a hospitalist whose sole role for the day is to admit patients.” Nationally up to 51.2% of hospitalist groups utilize a dedicated daytime admitter.

The report found that hospital services for which hospitalists are more likely to be attendings than consultants include GI/liver, 78.4%; palliative care, 77.3%; neurology/stroke, 73.6%; oncology, 67.8%; cardiology, 56.9%; and critical care, 50.7%. Conditions where hospitalists are more likely to consult rather than admit and attend include neurosurgery, orthopedics, general surgery, cardiovascular surgery, and other surgical subspecialties.

Other hospital services routinely provided by adult-only hospitalists include care of patients in an ICU setting (62.7%); primary responsibility for observation units (54.6%); primary clinical responsibility for rapid response teams (48.8%); primary responsibility for code blue or cardiac arrest teams (43.8%); nighttime admissions or tuck-in services (33.9%); and medical procedures (31.5%). For pediatric hospital medicine groups, care of healthy newborns and medical procedures were among the most common services provided, while for hospitalists serving adults and children, rapid response teams, ICUs, and specialty units were most common.

New models of payment for health care

As the larger health care system is being transformed by new payment models and benefit structures, including accountable care organizations (ACOs), value-based purchasing, bundled payments, and other forms of population-based coverage – which is described as a volume-to-value shift in health care – how are these new models affecting hospitalists?

Observers say penetration of these new models varies widely by locality but they haven’t had much direct impact on hospitalists’ practices – at least not yet. However, as hospitals and health systems find themselves needing to learn new ways to invest their resources differently in response to these trends, what matters to the hospital should be of great importance to the hospitalist group.

“I haven’t seen a lot of dramatic changes in how hospitalists engage with value-based purchasing,” Dr. White said. “If we know that someone is part of an ACO, the instinctual – and right – response is to treat them like any other patient. But we still need to be committed to not waste resources.”

Hospitalists are the best people to understand the intricacies of how the health care system works under value-based approaches, Dr. Huang said. “That’s why so many hospitalists have taken leadership positions in their hospitals. I think all of this translates to the practical, day-to-day work of hospitalists, reflected in our focus on readmissions and length of stay.”

Dr. Williams said the health care system still hasn’t turned the corner from fee-for-service to value-based purchasing. “It still represents a tiny fraction of the income of hospitalists. Hospitals still have to focus on the bottom line, as fee-for-service reimbursement for hospitalized patients continues to get squeezed, and ACOs aren’t exactly paying premium rates either. Ask almost any hospital CEO what drives their bottom line today and the answer is volume – along with optimizing productivity. Pretty much every place I look, the future does not look terribly rosy for hospitals.”

Ms. Himebaugh said she is bullish on hospital medicine, in the sense that it’s unlikely to go away anytime soon. “Hospitalists are needed and provide value. But I don’t think we have devised the right model yet. I’m not sure our current model is sustainable. We need to find new models we can afford that don’t require squeezing our providers.”

For more information about the 2018 State of Hospital Medicine Report, contact SHM’s Practice Management Department at: survey@hospitalmedicine.org or call 800-843-3360. See also: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/.

In a national health care environment undergoing unprecedented transformation, the specialty of hospital medicine appears to be an island of relative stability, a conclusion that is supported by the principal findings from SHM’s 2018 State of Hospital Medicine (SoHM) report.

The report of hospitalist group practice characteristics, as well as other key data defining the field’s current status, that the Society of Hospital Medicine puts out every 2 years reveals that overall salaries for hospitalist physicians are up by 3.8% since 2016. Although productivity, as measured by work relative value units (RVUs), remained largely flat over the same period, financial support per full-time equivalent (FTE) physician position to hospitalist groups from their hospitals and health systems is up significantly.

Total support per FTE averaged $176,657 in 2018, 12% higher than in 2016, noted Leslie Flores, MHA, SFHM, of Nelson Flores Hospital Medicine Consultants, and a member of SHM’s Practice Analysis Committee, which oversees the biennial survey. Compensation and productivity data were collected by the Medical Group Management Association and licensed by SHM for inclusion in its report.

How do hospitalists use the SoHM report?

Dr. White called the 2018 SoHM report the “most representative and balanced sample to date” of hospitalist group practices, with some of the highest quality data, thanks to more robust participation in the survey by pediatric groups and improved distribution among hospitalist management companies and academic programs.

“Not that past reports had major flaws, but this version is more authoritative, reflecting an intentional effort by our Practice Analysis Committee to bring in more participants from key groups,” he said.

The biennial report has been around long enough to achieve brand recognition in the field as the most authoritative source of information regarding hospitalist practice, he added. “We worked hard this year to balance the participants, with more of our responses than in the past coming from multi-hospital groups, whether 4 to 5 sites, or 20 to 30.”

Surveys were conducted online in January and February of 2018 in response to invitations mailed and emailed to targeted hospital medicine group leaders. A total of 569 groups completed the survey, representing 8,889 hospitalist FTEs, approximately 16% of the total hospitalist workforce. Responses were presented in several categories, including by size of program, region and employment model. Groups that care for adults only represented 87.9% of the surveys, while groups that care for children only were 6.7% and groups that care for both adults and children were 5.4%.

Calls for more productivity

Roberta Himebaugh, MBA, SFHM, senior vice president of acute care services for the national hospitalist management company TeamHealth, and cochair of the SHM Practice Administrators Special Interest Group, said her company’s clients have traditionally asked for greater productivity from their hospitalist contracts as a way to decrease overall costs. Some markets are starting to see a change in that approach, she noted.

“Recently there’s been an increased focus on paying hospitalists to focus on quality rather than just productivity. Some of our clients are willing to pay for that, and we are trying to assign value to this non-billable time or adjust our productivity standards appropriately. I think hospitals definitely understand the value of non-billable services from hospitalists, but still will push us on the productivity targets,” Ms. Himebaugh said.

How is hospitalist practice evolving?

In addition to payment and productivity data, the SoHM report provides a current picture of the evolving state of hospitalist group practices. A key thread is how the work hospitalists are doing, and the way they do it, is changing, with new information about comanagement roles, dedicated admitters, night coverage, geographic rounding, and the like.

Making greater use of nurse practitioners and physician assistants (NPs/PAs), may be one way to change the flat productivity trends, Dr. Brown said. With a cost per RVU that’s roughly half that of a doctor’s, NPs/PAs could contribute to the bottom line. But he sees surprisingly large variation in how hospitalist groups are using them. Typically, they are deployed at a ratio of four doctors to one NP/PA, but that ratio could be two to one or even one to one, he said.

The predominant scheduling model of hospital medicine, 7 days on duty followed by 7 days off, has diminished somewhat in recent years. There appears to be some fluctuation and a gradual move away from 7 on/7 off toward some kind of variable approach, since the former may not be physically sustainable for the doctor over the long haul, Dr. Brown said. Some groups are experimenting with a combined approach.

“I think balancing workload with manpower has always been a challenge for our field. Maybe we should be working shorter shifts or fewer days and making sure our hospitalists aren’t ever sitting around idle,” he said. “And could we come in on nonclinical days to do administrative tasks? I think the solution is out there, but we haven’t created the algorithms to define that yet. If you could somehow use the data for volume, number of beds, nurse staffing, etc., by year and seasonally, you might be able to reliably predict census. This is about applying data hospitals already have in their electronic health records, but utilizing the data in ways that are more helpful.”

Dr. McIlraith added that a big driver of the future of hospital medicine will be the evolution of the EHR and the digitalization of health care, as hospitals learn how to leverage more of what’s in their EHRs. “The impact will grow for hospitalists through the creation and maturation of big data systems – and the learning that can be extracted from what’s contained in the electronic health record.”

Another important question for hospitalist groups is their model of backup scheduling, to make sure there is a replacement available if a scheduled doctor calls in sick or if demand is unexpectedly high.

“In today’s world, this is how we have traditionally managed unpredictability,” Dr. Brown said. “You don’t know when you will need it, but if you need it, you want it immediately. So how do you pay for it – only when the doctor comes in, or also an amount just for being on call?” Some groups pay for both, he said, others for neither.

“We are a group of 70 hospitalists, and if someone is sick you can’t just shut down the service,” said Dr. Chadha. “We are one of the few to use incentives for both, which could include a 1-week decrease in clinical shifts in exchange for 2 weeks of backup. We have times with 25% usage of backup number 1, and 10% usage of backup number 2,” he noted. “But the goal is for our hospitalists to have assurances that there is a backup system and that it works.”

The presence of nocturnists in hospitals continues to rise, with 76.1% of adults-only groups having nocturnists, 27.6% of children-only groups, and 68.2% of adults and children groups. Geographic or unit-based hospital assignments have grown to 36.4% of adult-only groups.

What are hospitalists’ other new roles?

“We have a large group of 50 doctors, with about 40 FTEs, and we are evolving from the traditional generalist role toward more subspecialty comanagement,” said Bryan Huang, MD, physician adviser and associate clinical professor in the division of hospital medicine at the University of California–San Diego. “Our hospitalists are asking what it means to be an academic hospitalist as our teaching roles have shrunk.”

Dr. Huang recently took on a new role as physician adviser for his hospital in such areas as utilization review, patient flow, and length of stay. “I’m spearheading a work group to address quality issues – all of which involve collaboration with other professionals. We also developed an admitting role here for a hospitalist whose sole role for the day is to admit patients.” Nationally up to 51.2% of hospitalist groups utilize a dedicated daytime admitter.

The report found that hospital services for which hospitalists are more likely to be attendings than consultants include GI/liver, 78.4%; palliative care, 77.3%; neurology/stroke, 73.6%; oncology, 67.8%; cardiology, 56.9%; and critical care, 50.7%. Conditions where hospitalists are more likely to consult rather than admit and attend include neurosurgery, orthopedics, general surgery, cardiovascular surgery, and other surgical subspecialties.

Other hospital services routinely provided by adult-only hospitalists include care of patients in an ICU setting (62.7%); primary responsibility for observation units (54.6%); primary clinical responsibility for rapid response teams (48.8%); primary responsibility for code blue or cardiac arrest teams (43.8%); nighttime admissions or tuck-in services (33.9%); and medical procedures (31.5%). For pediatric hospital medicine groups, care of healthy newborns and medical procedures were among the most common services provided, while for hospitalists serving adults and children, rapid response teams, ICUs, and specialty units were most common.

New models of payment for health care

As the larger health care system is being transformed by new payment models and benefit structures, including accountable care organizations (ACOs), value-based purchasing, bundled payments, and other forms of population-based coverage – which is described as a volume-to-value shift in health care – how are these new models affecting hospitalists?

Observers say penetration of these new models varies widely by locality but they haven’t had much direct impact on hospitalists’ practices – at least not yet. However, as hospitals and health systems find themselves needing to learn new ways to invest their resources differently in response to these trends, what matters to the hospital should be of great importance to the hospitalist group.

“I haven’t seen a lot of dramatic changes in how hospitalists engage with value-based purchasing,” Dr. White said. “If we know that someone is part of an ACO, the instinctual – and right – response is to treat them like any other patient. But we still need to be committed to not waste resources.”

Hospitalists are the best people to understand the intricacies of how the health care system works under value-based approaches, Dr. Huang said. “That’s why so many hospitalists have taken leadership positions in their hospitals. I think all of this translates to the practical, day-to-day work of hospitalists, reflected in our focus on readmissions and length of stay.”

Dr. Williams said the health care system still hasn’t turned the corner from fee-for-service to value-based purchasing. “It still represents a tiny fraction of the income of hospitalists. Hospitals still have to focus on the bottom line, as fee-for-service reimbursement for hospitalized patients continues to get squeezed, and ACOs aren’t exactly paying premium rates either. Ask almost any hospital CEO what drives their bottom line today and the answer is volume – along with optimizing productivity. Pretty much every place I look, the future does not look terribly rosy for hospitals.”

Ms. Himebaugh said she is bullish on hospital medicine, in the sense that it’s unlikely to go away anytime soon. “Hospitalists are needed and provide value. But I don’t think we have devised the right model yet. I’m not sure our current model is sustainable. We need to find new models we can afford that don’t require squeezing our providers.”

For more information about the 2018 State of Hospital Medicine Report, contact SHM’s Practice Management Department at: survey@hospitalmedicine.org or call 800-843-3360. See also: https://www.hospitalmedicine.org/practice-management/shms-state-of-hospital-medicine/.

The Diagnosis: Ruptured Molluscum

Molluscum contagiosum (MC) is caused by a DNA virus (MC virus) belonging to the poxvirus family. Molluscum contagiosum is common and predominantly seen in children and young adults. In sexually active adults, the lesions commonly occur in the genital region, abdomen, and inner thighs. In immunocompromised individuals, including those with AIDS, the lesions are more extensive and may cause disfigurement.¹ Molluscum contagiosum involving epidermoid cysts has been reported.²

Histopathologically, MC can be classified as noninflammatory or inflammatory. In noninflamed lesions, multiple large, intracytoplasmic, eosinophilic inclusions (Henderson-Paterson bodies) appear within the lobulated endophytic and hyperplastic epidermis. Ultrastructurally, these bodies show membrane-bound collections of MC virus.¹ Replicating Henderson-Paterson bodies can result in rupture and inflammation. This case demonstrates a palisading granuloma containing keratin with few Henderson-Paterson bodies (quiz image) due to prior rupture of a molluscum or molluscoid cyst.

Rheumatoid nodules, the most characteristic histopathologic lesions of rheumatoid arthritis, are most commonly found in the subcutis at points of pressure and may occur in connective tissue of numerous organs. Rheumatoid nodules are firm, nontender, and mobile within the subcutaneous tissue but may be fixed to underlying structures including the periosteum, tendons, or bursae.^3,4 Occasionally, superficial nodules may perforate the epidermis.⁵ The inner central necrobiotic zone appears as intensely eosinophilic, amorphous fibrin and other cellular debris. This central area is surrounded by histiocytes in a palisaded configuration (Figure 1). Multinucleated foreign body giant cells also may be present. Occasionally, mast cells, eosinophils, and neutrophils are present.^6,7

Lupus miliaris disseminatus faciei presents with multiple discrete, smooth, yellow-brown to red, dome-shaped papules. The lesions typically are located on the central and lateral sides of the face and infrequently involve the neck. Other sites including the axillae, arms, hands, legs, and groin occasionally can be involved. Diascopy may reveal an apple jelly color.^8,9 The histopathologic hallmark of lupus miliaris disseminatus faciei is an epithelioid cell granuloma with central necrosis (Figure 2).

Epithelioid sarcoma (ES) is a soft tissue tumor with a known propensity for local recurrence, regional lymph node involvement, sporotrichoid spread, and distant metastases.¹⁰ The name was coined by Enzinger¹¹ in 1970 during a review of 62 cases of a “peculiar form of sarcoma that has repeatedly been confused with a chronic inflammatory process, a necrotizing granuloma, and a squamous cell carcinoma.” Epithelioid sarcoma tends to grow slowly in a nodular or multinodular manner along fascial structures and tendons, often with central necrosis and ulceration of the overlying skin. Histopathologically, classic ES shows nodular masses of uniform plump epithelioid cells with abundant eosinophilic cytoplasm and prominent central necrosis. A biphasic pattern is typical with spindle cells merging with epithelioid cells. Cellular atypia is relatively mild and mitoses are rare (Figure 3). Recurrent or metastatic lesions can show a greater degree of pleomorphism.¹² Given the low-grade atypia in early lesions, this sarcoma is easily misdiagnosed as granulomatous dermatitis. Immunohistochemically, the majority of ES cases are positive for cytokeratins and epithelial membrane antigen; SMARCB1/INI-1 expression is characteristically lost.¹³

Granulomatosis with polyangiitis (formerly Wegener granulomatosis) is an autoimmune vasculitis highly associated with antineutrophil cytoplasmic antibodies. Clinical manifestations include systemic necrotizing vasculitis; necrotizing glomerulonephritis; and granulomatous inflammation, which predominantly involves the upper respiratory tract, skin, and mucosa.^14,15 Skin involvement may be the initial manifestation of the disease and consists of palpable purpura, papules, ulcerations, vesicles, subcutaneous nodules, necrotizing ulcerations, papulonecrotic lesions, and petechiae. None of the findings are pathognomonic. The cutaneous histopathologic spectrum includes leukocytoclastic vasculitis, extravascular palisading granulomas, and granulomatous vasculitis.¹⁶ In the acute lesions of granulomatosis with polyangiitis, the predominant pattern of inflammation is not granulomatous but purulent with the appearance of an abscess. As it evolves, it develops a central zone of necrosis with extensive karyorrhectic debris and palisades of macrophages with scattered multinucleated giant cells (Figure 4).¹⁷

The Diagnosis: Ruptured Molluscum

Molluscum contagiosum (MC) is caused by a DNA virus (MC virus) belonging to the poxvirus family. Molluscum contagiosum is common and predominantly seen in children and young adults. In sexually active adults, the lesions commonly occur in the genital region, abdomen, and inner thighs. In immunocompromised individuals, including those with AIDS, the lesions are more extensive and may cause disfigurement.¹ Molluscum contagiosum involving epidermoid cysts has been reported.²

Histopathologically, MC can be classified as noninflammatory or inflammatory. In noninflamed lesions, multiple large, intracytoplasmic, eosinophilic inclusions (Henderson-Paterson bodies) appear within the lobulated endophytic and hyperplastic epidermis. Ultrastructurally, these bodies show membrane-bound collections of MC virus.¹ Replicating Henderson-Paterson bodies can result in rupture and inflammation. This case demonstrates a palisading granuloma containing keratin with few Henderson-Paterson bodies (quiz image) due to prior rupture of a molluscum or molluscoid cyst.

Rheumatoid nodules, the most characteristic histopathologic lesions of rheumatoid arthritis, are most commonly found in the subcutis at points of pressure and may occur in connective tissue of numerous organs. Rheumatoid nodules are firm, nontender, and mobile within the subcutaneous tissue but may be fixed to underlying structures including the periosteum, tendons, or bursae.^3,4 Occasionally, superficial nodules may perforate the epidermis.⁵ The inner central necrobiotic zone appears as intensely eosinophilic, amorphous fibrin and other cellular debris. This central area is surrounded by histiocytes in a palisaded configuration (Figure 1). Multinucleated foreign body giant cells also may be present. Occasionally, mast cells, eosinophils, and neutrophils are present.^6,7

Lupus miliaris disseminatus faciei presents with multiple discrete, smooth, yellow-brown to red, dome-shaped papules. The lesions typically are located on the central and lateral sides of the face and infrequently involve the neck. Other sites including the axillae, arms, hands, legs, and groin occasionally can be involved. Diascopy may reveal an apple jelly color.^8,9 The histopathologic hallmark of lupus miliaris disseminatus faciei is an epithelioid cell granuloma with central necrosis (Figure 2).

Epithelioid sarcoma (ES) is a soft tissue tumor with a known propensity for local recurrence, regional lymph node involvement, sporotrichoid spread, and distant metastases.¹⁰ The name was coined by Enzinger¹¹ in 1970 during a review of 62 cases of a “peculiar form of sarcoma that has repeatedly been confused with a chronic inflammatory process, a necrotizing granuloma, and a squamous cell carcinoma.” Epithelioid sarcoma tends to grow slowly in a nodular or multinodular manner along fascial structures and tendons, often with central necrosis and ulceration of the overlying skin. Histopathologically, classic ES shows nodular masses of uniform plump epithelioid cells with abundant eosinophilic cytoplasm and prominent central necrosis. A biphasic pattern is typical with spindle cells merging with epithelioid cells. Cellular atypia is relatively mild and mitoses are rare (Figure 3). Recurrent or metastatic lesions can show a greater degree of pleomorphism.¹² Given the low-grade atypia in early lesions, this sarcoma is easily misdiagnosed as granulomatous dermatitis. Immunohistochemically, the majority of ES cases are positive for cytokeratins and epithelial membrane antigen; SMARCB1/INI-1 expression is characteristically lost.¹³

Granulomatosis with polyangiitis (formerly Wegener granulomatosis) is an autoimmune vasculitis highly associated with antineutrophil cytoplasmic antibodies. Clinical manifestations include systemic necrotizing vasculitis; necrotizing glomerulonephritis; and granulomatous inflammation, which predominantly involves the upper respiratory tract, skin, and mucosa.^14,15 Skin involvement may be the initial manifestation of the disease and consists of palpable purpura, papules, ulcerations, vesicles, subcutaneous nodules, necrotizing ulcerations, papulonecrotic lesions, and petechiae. None of the findings are pathognomonic. The cutaneous histopathologic spectrum includes leukocytoclastic vasculitis, extravascular palisading granulomas, and granulomatous vasculitis.¹⁶ In the acute lesions of granulomatosis with polyangiitis, the predominant pattern of inflammation is not granulomatous but purulent with the appearance of an abscess. As it evolves, it develops a central zone of necrosis with extensive karyorrhectic debris and palisades of macrophages with scattered multinucleated giant cells (Figure 4).¹⁷

The Diagnosis: Ruptured Molluscum

Molluscum contagiosum (MC) is caused by a DNA virus (MC virus) belonging to the poxvirus family. Molluscum contagiosum is common and predominantly seen in children and young adults. In sexually active adults, the lesions commonly occur in the genital region, abdomen, and inner thighs. In immunocompromised individuals, including those with AIDS, the lesions are more extensive and may cause disfigurement.¹ Molluscum contagiosum involving epidermoid cysts has been reported.²

Histopathologically, MC can be classified as noninflammatory or inflammatory. In noninflamed lesions, multiple large, intracytoplasmic, eosinophilic inclusions (Henderson-Paterson bodies) appear within the lobulated endophytic and hyperplastic epidermis. Ultrastructurally, these bodies show membrane-bound collections of MC virus.¹ Replicating Henderson-Paterson bodies can result in rupture and inflammation. This case demonstrates a palisading granuloma containing keratin with few Henderson-Paterson bodies (quiz image) due to prior rupture of a molluscum or molluscoid cyst.

Rheumatoid nodules, the most characteristic histopathologic lesions of rheumatoid arthritis, are most commonly found in the subcutis at points of pressure and may occur in connective tissue of numerous organs. Rheumatoid nodules are firm, nontender, and mobile within the subcutaneous tissue but may be fixed to underlying structures including the periosteum, tendons, or bursae.^3,4 Occasionally, superficial nodules may perforate the epidermis.⁵ The inner central necrobiotic zone appears as intensely eosinophilic, amorphous fibrin and other cellular debris. This central area is surrounded by histiocytes in a palisaded configuration (Figure 1). Multinucleated foreign body giant cells also may be present. Occasionally, mast cells, eosinophils, and neutrophils are present.^6,7

Lupus miliaris disseminatus faciei presents with multiple discrete, smooth, yellow-brown to red, dome-shaped papules. The lesions typically are located on the central and lateral sides of the face and infrequently involve the neck. Other sites including the axillae, arms, hands, legs, and groin occasionally can be involved. Diascopy may reveal an apple jelly color.^8,9 The histopathologic hallmark of lupus miliaris disseminatus faciei is an epithelioid cell granuloma with central necrosis (Figure 2).

Epithelioid sarcoma (ES) is a soft tissue tumor with a known propensity for local recurrence, regional lymph node involvement, sporotrichoid spread, and distant metastases.¹⁰ The name was coined by Enzinger¹¹ in 1970 during a review of 62 cases of a “peculiar form of sarcoma that has repeatedly been confused with a chronic inflammatory process, a necrotizing granuloma, and a squamous cell carcinoma.” Epithelioid sarcoma tends to grow slowly in a nodular or multinodular manner along fascial structures and tendons, often with central necrosis and ulceration of the overlying skin. Histopathologically, classic ES shows nodular masses of uniform plump epithelioid cells with abundant eosinophilic cytoplasm and prominent central necrosis. A biphasic pattern is typical with spindle cells merging with epithelioid cells. Cellular atypia is relatively mild and mitoses are rare (Figure 3). Recurrent or metastatic lesions can show a greater degree of pleomorphism.¹² Given the low-grade atypia in early lesions, this sarcoma is easily misdiagnosed as granulomatous dermatitis. Immunohistochemically, the majority of ES cases are positive for cytokeratins and epithelial membrane antigen; SMARCB1/INI-1 expression is characteristically lost.¹³

Granulomatosis with polyangiitis (formerly Wegener granulomatosis) is an autoimmune vasculitis highly associated with antineutrophil cytoplasmic antibodies. Clinical manifestations include systemic necrotizing vasculitis; necrotizing glomerulonephritis; and granulomatous inflammation, which predominantly involves the upper respiratory tract, skin, and mucosa.^14,15 Skin involvement may be the initial manifestation of the disease and consists of palpable purpura, papules, ulcerations, vesicles, subcutaneous nodules, necrotizing ulcerations, papulonecrotic lesions, and petechiae. None of the findings are pathognomonic. The cutaneous histopathologic spectrum includes leukocytoclastic vasculitis, extravascular palisading granulomas, and granulomatous vasculitis.¹⁶ In the acute lesions of granulomatosis with polyangiitis, the predominant pattern of inflammation is not granulomatous but purulent with the appearance of an abscess. As it evolves, it develops a central zone of necrosis with extensive karyorrhectic debris and palisades of macrophages with scattered multinucleated giant cells (Figure 4).¹⁷

LOS ANGELES – When Derek LeRoith, MD, PhD, was a medical student, he remembers professors telling him that human tissue response to aging diminishes over time, and that individuals can develop insulin resistance purely from aging.

Doug Brunk/MDedge News

“Whether that was right or wrong I don’t know, but certainly it seems to be one of the major issues that leads to the increase in diabetes, with all of its associated aspects such as dyslipidemia and hypertension,” he said at the World Congress on Insulin Resistance, Diabetes & Cardiovascular Disease.

According to Dr. LeRoith, professor of medicine and director of research in the division of endocrinology at Icahn School of Medicine at Mount Sinai, New York, studies have demonstrated that the elderly have worse glucose tolerance, compared with younger adults. One such analysis found that the insulin secretion index and disposition index are lower in the elderly, compared with their younger patients (Diabetes 2003;52[7]:1738-48). “But it’s not just the insulin resistance per se,” he said. “It’s also a defect of the beta cell. Studies have shown that beta cell function declines with age regardless of diabetes status. This is characterized by abnormal pulsatile insulin response, decreased beta-cell responsiveness to glucose, increased proinsulin-to-insulin ratio, and decreased insulin production and secretion.”

Another major issue for aging patients is the impact of diabetes on cognitive decline and the formation of Alzheimer’s disease. “There’s a suggestion that the brain has insulin resistance and that this may also affect cognitive decline and Alzheimer’s,” Dr. LeRoith said. “But there are other aspects: insulin insufficiency, hyperglycemia, and, of course ... hypoglycemia. There is a debate as to what the major causes are. Is it amyloid beta accumulation, or is it vascular damage?”

In collaboration with Israeli researchers, Dr. LeRoith and his associates have been evaluating patients that belong to the Maccabi Health System in Tel Aviv, which has a diabetes registry with complete hemoglobin A_1c measurements since 1998. One study of 897 registry participants found a strong association between worse diabetes control and worse cognition (Am J Geriatr Psych 2014;22:1055-9). Specifically, an interaction of duration of type 2 diabetes with HbA_1c was associated with executive functioning (P = .006), semantic categorization (P = .019), attention/working memory (P = .011), and overall cognition (P = .006), such that the associations between duration of type 2 diabetes and cognitive impairment increased as HbA_1c levels increased – but not for episodic memory (P = .984).

In a separate analysis of patients from the same registry, Dr. LeRoith and his colleagues evaluated the relationships of long-term trajectories of glycemic control with cognitive performance in cognitively normal elderly with type 2 diabetes (PLoS ONE 9[6]:e97384 doi: 10.1371/journal.pone.0097384). They found that subjects with stable HbA_1c over time had the lowest HbA_1c at study entry and performed best on cognitive measures, “suggesting that the trajectile of HbA_1c over 10 or 12 years can really influence the cognitive ability in these patients,” he said.

Another, unrelated study found that insulin in combination with other diabetes medication is associated with less Alzheimer’s neuropathology (Neurology 2008;71:750-7), while an Alzheimer’s mouse model from Dr. LeRoith and his colleagues demonstrated that high dietary advanced glycation end products are associated with poorer spatial learning and accelerated amyloid beta deposition (Aging Cell 2016;15:309-16). “From that study we conclude that high dietary advance glycation end (AGE) products may be neurotoxic and that a diet low in AGEs may decrease dementia risk, particularly in diabetic elderly who are at increased risk and have higher levels of AGEs,” he said.

Potential ways to mitigate some of aging’s effects on the course of diabetes include caloric restriction, exercise, and taking metformin, Dr. LeRoith said. “There is a correlation between fitness and cognitive function, so the implication for clinical practice in individuals with diabetes is to encourage them to engage in physical activity on most days of the week,” he said. “It’s also known that depression makes the diabetes worse and depression makes cognitive function worse. It’s been suggested that if you have patients who are depressed, you should treat them with antidepressants if necessary, because this may help with their cognitive function.”

Meanwhile, an ongoing trial first announced in 2016 known as Targeting Aging with Metformin (TAME) is exploring the effects of metformin in helping to delay the aging process (Cell Metab 2016;23[6]:1060-5). Early support exists that metformin may delay cognitive decline and Alzheimer’s, even in non–type 2 diabetes. “An intended consequence of this effort is to create a paradigm for evaluation of pharmacologic approaches to delay aging,” the researchers wrote in an article describing the project, which is funded by the National Institute on Aging. “The randomized, controlled clinical trial we have proposed, if successful, could profoundly change the approach to aging and its diseases and affect health care delivery and costs.”

Dr. LeRoith reported having no financial disclosures.

dbrunk@mdedge.com

LOS ANGELES – When Derek LeRoith, MD, PhD, was a medical student, he remembers professors telling him that human tissue response to aging diminishes over time, and that individuals can develop insulin resistance purely from aging.

Doug Brunk/MDedge News

“Whether that was right or wrong I don’t know, but certainly it seems to be one of the major issues that leads to the increase in diabetes, with all of its associated aspects such as dyslipidemia and hypertension,” he said at the World Congress on Insulin Resistance, Diabetes & Cardiovascular Disease.

According to Dr. LeRoith, professor of medicine and director of research in the division of endocrinology at Icahn School of Medicine at Mount Sinai, New York, studies have demonstrated that the elderly have worse glucose tolerance, compared with younger adults. One such analysis found that the insulin secretion index and disposition index are lower in the elderly, compared with their younger patients (Diabetes 2003;52[7]:1738-48). “But it’s not just the insulin resistance per se,” he said. “It’s also a defect of the beta cell. Studies have shown that beta cell function declines with age regardless of diabetes status. This is characterized by abnormal pulsatile insulin response, decreased beta-cell responsiveness to glucose, increased proinsulin-to-insulin ratio, and decreased insulin production and secretion.”

Another major issue for aging patients is the impact of diabetes on cognitive decline and the formation of Alzheimer’s disease. “There’s a suggestion that the brain has insulin resistance and that this may also affect cognitive decline and Alzheimer’s,” Dr. LeRoith said. “But there are other aspects: insulin insufficiency, hyperglycemia, and, of course ... hypoglycemia. There is a debate as to what the major causes are. Is it amyloid beta accumulation, or is it vascular damage?”

In collaboration with Israeli researchers, Dr. LeRoith and his associates have been evaluating patients that belong to the Maccabi Health System in Tel Aviv, which has a diabetes registry with complete hemoglobin A_1c measurements since 1998. One study of 897 registry participants found a strong association between worse diabetes control and worse cognition (Am J Geriatr Psych 2014;22:1055-9). Specifically, an interaction of duration of type 2 diabetes with HbA_1c was associated with executive functioning (P = .006), semantic categorization (P = .019), attention/working memory (P = .011), and overall cognition (P = .006), such that the associations between duration of type 2 diabetes and cognitive impairment increased as HbA_1c levels increased – but not for episodic memory (P = .984).

In a separate analysis of patients from the same registry, Dr. LeRoith and his colleagues evaluated the relationships of long-term trajectories of glycemic control with cognitive performance in cognitively normal elderly with type 2 diabetes (PLoS ONE 9[6]:e97384 doi: 10.1371/journal.pone.0097384). They found that subjects with stable HbA_1c over time had the lowest HbA_1c at study entry and performed best on cognitive measures, “suggesting that the trajectile of HbA_1c over 10 or 12 years can really influence the cognitive ability in these patients,” he said.

Another, unrelated study found that insulin in combination with other diabetes medication is associated with less Alzheimer’s neuropathology (Neurology 2008;71:750-7), while an Alzheimer’s mouse model from Dr. LeRoith and his colleagues demonstrated that high dietary advanced glycation end products are associated with poorer spatial learning and accelerated amyloid beta deposition (Aging Cell 2016;15:309-16). “From that study we conclude that high dietary advance glycation end (AGE) products may be neurotoxic and that a diet low in AGEs may decrease dementia risk, particularly in diabetic elderly who are at increased risk and have higher levels of AGEs,” he said.

Potential ways to mitigate some of aging’s effects on the course of diabetes include caloric restriction, exercise, and taking metformin, Dr. LeRoith said. “There is a correlation between fitness and cognitive function, so the implication for clinical practice in individuals with diabetes is to encourage them to engage in physical activity on most days of the week,” he said. “It’s also known that depression makes the diabetes worse and depression makes cognitive function worse. It’s been suggested that if you have patients who are depressed, you should treat them with antidepressants if necessary, because this may help with their cognitive function.”

Meanwhile, an ongoing trial first announced in 2016 known as Targeting Aging with Metformin (TAME) is exploring the effects of metformin in helping to delay the aging process (Cell Metab 2016;23[6]:1060-5). Early support exists that metformin may delay cognitive decline and Alzheimer’s, even in non–type 2 diabetes. “An intended consequence of this effort is to create a paradigm for evaluation of pharmacologic approaches to delay aging,” the researchers wrote in an article describing the project, which is funded by the National Institute on Aging. “The randomized, controlled clinical trial we have proposed, if successful, could profoundly change the approach to aging and its diseases and affect health care delivery and costs.”

Dr. LeRoith reported having no financial disclosures.

dbrunk@mdedge.com

LOS ANGELES – When Derek LeRoith, MD, PhD, was a medical student, he remembers professors telling him that human tissue response to aging diminishes over time, and that individuals can develop insulin resistance purely from aging.

Doug Brunk/MDedge News

“Whether that was right or wrong I don’t know, but certainly it seems to be one of the major issues that leads to the increase in diabetes, with all of its associated aspects such as dyslipidemia and hypertension,” he said at the World Congress on Insulin Resistance, Diabetes & Cardiovascular Disease.

According to Dr. LeRoith, professor of medicine and director of research in the division of endocrinology at Icahn School of Medicine at Mount Sinai, New York, studies have demonstrated that the elderly have worse glucose tolerance, compared with younger adults. One such analysis found that the insulin secretion index and disposition index are lower in the elderly, compared with their younger patients (Diabetes 2003;52[7]:1738-48). “But it’s not just the insulin resistance per se,” he said. “It’s also a defect of the beta cell. Studies have shown that beta cell function declines with age regardless of diabetes status. This is characterized by abnormal pulsatile insulin response, decreased beta-cell responsiveness to glucose, increased proinsulin-to-insulin ratio, and decreased insulin production and secretion.”

Another major issue for aging patients is the impact of diabetes on cognitive decline and the formation of Alzheimer’s disease. “There’s a suggestion that the brain has insulin resistance and that this may also affect cognitive decline and Alzheimer’s,” Dr. LeRoith said. “But there are other aspects: insulin insufficiency, hyperglycemia, and, of course ... hypoglycemia. There is a debate as to what the major causes are. Is it amyloid beta accumulation, or is it vascular damage?”

In collaboration with Israeli researchers, Dr. LeRoith and his associates have been evaluating patients that belong to the Maccabi Health System in Tel Aviv, which has a diabetes registry with complete hemoglobin A_1c measurements since 1998. One study of 897 registry participants found a strong association between worse diabetes control and worse cognition (Am J Geriatr Psych 2014;22:1055-9). Specifically, an interaction of duration of type 2 diabetes with HbA_1c was associated with executive functioning (P = .006), semantic categorization (P = .019), attention/working memory (P = .011), and overall cognition (P = .006), such that the associations between duration of type 2 diabetes and cognitive impairment increased as HbA_1c levels increased – but not for episodic memory (P = .984).

In a separate analysis of patients from the same registry, Dr. LeRoith and his colleagues evaluated the relationships of long-term trajectories of glycemic control with cognitive performance in cognitively normal elderly with type 2 diabetes (PLoS ONE 9[6]:e97384 doi: 10.1371/journal.pone.0097384). They found that subjects with stable HbA_1c over time had the lowest HbA_1c at study entry and performed best on cognitive measures, “suggesting that the trajectile of HbA_1c over 10 or 12 years can really influence the cognitive ability in these patients,” he said.

Another, unrelated study found that insulin in combination with other diabetes medication is associated with less Alzheimer’s neuropathology (Neurology 2008;71:750-7), while an Alzheimer’s mouse model from Dr. LeRoith and his colleagues demonstrated that high dietary advanced glycation end products are associated with poorer spatial learning and accelerated amyloid beta deposition (Aging Cell 2016;15:309-16). “From that study we conclude that high dietary advance glycation end (AGE) products may be neurotoxic and that a diet low in AGEs may decrease dementia risk, particularly in diabetic elderly who are at increased risk and have higher levels of AGEs,” he said.

Potential ways to mitigate some of aging’s effects on the course of diabetes include caloric restriction, exercise, and taking metformin, Dr. LeRoith said. “There is a correlation between fitness and cognitive function, so the implication for clinical practice in individuals with diabetes is to encourage them to engage in physical activity on most days of the week,” he said. “It’s also known that depression makes the diabetes worse and depression makes cognitive function worse. It’s been suggested that if you have patients who are depressed, you should treat them with antidepressants if necessary, because this may help with their cognitive function.”

Meanwhile, an ongoing trial first announced in 2016 known as Targeting Aging with Metformin (TAME) is exploring the effects of metformin in helping to delay the aging process (Cell Metab 2016;23[6]:1060-5). Early support exists that metformin may delay cognitive decline and Alzheimer’s, even in non–type 2 diabetes. “An intended consequence of this effort is to create a paradigm for evaluation of pharmacologic approaches to delay aging,” the researchers wrote in an article describing the project, which is funded by the National Institute on Aging. “The randomized, controlled clinical trial we have proposed, if successful, could profoundly change the approach to aging and its diseases and affect health care delivery and costs.”

Dr. LeRoith reported having no financial disclosures.

dbrunk@mdedge.com