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Scarring Head Wound
The Diagnosis: Brunsting-Perry Cicatricial Pemphigoid
Physical examination and histopathology are paramount in diagnosing Brunsting-Perry cicatricial pemphigoid (BPCP). In our patient, histopathology showed subepidermal blistering with a mixed superficial dermal inflammatory cell infiltrate. Direct immunofluorescence was positive for linear IgG and C3 antibodies along the basement membrane. The scarring erosions on the scalp combined with the autoantibody findings on direct immunofluorescence were consistent with BPCP. He was started on dapsone 100 mg daily and demonstrated complete resolution of symptoms after 10 months, with the exception of persistent scarring hair loss (Figure).
Brunsting-Perry cicatricial pemphigoid is a rare dermatologic condition. It was first defined in 1957 when Brunsting and Perry1 examined 7 patients with cicatricial pemphigoid that predominantly affected the head and neck region, with occasional mucous membrane involvement but no mucosal scarring. Characteristically, BPCP manifests as scarring herpetiform plaques with varied blisters, erosions, crusts, and scarring.1 It primarily affects middle-aged men.2
Historically, BPCP has been considered a variant of cicatricial pemphigoid (now known as mucous membrane pemphigoid), bullous pemphigoid, or epidermolysis bullosa acquisita.3 The antigen target has not been established clearly; however, autoantibodies against laminin 332, collagen VII, and BP180 and BP230 have been proposed.2,4,5 Jacoby et al6 described BPCP on a spectrum with bullous pemphigoid and cicatricial pemphigoid, with primarily circulating autoantibodies on one end and tissue-fixed autoantibodies on the other.
The differential for BPCP also includes anti-p200 pemphigoid and anti–laminin 332 pemphigoid. Anti-p200 pemphigoid also is known as bullous pemphigoid with antibodies against the 200-kDa protein.7 It may clinically manifest similar to bullous pemphigoid and other subepidermal autoimmune blistering diseases; thus, immunopathologic differentiation can be helpful. Anti–laminin 332 pemphigoid (also known as anti–laminin gamma-1 pemphigoid) is characterized by autoantibodies targeting the laminin 332 protein in the basement membrane zone, resulting in blistering and erosions.8 Similar to BPCP and epidermolysis bullosa aquisita, anti–laminin 332 pemphigoid may affect cephalic regions and mucous membrane surfaces, resulting in scarring and cicatricial changes. Anti–laminin 332 pemphigoid also has been associated with internal malignancy.8 The use of the salt-split skin technique can be utilized to differentiate these entities based on their autoantibody-binding patterns in relation to the lamina densa.
Treatment options for mild BPCP include potent topical or intralesional steroids and dapsone, while more severe cases may require systemic therapy with rituximab, azathioprine, mycophenolate mofetil, or cyclophosphamide.4
This case highlights the importance of histopathologic examination of skin lesions with an unusual history or clinical presentation. Dermatologists should consider BPCP when presented with erosions, ulcerations, or blisters of the head and neck in middle-aged male patients.
- Brunsting LA, Perry HO. Benign pemphigoid? a report of seven cases with chronic, scarring, herpetiform plaques about the head and neck. AMA Arch Derm. 1957;75:489-501. doi:10.1001 /archderm.1957.01550160015002
- Jedlickova H, Neidermeier A, Zgažarová S, et al. Brunsting-Perry pemphigoid of the scalp with antibodies against laminin 332. Dermatology. 2011;222:193-195. doi:10.1159/000322842
- Eichhoff G. Brunsting-Perry pemphigoid as differential diagnosis of nonmelanoma skin cancer. Cureus. 2019;11:E5400. doi:10.7759/cureus.5400
- Asfour L, Chong H, Mee J, et al. Epidermolysis bullosa acquisita (Brunsting-Perry pemphigoid variant) localized to the face and diagnosed with antigen identification using skin deficient in type VII collagen. Am J Dermatopathol. 2017;39:e90-e96. doi:10.1097 /DAD.0000000000000829
- Zhou S, Zou Y, Pan M. Brunsting-Perry pemphigoid transitioning from previous bullous pemphigoid. JAAD Case Rep. 2020;6:192-194. doi:10.1016/j.jdcr.2019.12.018
- Jacoby WD Jr, Bartholome CW, Ramchand SC, et al. Cicatricial pemphigoid (Brunsting-Perry type). case report and immunofluorescence findings. Arch Dermatol. 1978;114:779-781. doi:10.1001/archderm.1978.01640170079018
- Kridin K, Ahmed AR. Anti-p200 pemphigoid: a systematic review. Front Immunol. 2019;10:2466. doi:10.3389/fimmu.2019.02466
- Shi L, Li X, Qian H. Anti-laminin 332-type mucous membrane pemphigoid. Biomolecules. 2022;12:1461. doi:10.3390/biom12101461
The Diagnosis: Brunsting-Perry Cicatricial Pemphigoid
Physical examination and histopathology are paramount in diagnosing Brunsting-Perry cicatricial pemphigoid (BPCP). In our patient, histopathology showed subepidermal blistering with a mixed superficial dermal inflammatory cell infiltrate. Direct immunofluorescence was positive for linear IgG and C3 antibodies along the basement membrane. The scarring erosions on the scalp combined with the autoantibody findings on direct immunofluorescence were consistent with BPCP. He was started on dapsone 100 mg daily and demonstrated complete resolution of symptoms after 10 months, with the exception of persistent scarring hair loss (Figure).
Brunsting-Perry cicatricial pemphigoid is a rare dermatologic condition. It was first defined in 1957 when Brunsting and Perry1 examined 7 patients with cicatricial pemphigoid that predominantly affected the head and neck region, with occasional mucous membrane involvement but no mucosal scarring. Characteristically, BPCP manifests as scarring herpetiform plaques with varied blisters, erosions, crusts, and scarring.1 It primarily affects middle-aged men.2
Historically, BPCP has been considered a variant of cicatricial pemphigoid (now known as mucous membrane pemphigoid), bullous pemphigoid, or epidermolysis bullosa acquisita.3 The antigen target has not been established clearly; however, autoantibodies against laminin 332, collagen VII, and BP180 and BP230 have been proposed.2,4,5 Jacoby et al6 described BPCP on a spectrum with bullous pemphigoid and cicatricial pemphigoid, with primarily circulating autoantibodies on one end and tissue-fixed autoantibodies on the other.
The differential for BPCP also includes anti-p200 pemphigoid and anti–laminin 332 pemphigoid. Anti-p200 pemphigoid also is known as bullous pemphigoid with antibodies against the 200-kDa protein.7 It may clinically manifest similar to bullous pemphigoid and other subepidermal autoimmune blistering diseases; thus, immunopathologic differentiation can be helpful. Anti–laminin 332 pemphigoid (also known as anti–laminin gamma-1 pemphigoid) is characterized by autoantibodies targeting the laminin 332 protein in the basement membrane zone, resulting in blistering and erosions.8 Similar to BPCP and epidermolysis bullosa aquisita, anti–laminin 332 pemphigoid may affect cephalic regions and mucous membrane surfaces, resulting in scarring and cicatricial changes. Anti–laminin 332 pemphigoid also has been associated with internal malignancy.8 The use of the salt-split skin technique can be utilized to differentiate these entities based on their autoantibody-binding patterns in relation to the lamina densa.
Treatment options for mild BPCP include potent topical or intralesional steroids and dapsone, while more severe cases may require systemic therapy with rituximab, azathioprine, mycophenolate mofetil, or cyclophosphamide.4
This case highlights the importance of histopathologic examination of skin lesions with an unusual history or clinical presentation. Dermatologists should consider BPCP when presented with erosions, ulcerations, or blisters of the head and neck in middle-aged male patients.
The Diagnosis: Brunsting-Perry Cicatricial Pemphigoid
Physical examination and histopathology are paramount in diagnosing Brunsting-Perry cicatricial pemphigoid (BPCP). In our patient, histopathology showed subepidermal blistering with a mixed superficial dermal inflammatory cell infiltrate. Direct immunofluorescence was positive for linear IgG and C3 antibodies along the basement membrane. The scarring erosions on the scalp combined with the autoantibody findings on direct immunofluorescence were consistent with BPCP. He was started on dapsone 100 mg daily and demonstrated complete resolution of symptoms after 10 months, with the exception of persistent scarring hair loss (Figure).
Brunsting-Perry cicatricial pemphigoid is a rare dermatologic condition. It was first defined in 1957 when Brunsting and Perry1 examined 7 patients with cicatricial pemphigoid that predominantly affected the head and neck region, with occasional mucous membrane involvement but no mucosal scarring. Characteristically, BPCP manifests as scarring herpetiform plaques with varied blisters, erosions, crusts, and scarring.1 It primarily affects middle-aged men.2
Historically, BPCP has been considered a variant of cicatricial pemphigoid (now known as mucous membrane pemphigoid), bullous pemphigoid, or epidermolysis bullosa acquisita.3 The antigen target has not been established clearly; however, autoantibodies against laminin 332, collagen VII, and BP180 and BP230 have been proposed.2,4,5 Jacoby et al6 described BPCP on a spectrum with bullous pemphigoid and cicatricial pemphigoid, with primarily circulating autoantibodies on one end and tissue-fixed autoantibodies on the other.
The differential for BPCP also includes anti-p200 pemphigoid and anti–laminin 332 pemphigoid. Anti-p200 pemphigoid also is known as bullous pemphigoid with antibodies against the 200-kDa protein.7 It may clinically manifest similar to bullous pemphigoid and other subepidermal autoimmune blistering diseases; thus, immunopathologic differentiation can be helpful. Anti–laminin 332 pemphigoid (also known as anti–laminin gamma-1 pemphigoid) is characterized by autoantibodies targeting the laminin 332 protein in the basement membrane zone, resulting in blistering and erosions.8 Similar to BPCP and epidermolysis bullosa aquisita, anti–laminin 332 pemphigoid may affect cephalic regions and mucous membrane surfaces, resulting in scarring and cicatricial changes. Anti–laminin 332 pemphigoid also has been associated with internal malignancy.8 The use of the salt-split skin technique can be utilized to differentiate these entities based on their autoantibody-binding patterns in relation to the lamina densa.
Treatment options for mild BPCP include potent topical or intralesional steroids and dapsone, while more severe cases may require systemic therapy with rituximab, azathioprine, mycophenolate mofetil, or cyclophosphamide.4
This case highlights the importance of histopathologic examination of skin lesions with an unusual history or clinical presentation. Dermatologists should consider BPCP when presented with erosions, ulcerations, or blisters of the head and neck in middle-aged male patients.
- Brunsting LA, Perry HO. Benign pemphigoid? a report of seven cases with chronic, scarring, herpetiform plaques about the head and neck. AMA Arch Derm. 1957;75:489-501. doi:10.1001 /archderm.1957.01550160015002
- Jedlickova H, Neidermeier A, Zgažarová S, et al. Brunsting-Perry pemphigoid of the scalp with antibodies against laminin 332. Dermatology. 2011;222:193-195. doi:10.1159/000322842
- Eichhoff G. Brunsting-Perry pemphigoid as differential diagnosis of nonmelanoma skin cancer. Cureus. 2019;11:E5400. doi:10.7759/cureus.5400
- Asfour L, Chong H, Mee J, et al. Epidermolysis bullosa acquisita (Brunsting-Perry pemphigoid variant) localized to the face and diagnosed with antigen identification using skin deficient in type VII collagen. Am J Dermatopathol. 2017;39:e90-e96. doi:10.1097 /DAD.0000000000000829
- Zhou S, Zou Y, Pan M. Brunsting-Perry pemphigoid transitioning from previous bullous pemphigoid. JAAD Case Rep. 2020;6:192-194. doi:10.1016/j.jdcr.2019.12.018
- Jacoby WD Jr, Bartholome CW, Ramchand SC, et al. Cicatricial pemphigoid (Brunsting-Perry type). case report and immunofluorescence findings. Arch Dermatol. 1978;114:779-781. doi:10.1001/archderm.1978.01640170079018
- Kridin K, Ahmed AR. Anti-p200 pemphigoid: a systematic review. Front Immunol. 2019;10:2466. doi:10.3389/fimmu.2019.02466
- Shi L, Li X, Qian H. Anti-laminin 332-type mucous membrane pemphigoid. Biomolecules. 2022;12:1461. doi:10.3390/biom12101461
- Brunsting LA, Perry HO. Benign pemphigoid? a report of seven cases with chronic, scarring, herpetiform plaques about the head and neck. AMA Arch Derm. 1957;75:489-501. doi:10.1001 /archderm.1957.01550160015002
- Jedlickova H, Neidermeier A, Zgažarová S, et al. Brunsting-Perry pemphigoid of the scalp with antibodies against laminin 332. Dermatology. 2011;222:193-195. doi:10.1159/000322842
- Eichhoff G. Brunsting-Perry pemphigoid as differential diagnosis of nonmelanoma skin cancer. Cureus. 2019;11:E5400. doi:10.7759/cureus.5400
- Asfour L, Chong H, Mee J, et al. Epidermolysis bullosa acquisita (Brunsting-Perry pemphigoid variant) localized to the face and diagnosed with antigen identification using skin deficient in type VII collagen. Am J Dermatopathol. 2017;39:e90-e96. doi:10.1097 /DAD.0000000000000829
- Zhou S, Zou Y, Pan M. Brunsting-Perry pemphigoid transitioning from previous bullous pemphigoid. JAAD Case Rep. 2020;6:192-194. doi:10.1016/j.jdcr.2019.12.018
- Jacoby WD Jr, Bartholome CW, Ramchand SC, et al. Cicatricial pemphigoid (Brunsting-Perry type). case report and immunofluorescence findings. Arch Dermatol. 1978;114:779-781. doi:10.1001/archderm.1978.01640170079018
- Kridin K, Ahmed AR. Anti-p200 pemphigoid: a systematic review. Front Immunol. 2019;10:2466. doi:10.3389/fimmu.2019.02466
- Shi L, Li X, Qian H. Anti-laminin 332-type mucous membrane pemphigoid. Biomolecules. 2022;12:1461. doi:10.3390/biom12101461
A 60-year-old man presented to a dermatology clinic with a wound on the scalp that had persisted for 11 months. The lesion started as a small erosion that eventually progressed to involve the entire parietal scalp. He had a history of type 2 diabetes mellitus, hypertension, and Graves disease. Physical examination demonstrated a large scar over the vertex scalp with central erosion, overlying crust, peripheral scalp atrophy, hypopigmentation at the periphery, and exaggerated superficial vasculature. Some oral erosions also were observed. A review of systems was negative for any constitutional symptoms. A month prior, the patient had been started on dapsone 50 mg with a prednisone taper by an outside dermatologist and noticed some improvement.
Family Size, Dog Ownership Linked With Reduced Risk of Crohn’s
, according to investigators.
Those who live with a pet bird may be more likely to develop CD, although few participants in the study lived with birds, requiring a cautious interpretation of this latter finding, lead author Mingyue Xue, PhD, of Mount Sinai Hospital, Toronto, Ontario, Canada, and colleagues reported.
“Environmental factors, such as smoking, large families, urban environments, and exposure to pets, have been shown to be associated with the risk of CD development,” the investigators wrote in Clinical Gastroenterology and Hepatology. “However, most of these studies were based on a retrospective study design, which makes it challenging to understand when and how environmental factors trigger the biological changes that lead to disease.”
The present study prospectively followed 4289 asymptomatic first-degree relatives (FDRs) of patients with CD. Environmental factors were identified via regression models that also considered biological factors, including gut inflammation via fecal calprotectin (FCP) levels, altered intestinal permeability measured by urinary fractional excretion of lactulose to mannitol ratio (LMR), and fecal microbiome composition through 16S rRNA sequencing.
After a median follow-up period of 5.62 years, 86 FDRs (1.9%) developed CD.
Living in a household of at least three people in the first year of life was associated with a 57% reduced risk of CD development (hazard ratio [HR], 0.43; P = .019). Similarly, living with a pet dog between the ages of 5 and 15 also demonstrated a protective effect, dropping risk of CD by 39% (HR, 0.61; P = .025).
“Our analysis revealed a protective trend of living with dogs that transcends the age of exposure, suggesting that dog ownership could confer health benefits in reducing the risk of CD,” the investigators wrote. “Our study also found that living in a large family during the first year of life is significantly associated with the future onset of CD, aligning with prior research that indicates that a larger family size in the first year of life can reduce the risk of developing IBD.”
In contrast, the study identified bird ownership at time of recruitment as a risk factor for CD, increasing risk almost three-fold (HR, 2.84; P = .005). The investigators urged a careful interpretation of this latter finding, however, as relatively few FDRs lived with birds.
“[A]lthough our sample size can be considered large, some environmental variables were uncommon, such as the participants having birds as pets, and would greatly benefit from replication of our findings in other cohorts,” Dr. Xue and colleagues noted.
They suggested several possible ways in which the above environmental factors may impact CD risk, including effects on subclinical inflammation, microbiome composition, and gut permeability.
“Understanding the relationship between CD-related environmental factors and these predisease biomarkers may shed light on the underlying mechanisms by which environmental factors impact host health and ultimately lead to CD onset,” the investigators concluded.
The study was supported by Crohn’s and Colitis Canada, Canadian Institutes of Health Research, the Helmsley Charitable Trust, and others. The investigators disclosed no conflicts of interest.
, according to investigators.
Those who live with a pet bird may be more likely to develop CD, although few participants in the study lived with birds, requiring a cautious interpretation of this latter finding, lead author Mingyue Xue, PhD, of Mount Sinai Hospital, Toronto, Ontario, Canada, and colleagues reported.
“Environmental factors, such as smoking, large families, urban environments, and exposure to pets, have been shown to be associated with the risk of CD development,” the investigators wrote in Clinical Gastroenterology and Hepatology. “However, most of these studies were based on a retrospective study design, which makes it challenging to understand when and how environmental factors trigger the biological changes that lead to disease.”
The present study prospectively followed 4289 asymptomatic first-degree relatives (FDRs) of patients with CD. Environmental factors were identified via regression models that also considered biological factors, including gut inflammation via fecal calprotectin (FCP) levels, altered intestinal permeability measured by urinary fractional excretion of lactulose to mannitol ratio (LMR), and fecal microbiome composition through 16S rRNA sequencing.
After a median follow-up period of 5.62 years, 86 FDRs (1.9%) developed CD.
Living in a household of at least three people in the first year of life was associated with a 57% reduced risk of CD development (hazard ratio [HR], 0.43; P = .019). Similarly, living with a pet dog between the ages of 5 and 15 also demonstrated a protective effect, dropping risk of CD by 39% (HR, 0.61; P = .025).
“Our analysis revealed a protective trend of living with dogs that transcends the age of exposure, suggesting that dog ownership could confer health benefits in reducing the risk of CD,” the investigators wrote. “Our study also found that living in a large family during the first year of life is significantly associated with the future onset of CD, aligning with prior research that indicates that a larger family size in the first year of life can reduce the risk of developing IBD.”
In contrast, the study identified bird ownership at time of recruitment as a risk factor for CD, increasing risk almost three-fold (HR, 2.84; P = .005). The investigators urged a careful interpretation of this latter finding, however, as relatively few FDRs lived with birds.
“[A]lthough our sample size can be considered large, some environmental variables were uncommon, such as the participants having birds as pets, and would greatly benefit from replication of our findings in other cohorts,” Dr. Xue and colleagues noted.
They suggested several possible ways in which the above environmental factors may impact CD risk, including effects on subclinical inflammation, microbiome composition, and gut permeability.
“Understanding the relationship between CD-related environmental factors and these predisease biomarkers may shed light on the underlying mechanisms by which environmental factors impact host health and ultimately lead to CD onset,” the investigators concluded.
The study was supported by Crohn’s and Colitis Canada, Canadian Institutes of Health Research, the Helmsley Charitable Trust, and others. The investigators disclosed no conflicts of interest.
, according to investigators.
Those who live with a pet bird may be more likely to develop CD, although few participants in the study lived with birds, requiring a cautious interpretation of this latter finding, lead author Mingyue Xue, PhD, of Mount Sinai Hospital, Toronto, Ontario, Canada, and colleagues reported.
“Environmental factors, such as smoking, large families, urban environments, and exposure to pets, have been shown to be associated with the risk of CD development,” the investigators wrote in Clinical Gastroenterology and Hepatology. “However, most of these studies were based on a retrospective study design, which makes it challenging to understand when and how environmental factors trigger the biological changes that lead to disease.”
The present study prospectively followed 4289 asymptomatic first-degree relatives (FDRs) of patients with CD. Environmental factors were identified via regression models that also considered biological factors, including gut inflammation via fecal calprotectin (FCP) levels, altered intestinal permeability measured by urinary fractional excretion of lactulose to mannitol ratio (LMR), and fecal microbiome composition through 16S rRNA sequencing.
After a median follow-up period of 5.62 years, 86 FDRs (1.9%) developed CD.
Living in a household of at least three people in the first year of life was associated with a 57% reduced risk of CD development (hazard ratio [HR], 0.43; P = .019). Similarly, living with a pet dog between the ages of 5 and 15 also demonstrated a protective effect, dropping risk of CD by 39% (HR, 0.61; P = .025).
“Our analysis revealed a protective trend of living with dogs that transcends the age of exposure, suggesting that dog ownership could confer health benefits in reducing the risk of CD,” the investigators wrote. “Our study also found that living in a large family during the first year of life is significantly associated with the future onset of CD, aligning with prior research that indicates that a larger family size in the first year of life can reduce the risk of developing IBD.”
In contrast, the study identified bird ownership at time of recruitment as a risk factor for CD, increasing risk almost three-fold (HR, 2.84; P = .005). The investigators urged a careful interpretation of this latter finding, however, as relatively few FDRs lived with birds.
“[A]lthough our sample size can be considered large, some environmental variables were uncommon, such as the participants having birds as pets, and would greatly benefit from replication of our findings in other cohorts,” Dr. Xue and colleagues noted.
They suggested several possible ways in which the above environmental factors may impact CD risk, including effects on subclinical inflammation, microbiome composition, and gut permeability.
“Understanding the relationship between CD-related environmental factors and these predisease biomarkers may shed light on the underlying mechanisms by which environmental factors impact host health and ultimately lead to CD onset,” the investigators concluded.
The study was supported by Crohn’s and Colitis Canada, Canadian Institutes of Health Research, the Helmsley Charitable Trust, and others. The investigators disclosed no conflicts of interest.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Is Buprenorphine/Naloxone Safer Than Buprenorphine Alone During Pregnancy?
TOPLINE:
Buprenorphine combined with naloxone during pregnancy is associated with lower risks for neonatal abstinence syndrome and neonatal intensive care unit admission than buprenorphine alone. The study also found no significant differences in major congenital malformations between the two treatments.
METHODOLOGY:
- Researchers conducted a population-based cohort study using healthcare utilization data of people who were insured by Medicaid between 2000 and 2018.
- A total of 8695 pregnant individuals were included, with 3369 exposed to buprenorphine/naloxone and 5326 exposed to buprenorphine alone during the first trimester.
- Outcome measures included major congenital malformations, low birth weight, neonatal abstinence syndrome, neonatal intensive care unit admission, preterm birth, respiratory symptoms, small for gestational age, cesarean delivery, and maternal morbidity.
- The study excluded pregnancies with chromosomal anomalies, first-trimester exposure to known teratogens, or methadone use during baseline or the first trimester.
TAKEAWAY:
- According to the authors, buprenorphine/naloxone exposure during pregnancy was associated with a lower risk for neonatal abstinence syndrome (weighted risk ratio [RR], 0.77; 95% CI, 0.70-0.84) than buprenorphine alone.
- The researchers found a modestly lower risk for neonatal intensive care unit admission (weighted RR, 0.91; 95% CI, 0.85-0.98) and small risk for gestational age (weighted RR, 0.86; 95% CI, 0.75-0.98) in the buprenorphine/naloxone group.
- No significant differences were observed between the two groups in major congenital malformations, low birth weight, preterm birth, respiratory symptoms, or cesarean delivery.
IN PRACTICE:
“For the outcomes assessed, compared with buprenorphine alone, buprenorphine combined with naloxone during pregnancy appears to be a safe treatment option. This supports the view that both formulations are reasonable options for treatment of OUD in pregnancy, affirming flexibility in collaborative treatment decision-making,” the study authors wrote.
SOURCE:
The study was led by Loreen Straub, MD, MS, of the Division of Pharmacoepidemiology and Pharmacoeconomics at Brigham and Women’s Hospital and Harvard Medical School in Boston. It was published online in JAMA.
LIMITATIONS:
Some potential confounders, such as alcohol use and cigarette smoking, may not have been recorded in claims data. The findings for many of the neonatal and maternal outcomes suggest that confounding by unmeasured factors is an unlikely explanation for the associations observed. Individuals identified as exposed based on filled prescriptions might not have used the medication. The study used outcome algorithms with relatively high positive predictive values to minimize outcome misclassification. The cohort was restricted to live births to enable linkage to infants and to assess neonatal outcomes.
DISCLOSURES:
Various authors reported receiving grants and personal fees from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institute on Drug Abuse, Roche, Moderna, Takeda, and Janssen Global, among others.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Buprenorphine combined with naloxone during pregnancy is associated with lower risks for neonatal abstinence syndrome and neonatal intensive care unit admission than buprenorphine alone. The study also found no significant differences in major congenital malformations between the two treatments.
METHODOLOGY:
- Researchers conducted a population-based cohort study using healthcare utilization data of people who were insured by Medicaid between 2000 and 2018.
- A total of 8695 pregnant individuals were included, with 3369 exposed to buprenorphine/naloxone and 5326 exposed to buprenorphine alone during the first trimester.
- Outcome measures included major congenital malformations, low birth weight, neonatal abstinence syndrome, neonatal intensive care unit admission, preterm birth, respiratory symptoms, small for gestational age, cesarean delivery, and maternal morbidity.
- The study excluded pregnancies with chromosomal anomalies, first-trimester exposure to known teratogens, or methadone use during baseline or the first trimester.
TAKEAWAY:
- According to the authors, buprenorphine/naloxone exposure during pregnancy was associated with a lower risk for neonatal abstinence syndrome (weighted risk ratio [RR], 0.77; 95% CI, 0.70-0.84) than buprenorphine alone.
- The researchers found a modestly lower risk for neonatal intensive care unit admission (weighted RR, 0.91; 95% CI, 0.85-0.98) and small risk for gestational age (weighted RR, 0.86; 95% CI, 0.75-0.98) in the buprenorphine/naloxone group.
- No significant differences were observed between the two groups in major congenital malformations, low birth weight, preterm birth, respiratory symptoms, or cesarean delivery.
IN PRACTICE:
“For the outcomes assessed, compared with buprenorphine alone, buprenorphine combined with naloxone during pregnancy appears to be a safe treatment option. This supports the view that both formulations are reasonable options for treatment of OUD in pregnancy, affirming flexibility in collaborative treatment decision-making,” the study authors wrote.
SOURCE:
The study was led by Loreen Straub, MD, MS, of the Division of Pharmacoepidemiology and Pharmacoeconomics at Brigham and Women’s Hospital and Harvard Medical School in Boston. It was published online in JAMA.
LIMITATIONS:
Some potential confounders, such as alcohol use and cigarette smoking, may not have been recorded in claims data. The findings for many of the neonatal and maternal outcomes suggest that confounding by unmeasured factors is an unlikely explanation for the associations observed. Individuals identified as exposed based on filled prescriptions might not have used the medication. The study used outcome algorithms with relatively high positive predictive values to minimize outcome misclassification. The cohort was restricted to live births to enable linkage to infants and to assess neonatal outcomes.
DISCLOSURES:
Various authors reported receiving grants and personal fees from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institute on Drug Abuse, Roche, Moderna, Takeda, and Janssen Global, among others.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Buprenorphine combined with naloxone during pregnancy is associated with lower risks for neonatal abstinence syndrome and neonatal intensive care unit admission than buprenorphine alone. The study also found no significant differences in major congenital malformations between the two treatments.
METHODOLOGY:
- Researchers conducted a population-based cohort study using healthcare utilization data of people who were insured by Medicaid between 2000 and 2018.
- A total of 8695 pregnant individuals were included, with 3369 exposed to buprenorphine/naloxone and 5326 exposed to buprenorphine alone during the first trimester.
- Outcome measures included major congenital malformations, low birth weight, neonatal abstinence syndrome, neonatal intensive care unit admission, preterm birth, respiratory symptoms, small for gestational age, cesarean delivery, and maternal morbidity.
- The study excluded pregnancies with chromosomal anomalies, first-trimester exposure to known teratogens, or methadone use during baseline or the first trimester.
TAKEAWAY:
- According to the authors, buprenorphine/naloxone exposure during pregnancy was associated with a lower risk for neonatal abstinence syndrome (weighted risk ratio [RR], 0.77; 95% CI, 0.70-0.84) than buprenorphine alone.
- The researchers found a modestly lower risk for neonatal intensive care unit admission (weighted RR, 0.91; 95% CI, 0.85-0.98) and small risk for gestational age (weighted RR, 0.86; 95% CI, 0.75-0.98) in the buprenorphine/naloxone group.
- No significant differences were observed between the two groups in major congenital malformations, low birth weight, preterm birth, respiratory symptoms, or cesarean delivery.
IN PRACTICE:
“For the outcomes assessed, compared with buprenorphine alone, buprenorphine combined with naloxone during pregnancy appears to be a safe treatment option. This supports the view that both formulations are reasonable options for treatment of OUD in pregnancy, affirming flexibility in collaborative treatment decision-making,” the study authors wrote.
SOURCE:
The study was led by Loreen Straub, MD, MS, of the Division of Pharmacoepidemiology and Pharmacoeconomics at Brigham and Women’s Hospital and Harvard Medical School in Boston. It was published online in JAMA.
LIMITATIONS:
Some potential confounders, such as alcohol use and cigarette smoking, may not have been recorded in claims data. The findings for many of the neonatal and maternal outcomes suggest that confounding by unmeasured factors is an unlikely explanation for the associations observed. Individuals identified as exposed based on filled prescriptions might not have used the medication. The study used outcome algorithms with relatively high positive predictive values to minimize outcome misclassification. The cohort was restricted to live births to enable linkage to infants and to assess neonatal outcomes.
DISCLOSURES:
Various authors reported receiving grants and personal fees from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institute on Drug Abuse, Roche, Moderna, Takeda, and Janssen Global, among others.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
E-Bikes: The Good ... and the Ugly
Bicycles have been woven into my life since I first straddled a hand-me-down with a fan belt drive when I was 3. At age 12 my friend Ricky and I took a 250 mile–plus 2-night adventure on our 3-speed “English” style bikes. We still marvel that our parents let us do it when neither cell phones nor GPS existed.
I have always bike commuted to work, including the years when that involved a perilous navigation into Boston from the suburbs. In our mid-50s my wife and I biked from Washington state back here to Maine with another couple unsupported. We continue to do at least one self-guided cycle tour out of the country each year.
Not surprisingly, I keep a close eye on what’s happening in the bicycle market. For decades the trends have shifted back and forth between sleek road models and beefier off-roaders. There have been boom years here and there for the dealers and manufacturers, but nothing like what the bike industry is experiencing now with the arrival of e-bikes on the market. Driven primarily by electrification, micromobility ridership (which includes conventional bikes and scooters) has grown more than 50-fold over the last 10 years. Projections suggest the market’s value will be $300 billion by 2030.
It doesn’t take an MBA with a major in marketing to understand the broad appeal of electrification. Most adults have ridden a bicycle as children, but several decades of gap years has left many of them with a level of fitness that makes pedaling against the wind or up any incline difficult and unappealing. An e-bike can put even the least fitness conscious back in the saddle and open the options for outdoor recreation they haven’t dreamed of since childhood.
In large part the people flocking to e-bikes are retiree’s who thought they were “over the hill.” They are having so much fun they don’t care if the Lycra-clad “serious” cyclists notice the battery bulge in the frame on their e-bikes. Another group of e-bike adopters are motivated by the “greenness” of a fossil-fuel–free electric powered transportation which, with minimal compromise, can be used as they would a car around town and for longer commutes than they would have considered on a purely pedal-powered bicycle.
Unfortunately, there is a growing group of younger e-bike riders who are motivated and uninhibited by the potential that the power boost of a small electric motor can provide. And here is where the ugliness begins to intrude on what was otherwise a beautiful and expanding landscape. However, it is the young who are, not surprisingly, drawn to the speed, and with any vehicle – motorized or conventional – as speed increases so does the frequency and seriousness of accidents.
The term e-bike covers a broad range of vehicles, from those designated class 1, which require pedaling and are limited to 20 miles per hour, to class 3, which may have a throttle and unmodified can hit 28 mph. Class 2 bikes have a throttle that will allow the rider to reach 20 mph without pedaling. Modifying any class of e-bike can substantially increase its speed, but this is more common in classes 2 and 3. As an example, some very fast micromobiles are considered unclassified e-bikes and avoid being labeled motorcycles simply because they have pedals.
One has to give some credit to the e-bike industry for eventually adopting this classification system. But, we must give the rest of us, including parents and public safety officials, a failing grade for doing a poor job of translating these scores into enforceable regulations to protect both riders and pedestrians from serious injury.
On the governmental side only a little more than half of US states have used the three category classification to craft their regulations. Many jurisdictions have failed to differentiate between streets, sidewalks, and trails. Regulations vary from state to state, and many states leave it up to local communities. From my experience chairing our town’s Bicycle and Pedestrian Advisory Committee, I can tell you that even “progressive” communities are struggling to decide who can ride what where. The result has been that people of all ages, but mostly adolescents, are traveling on busy streets and sidewalks at speeds that put themselves and pedestrians at risk.
On the parental side of the problem are families that have either allowed or enabled their children to ride class 2 and 3 e-bikes without proper safety equipment or consideration for the safety of the rest of the community. Currently, this is not much of a problem here in Maine thanks to the weather and the high price of e-bikes. However, I frequently visit an affluent community in the San Francisco Bay Area, where it is not uncommon to see middle school children speeding along well in excess of 20 mph.
Unfortunately this is another example, like television and cell phone, in which our society has been unable to keep up with technology by molding the behavior of our children and/or creating enforceable rules that allow us to reap the benefits of new discoveries while minimizing the collateral damage that can accompany them.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
Bicycles have been woven into my life since I first straddled a hand-me-down with a fan belt drive when I was 3. At age 12 my friend Ricky and I took a 250 mile–plus 2-night adventure on our 3-speed “English” style bikes. We still marvel that our parents let us do it when neither cell phones nor GPS existed.
I have always bike commuted to work, including the years when that involved a perilous navigation into Boston from the suburbs. In our mid-50s my wife and I biked from Washington state back here to Maine with another couple unsupported. We continue to do at least one self-guided cycle tour out of the country each year.
Not surprisingly, I keep a close eye on what’s happening in the bicycle market. For decades the trends have shifted back and forth between sleek road models and beefier off-roaders. There have been boom years here and there for the dealers and manufacturers, but nothing like what the bike industry is experiencing now with the arrival of e-bikes on the market. Driven primarily by electrification, micromobility ridership (which includes conventional bikes and scooters) has grown more than 50-fold over the last 10 years. Projections suggest the market’s value will be $300 billion by 2030.
It doesn’t take an MBA with a major in marketing to understand the broad appeal of electrification. Most adults have ridden a bicycle as children, but several decades of gap years has left many of them with a level of fitness that makes pedaling against the wind or up any incline difficult and unappealing. An e-bike can put even the least fitness conscious back in the saddle and open the options for outdoor recreation they haven’t dreamed of since childhood.
In large part the people flocking to e-bikes are retiree’s who thought they were “over the hill.” They are having so much fun they don’t care if the Lycra-clad “serious” cyclists notice the battery bulge in the frame on their e-bikes. Another group of e-bike adopters are motivated by the “greenness” of a fossil-fuel–free electric powered transportation which, with minimal compromise, can be used as they would a car around town and for longer commutes than they would have considered on a purely pedal-powered bicycle.
Unfortunately, there is a growing group of younger e-bike riders who are motivated and uninhibited by the potential that the power boost of a small electric motor can provide. And here is where the ugliness begins to intrude on what was otherwise a beautiful and expanding landscape. However, it is the young who are, not surprisingly, drawn to the speed, and with any vehicle – motorized or conventional – as speed increases so does the frequency and seriousness of accidents.
The term e-bike covers a broad range of vehicles, from those designated class 1, which require pedaling and are limited to 20 miles per hour, to class 3, which may have a throttle and unmodified can hit 28 mph. Class 2 bikes have a throttle that will allow the rider to reach 20 mph without pedaling. Modifying any class of e-bike can substantially increase its speed, but this is more common in classes 2 and 3. As an example, some very fast micromobiles are considered unclassified e-bikes and avoid being labeled motorcycles simply because they have pedals.
One has to give some credit to the e-bike industry for eventually adopting this classification system. But, we must give the rest of us, including parents and public safety officials, a failing grade for doing a poor job of translating these scores into enforceable regulations to protect both riders and pedestrians from serious injury.
On the governmental side only a little more than half of US states have used the three category classification to craft their regulations. Many jurisdictions have failed to differentiate between streets, sidewalks, and trails. Regulations vary from state to state, and many states leave it up to local communities. From my experience chairing our town’s Bicycle and Pedestrian Advisory Committee, I can tell you that even “progressive” communities are struggling to decide who can ride what where. The result has been that people of all ages, but mostly adolescents, are traveling on busy streets and sidewalks at speeds that put themselves and pedestrians at risk.
On the parental side of the problem are families that have either allowed or enabled their children to ride class 2 and 3 e-bikes without proper safety equipment or consideration for the safety of the rest of the community. Currently, this is not much of a problem here in Maine thanks to the weather and the high price of e-bikes. However, I frequently visit an affluent community in the San Francisco Bay Area, where it is not uncommon to see middle school children speeding along well in excess of 20 mph.
Unfortunately this is another example, like television and cell phone, in which our society has been unable to keep up with technology by molding the behavior of our children and/or creating enforceable rules that allow us to reap the benefits of new discoveries while minimizing the collateral damage that can accompany them.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
Bicycles have been woven into my life since I first straddled a hand-me-down with a fan belt drive when I was 3. At age 12 my friend Ricky and I took a 250 mile–plus 2-night adventure on our 3-speed “English” style bikes. We still marvel that our parents let us do it when neither cell phones nor GPS existed.
I have always bike commuted to work, including the years when that involved a perilous navigation into Boston from the suburbs. In our mid-50s my wife and I biked from Washington state back here to Maine with another couple unsupported. We continue to do at least one self-guided cycle tour out of the country each year.
Not surprisingly, I keep a close eye on what’s happening in the bicycle market. For decades the trends have shifted back and forth between sleek road models and beefier off-roaders. There have been boom years here and there for the dealers and manufacturers, but nothing like what the bike industry is experiencing now with the arrival of e-bikes on the market. Driven primarily by electrification, micromobility ridership (which includes conventional bikes and scooters) has grown more than 50-fold over the last 10 years. Projections suggest the market’s value will be $300 billion by 2030.
It doesn’t take an MBA with a major in marketing to understand the broad appeal of electrification. Most adults have ridden a bicycle as children, but several decades of gap years has left many of them with a level of fitness that makes pedaling against the wind or up any incline difficult and unappealing. An e-bike can put even the least fitness conscious back in the saddle and open the options for outdoor recreation they haven’t dreamed of since childhood.
In large part the people flocking to e-bikes are retiree’s who thought they were “over the hill.” They are having so much fun they don’t care if the Lycra-clad “serious” cyclists notice the battery bulge in the frame on their e-bikes. Another group of e-bike adopters are motivated by the “greenness” of a fossil-fuel–free electric powered transportation which, with minimal compromise, can be used as they would a car around town and for longer commutes than they would have considered on a purely pedal-powered bicycle.
Unfortunately, there is a growing group of younger e-bike riders who are motivated and uninhibited by the potential that the power boost of a small electric motor can provide. And here is where the ugliness begins to intrude on what was otherwise a beautiful and expanding landscape. However, it is the young who are, not surprisingly, drawn to the speed, and with any vehicle – motorized or conventional – as speed increases so does the frequency and seriousness of accidents.
The term e-bike covers a broad range of vehicles, from those designated class 1, which require pedaling and are limited to 20 miles per hour, to class 3, which may have a throttle and unmodified can hit 28 mph. Class 2 bikes have a throttle that will allow the rider to reach 20 mph without pedaling. Modifying any class of e-bike can substantially increase its speed, but this is more common in classes 2 and 3. As an example, some very fast micromobiles are considered unclassified e-bikes and avoid being labeled motorcycles simply because they have pedals.
One has to give some credit to the e-bike industry for eventually adopting this classification system. But, we must give the rest of us, including parents and public safety officials, a failing grade for doing a poor job of translating these scores into enforceable regulations to protect both riders and pedestrians from serious injury.
On the governmental side only a little more than half of US states have used the three category classification to craft their regulations. Many jurisdictions have failed to differentiate between streets, sidewalks, and trails. Regulations vary from state to state, and many states leave it up to local communities. From my experience chairing our town’s Bicycle and Pedestrian Advisory Committee, I can tell you that even “progressive” communities are struggling to decide who can ride what where. The result has been that people of all ages, but mostly adolescents, are traveling on busy streets and sidewalks at speeds that put themselves and pedestrians at risk.
On the parental side of the problem are families that have either allowed or enabled their children to ride class 2 and 3 e-bikes without proper safety equipment or consideration for the safety of the rest of the community. Currently, this is not much of a problem here in Maine thanks to the weather and the high price of e-bikes. However, I frequently visit an affluent community in the San Francisco Bay Area, where it is not uncommon to see middle school children speeding along well in excess of 20 mph.
Unfortunately this is another example, like television and cell phone, in which our society has been unable to keep up with technology by molding the behavior of our children and/or creating enforceable rules that allow us to reap the benefits of new discoveries while minimizing the collateral damage that can accompany them.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
A Racing Heart Signals Trouble in Chronic Kidney Disease
TOPLINE:
A higher resting heart rate, even within the normal range, is linked to an increased risk for mortality and cardiovascular events in patients with non–dialysis-dependent chronic kidney disease (CKD).
METHODOLOGY:
- An elevated resting heart rate is an independent risk factor for all-cause mortality and cardiovascular events in the general population; however, the correlation between heart rate and mortality in patients with CKD is unclear.
- Researchers analyzed the longitudinal data of patients with non–dialysis-dependent CKD enrolled in the Fukushima CKD Cohort Study to investigate the association between resting heart rate and adverse clinical outcomes.
- The patient cohort was stratified into four groups on the basis of resting heart rates: < 70, 70-79, 80-89, and ≥ 90 beats/min.
- The primary and secondary outcomes were all-cause mortality and cardiovascular events, respectively, the latter category including myocardial infarction, angina pectoris, and heart failure.
TAKEAWAY:
- Researchers enrolled 1353 patients with non–dialysis-dependent CKD (median age, 65 years; 56.7% men; median estimated glomerular filtration rate, 52.2 mL/min/1.73 m2) who had a median heart rate of 76 beats/min.
- During the median observation period of 4.9 years, 123 patients died and 163 developed cardiovascular events.
- Compared with patients with a resting heart rate < 70 beats/min, those with a resting heart rate of 80-89 and ≥ 90 beats/min had an adjusted hazard ratio of 1.74 and 2.61 for all-cause mortality, respectively.
- Similarly, the risk for cardiovascular events was higher in patients with a heart rate of 80-89 beats/min than in those with a heart rate < 70 beats/min (adjusted hazard ratio, 1.70).
IN PRACTICE:
“The present study supported the idea that reducing heart rate might be effective for CKD patients with a heart rate ≥ 70/min, since the lowest risk of mortality was seen in patients with heart rate < 70/min,” the authors concluded.
SOURCE:
This study was led by Hirotaka Saito, Department of Nephrology and Hypertension, Fukushima Medical University, Fukushima City, Japan. It was published online in Scientific Reports.
LIMITATIONS:
Heart rate was measured using a standard sphygmomanometer or an automated device, rather than an electrocardiograph, which may have introduced measurement variability. The observational nature of the study precluded the establishment of cause-and-effect relationships between heart rate and clinical outcomes. Additionally, variables such as lifestyle factors, underlying health conditions, and socioeconomic factors were not measured, which could have affected the results.
DISCLOSURES:
Some authors received research funding from Chugai Pharmaceutical, Kowa Pharmaceutical, Ono Pharmaceutical, and other sources. They declared having no competing interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
A higher resting heart rate, even within the normal range, is linked to an increased risk for mortality and cardiovascular events in patients with non–dialysis-dependent chronic kidney disease (CKD).
METHODOLOGY:
- An elevated resting heart rate is an independent risk factor for all-cause mortality and cardiovascular events in the general population; however, the correlation between heart rate and mortality in patients with CKD is unclear.
- Researchers analyzed the longitudinal data of patients with non–dialysis-dependent CKD enrolled in the Fukushima CKD Cohort Study to investigate the association between resting heart rate and adverse clinical outcomes.
- The patient cohort was stratified into four groups on the basis of resting heart rates: < 70, 70-79, 80-89, and ≥ 90 beats/min.
- The primary and secondary outcomes were all-cause mortality and cardiovascular events, respectively, the latter category including myocardial infarction, angina pectoris, and heart failure.
TAKEAWAY:
- Researchers enrolled 1353 patients with non–dialysis-dependent CKD (median age, 65 years; 56.7% men; median estimated glomerular filtration rate, 52.2 mL/min/1.73 m2) who had a median heart rate of 76 beats/min.
- During the median observation period of 4.9 years, 123 patients died and 163 developed cardiovascular events.
- Compared with patients with a resting heart rate < 70 beats/min, those with a resting heart rate of 80-89 and ≥ 90 beats/min had an adjusted hazard ratio of 1.74 and 2.61 for all-cause mortality, respectively.
- Similarly, the risk for cardiovascular events was higher in patients with a heart rate of 80-89 beats/min than in those with a heart rate < 70 beats/min (adjusted hazard ratio, 1.70).
IN PRACTICE:
“The present study supported the idea that reducing heart rate might be effective for CKD patients with a heart rate ≥ 70/min, since the lowest risk of mortality was seen in patients with heart rate < 70/min,” the authors concluded.
SOURCE:
This study was led by Hirotaka Saito, Department of Nephrology and Hypertension, Fukushima Medical University, Fukushima City, Japan. It was published online in Scientific Reports.
LIMITATIONS:
Heart rate was measured using a standard sphygmomanometer or an automated device, rather than an electrocardiograph, which may have introduced measurement variability. The observational nature of the study precluded the establishment of cause-and-effect relationships between heart rate and clinical outcomes. Additionally, variables such as lifestyle factors, underlying health conditions, and socioeconomic factors were not measured, which could have affected the results.
DISCLOSURES:
Some authors received research funding from Chugai Pharmaceutical, Kowa Pharmaceutical, Ono Pharmaceutical, and other sources. They declared having no competing interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
A higher resting heart rate, even within the normal range, is linked to an increased risk for mortality and cardiovascular events in patients with non–dialysis-dependent chronic kidney disease (CKD).
METHODOLOGY:
- An elevated resting heart rate is an independent risk factor for all-cause mortality and cardiovascular events in the general population; however, the correlation between heart rate and mortality in patients with CKD is unclear.
- Researchers analyzed the longitudinal data of patients with non–dialysis-dependent CKD enrolled in the Fukushima CKD Cohort Study to investigate the association between resting heart rate and adverse clinical outcomes.
- The patient cohort was stratified into four groups on the basis of resting heart rates: < 70, 70-79, 80-89, and ≥ 90 beats/min.
- The primary and secondary outcomes were all-cause mortality and cardiovascular events, respectively, the latter category including myocardial infarction, angina pectoris, and heart failure.
TAKEAWAY:
- Researchers enrolled 1353 patients with non–dialysis-dependent CKD (median age, 65 years; 56.7% men; median estimated glomerular filtration rate, 52.2 mL/min/1.73 m2) who had a median heart rate of 76 beats/min.
- During the median observation period of 4.9 years, 123 patients died and 163 developed cardiovascular events.
- Compared with patients with a resting heart rate < 70 beats/min, those with a resting heart rate of 80-89 and ≥ 90 beats/min had an adjusted hazard ratio of 1.74 and 2.61 for all-cause mortality, respectively.
- Similarly, the risk for cardiovascular events was higher in patients with a heart rate of 80-89 beats/min than in those with a heart rate < 70 beats/min (adjusted hazard ratio, 1.70).
IN PRACTICE:
“The present study supported the idea that reducing heart rate might be effective for CKD patients with a heart rate ≥ 70/min, since the lowest risk of mortality was seen in patients with heart rate < 70/min,” the authors concluded.
SOURCE:
This study was led by Hirotaka Saito, Department of Nephrology and Hypertension, Fukushima Medical University, Fukushima City, Japan. It was published online in Scientific Reports.
LIMITATIONS:
Heart rate was measured using a standard sphygmomanometer or an automated device, rather than an electrocardiograph, which may have introduced measurement variability. The observational nature of the study precluded the establishment of cause-and-effect relationships between heart rate and clinical outcomes. Additionally, variables such as lifestyle factors, underlying health conditions, and socioeconomic factors were not measured, which could have affected the results.
DISCLOSURES:
Some authors received research funding from Chugai Pharmaceutical, Kowa Pharmaceutical, Ono Pharmaceutical, and other sources. They declared having no competing interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
PCOS Increases Eating Disorder Risk
TOPLINE:
Women with polycystic ovary syndrome (PCOS) have higher odds of some eating disorders, including bulimia nervosa, binge eating disorder, and disordered eating, regardless of weight.
METHODOLOGY:
- A small systematic review and meta-analysis showed increased odds of any eating disorders and disordered eating scores in adult women with PCOS compared with women without PCOS.
- As part of the 2023 update of the International Evidence-based Guideline for the Assessment of and Management of PCOS, the same researchers updated and expanded their analysis to include adolescents and specific eating disorders and to evaluate the effect of body mass index (BMI) on these risks.
- They included 20 cross-sectional studies involving 28,922 women with PCOS and 258,619 women without PCOS; PCOS was diagnosed by either National Institutes of Health or Rotterdam criteria, as well as by patient self-report or hospital records.
- Eating disorders were screened using a validated disordered eating screening tool or diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders.
- The outcomes of interest included the prevalence of any eating disorder, individual eating disorders, disordered eating, and mean disordered eating scores.
TAKEAWAY:
- Women with PCOS had 53% higher odds (odds ratio [OR], 1.53; 95% CI, 1.29-1.82; eight studies) of any eating disorder than control individuals without PCOS.
- The likelihood of bulimia nervosa (OR, 1.34; 95% CI, 1.17-1.54; five studies) and binge eating disorder (OR, 2.09; 95% CI, 1.18-3.72; four studies) was higher in women with PCOS, but no significant association was found for anorexia nervosa.
- The mean disordered eating scores and odds of disordered eating were higher in women with PCOS (standardized mean difference [SMD], 0.52; 95% CI, 0.28-0.77; 13 studies; and OR, 2.84; 95% CI, 1.0-8.04; eight studies; respectively).
- Disordered eating scores were higher in both the normal and higher weight categories (BMI < 25; SMD, 0.36; 95% CI, 0.15-0.58; five studies; and BMI ≥ 25; SMD, 0.68; 95% CI, 0.22-1.13; four studies; respectively).
IN PRACTICE:
“Our findings emphasize the importance of screening women with PCOS for eating disorders before clinicians share any lifestyle advice,” the lead author said in a press release. “The lifestyle modifications we often recommend for women with PCOS — including physical activity, healthy diet, and behavior modifications — could hinder the recovery process for eating disorders.”
SOURCE:
The study was led by Laura G. Cooney, MD, MSCE, University of Wisconsin, Madison, and published online in the Journal of Clinical Endocrinology & Metabolism.
LIMITATIONS:
The included studies were observational in nature, limiting the ability to adjust for potential confounders. The cross-sectional design of the included studies precluded determining whether the diagnosis of PCOS or the symptoms of disordered eating occurred first. Studies from 10 countries were included, but limited data from developing or Asian countries restrict the generalizability of the results.
DISCLOSURES:
This study was conducted to inform recommendations of the 2023 International Evidence-based Guideline in PCOS, which was funded by the Australian National Health and Medical Research Council, Centre for Research Excellence in Polycystic Ovary Syndrome, and other sources. The authors declared no conflicts of interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Women with polycystic ovary syndrome (PCOS) have higher odds of some eating disorders, including bulimia nervosa, binge eating disorder, and disordered eating, regardless of weight.
METHODOLOGY:
- A small systematic review and meta-analysis showed increased odds of any eating disorders and disordered eating scores in adult women with PCOS compared with women without PCOS.
- As part of the 2023 update of the International Evidence-based Guideline for the Assessment of and Management of PCOS, the same researchers updated and expanded their analysis to include adolescents and specific eating disorders and to evaluate the effect of body mass index (BMI) on these risks.
- They included 20 cross-sectional studies involving 28,922 women with PCOS and 258,619 women without PCOS; PCOS was diagnosed by either National Institutes of Health or Rotterdam criteria, as well as by patient self-report or hospital records.
- Eating disorders were screened using a validated disordered eating screening tool or diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders.
- The outcomes of interest included the prevalence of any eating disorder, individual eating disorders, disordered eating, and mean disordered eating scores.
TAKEAWAY:
- Women with PCOS had 53% higher odds (odds ratio [OR], 1.53; 95% CI, 1.29-1.82; eight studies) of any eating disorder than control individuals without PCOS.
- The likelihood of bulimia nervosa (OR, 1.34; 95% CI, 1.17-1.54; five studies) and binge eating disorder (OR, 2.09; 95% CI, 1.18-3.72; four studies) was higher in women with PCOS, but no significant association was found for anorexia nervosa.
- The mean disordered eating scores and odds of disordered eating were higher in women with PCOS (standardized mean difference [SMD], 0.52; 95% CI, 0.28-0.77; 13 studies; and OR, 2.84; 95% CI, 1.0-8.04; eight studies; respectively).
- Disordered eating scores were higher in both the normal and higher weight categories (BMI < 25; SMD, 0.36; 95% CI, 0.15-0.58; five studies; and BMI ≥ 25; SMD, 0.68; 95% CI, 0.22-1.13; four studies; respectively).
IN PRACTICE:
“Our findings emphasize the importance of screening women with PCOS for eating disorders before clinicians share any lifestyle advice,” the lead author said in a press release. “The lifestyle modifications we often recommend for women with PCOS — including physical activity, healthy diet, and behavior modifications — could hinder the recovery process for eating disorders.”
SOURCE:
The study was led by Laura G. Cooney, MD, MSCE, University of Wisconsin, Madison, and published online in the Journal of Clinical Endocrinology & Metabolism.
LIMITATIONS:
The included studies were observational in nature, limiting the ability to adjust for potential confounders. The cross-sectional design of the included studies precluded determining whether the diagnosis of PCOS or the symptoms of disordered eating occurred first. Studies from 10 countries were included, but limited data from developing or Asian countries restrict the generalizability of the results.
DISCLOSURES:
This study was conducted to inform recommendations of the 2023 International Evidence-based Guideline in PCOS, which was funded by the Australian National Health and Medical Research Council, Centre for Research Excellence in Polycystic Ovary Syndrome, and other sources. The authors declared no conflicts of interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Women with polycystic ovary syndrome (PCOS) have higher odds of some eating disorders, including bulimia nervosa, binge eating disorder, and disordered eating, regardless of weight.
METHODOLOGY:
- A small systematic review and meta-analysis showed increased odds of any eating disorders and disordered eating scores in adult women with PCOS compared with women without PCOS.
- As part of the 2023 update of the International Evidence-based Guideline for the Assessment of and Management of PCOS, the same researchers updated and expanded their analysis to include adolescents and specific eating disorders and to evaluate the effect of body mass index (BMI) on these risks.
- They included 20 cross-sectional studies involving 28,922 women with PCOS and 258,619 women without PCOS; PCOS was diagnosed by either National Institutes of Health or Rotterdam criteria, as well as by patient self-report or hospital records.
- Eating disorders were screened using a validated disordered eating screening tool or diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders.
- The outcomes of interest included the prevalence of any eating disorder, individual eating disorders, disordered eating, and mean disordered eating scores.
TAKEAWAY:
- Women with PCOS had 53% higher odds (odds ratio [OR], 1.53; 95% CI, 1.29-1.82; eight studies) of any eating disorder than control individuals without PCOS.
- The likelihood of bulimia nervosa (OR, 1.34; 95% CI, 1.17-1.54; five studies) and binge eating disorder (OR, 2.09; 95% CI, 1.18-3.72; four studies) was higher in women with PCOS, but no significant association was found for anorexia nervosa.
- The mean disordered eating scores and odds of disordered eating were higher in women with PCOS (standardized mean difference [SMD], 0.52; 95% CI, 0.28-0.77; 13 studies; and OR, 2.84; 95% CI, 1.0-8.04; eight studies; respectively).
- Disordered eating scores were higher in both the normal and higher weight categories (BMI < 25; SMD, 0.36; 95% CI, 0.15-0.58; five studies; and BMI ≥ 25; SMD, 0.68; 95% CI, 0.22-1.13; four studies; respectively).
IN PRACTICE:
“Our findings emphasize the importance of screening women with PCOS for eating disorders before clinicians share any lifestyle advice,” the lead author said in a press release. “The lifestyle modifications we often recommend for women with PCOS — including physical activity, healthy diet, and behavior modifications — could hinder the recovery process for eating disorders.”
SOURCE:
The study was led by Laura G. Cooney, MD, MSCE, University of Wisconsin, Madison, and published online in the Journal of Clinical Endocrinology & Metabolism.
LIMITATIONS:
The included studies were observational in nature, limiting the ability to adjust for potential confounders. The cross-sectional design of the included studies precluded determining whether the diagnosis of PCOS or the symptoms of disordered eating occurred first. Studies from 10 countries were included, but limited data from developing or Asian countries restrict the generalizability of the results.
DISCLOSURES:
This study was conducted to inform recommendations of the 2023 International Evidence-based Guideline in PCOS, which was funded by the Australian National Health and Medical Research Council, Centre for Research Excellence in Polycystic Ovary Syndrome, and other sources. The authors declared no conflicts of interests.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
Viral Season 2024-2025: Try for An Ounce of Prevention
We are quickly approaching the typical cold and flu season. But can we call anything typical since 2020? Since 2020, there have been different recommendations for prevention, testing, return to work, and treatment since our world was rocked by the pandemic. Now that we are in the “post-pandemic” era, family physicians and other primary care professionals are the front line for discussions on prevention, evaluation, and treatment of the typical upper-respiratory infections, influenza, and COVID-19.
Let’s start with prevention. We have all heard the old adage, an ounce of prevention is worth a pound of cure. In primary care, we need to focus on prevention. Vaccination is often one of our best tools against the myriad of infections we are hoping to help patients prevent during cold and flu season. Most recently, we have fall vaccinations aimed to prevent COVID-19, influenza, and respiratory syncytial virus (RSV).
The number and timing of each of these vaccinations has different recommendations based on a variety of factors including age, pregnancy status, and whether or not the patient is immunocompromised. For the 2024-2025 season, the Centers for Disease Control and Prevention has recommended updated vaccines for both influenza and COVID-19.1
They have also updated the RSV vaccine recommendations to “People 75 or older, or between 60-74 with certain chronic health conditions or living in a nursing home should get one dose of the RSV vaccine to provide an extra layer of protection.”2
In addition to vaccines as prevention, there is also hygiene, staying home when sick and away from others who are sick, following guidelines for where and when to wear a face mask, and the general tools of eating well, and getting sufficient sleep and exercise to help maintain the healthiest immune system.
Despite the best of intentions, there will still be many who experience viral infections in this upcoming season. The CDC is currently recommending persons to stay away from others for at least 24 hours after their symptoms improve and they are fever-free without antipyretics. In addition to isolation while sick, general symptom management is something that we can recommend for all of these illnesses.
There is more to consider, though, as our patients face these illnesses. The first question is how to determine the diagnosis — and if that diagnosis is even necessary. Unfortunately, many of these viral illnesses can look the same. They can all cause fevers, chills, and other upper respiratory symptoms. They are all fairly contagious. All of these viruses can cause serious illness associated with additional complications. It is not truly possible to determine which virus someone has by symptoms alone, our patients can have multiple viruses at the same time and diagnosis of one does not preclude having another.3
Instead, we truly do need a test for diagnosis. In-office testing is available for RSV, influenza, and COVID-19. Additionally, despite not being as freely available as they were during the pandemic, patients are able to do home COVID tests and then call in with their results. At the time of writing this, at-home rapid influenza tests have also been approved by the FDA but are not yet readily available to the public. These tests are important for determining if the patient is eligible for treatment. Both influenza and COVID-19 have antiviral treatments available to help decrease the severity of the illness and potentially the length of illness and time contagious. According to the CDC, both treatments are underutilized.
This could be because of a lack of testing and diagnosis. It may also be because of a lack of familiarity with the available treatments.4,5
Influenza treatment is recommended as soon as possible for those with suspected or confirmed diagnosis, immediately for anyone hospitalized, anyone with severe, complicated, or progressing illness, and for those at high risk of severe illness including but not limited to those under 2 years old, those over 65, those who are pregnant, and those with many chronic conditions.
Treatment can also be used for those who are not high risk when diagnosed within 48 hours. In the United States, four antivirals are recommended to treat influenza: oseltamivir phosphate, zanamivir, peramivir, and baloxavir marboxil. For COVID-19, treatments are also available for mild or moderate disease in those at risk for severe disease. Both remdesivir and nimatrelvir with ritonavir are treatment options that can be used for COVID-19 infection. Unfortunately, no specific antiviral is available for the other viral illnesses we see often during this season.
In primary care, we have some important roles to play. We need to continue to discuss all methods of prevention. Not only do vaccine recommendations change at least annually, our patients’ situations change and we have to reassess them. Additionally, people often need to hear things more than once before committing — so it never hurts to continue having those conversations. Combining the conversation about vaccines with other prevention measures is also important so that it does not seem like we are only recommending one thing. We should also start talking about treatment options before our patients are sick. We can communicate what is available as long as they let us know they are sick early. We can also be there to help our patients determine when they are at risk for severe illness and when they should consider a higher level of care.
The availability of home testing gives us the opportunity to provide these treatments via telehealth and even potentially in times when these illnesses are everywhere — with standing orders with our clinical teams. Although it is a busy time for us in the clinic, “cold and flu” season is definitely one of those times when our primary care relationship can truly help our patients.
References
1. CDC Recommends Updated 2024-2025 COVID-19 and Flu Vaccines for Fall/Winter Virus Season. https://www.cdc.gov/media/releases/2024/s-t0627-vaccine-recommendations.html. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention.
2. CDC Updates RSV Vaccination Recommendation for Adults. https://www.cdc.gov/media/releases/2024/s-0626-vaccination-adults.html. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention.
3. Similarities and Differences between Flu and COVID-19. https://www.cdc.gov/flu/symptoms/flu-vs-covid19.htm. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention, National Center for Immunization and Respiratory Diseases.
4. Respiratory Virus Guidance. https://www.cdc.gov/respiratory-viruses/guidance/index.html. Accessed August 9, 2024. Source: National Center for Immunization and Respiratory Diseases.
5. Provider Toolkit: Preparing Patients for the Fall and Winter Virus Season. https://www.cdc.gov/respiratory-viruses/hcp/tools-resources/index.html. Accessed August 9, 2024. Source: Centers for Disease Control and Prevention.
We are quickly approaching the typical cold and flu season. But can we call anything typical since 2020? Since 2020, there have been different recommendations for prevention, testing, return to work, and treatment since our world was rocked by the pandemic. Now that we are in the “post-pandemic” era, family physicians and other primary care professionals are the front line for discussions on prevention, evaluation, and treatment of the typical upper-respiratory infections, influenza, and COVID-19.
Let’s start with prevention. We have all heard the old adage, an ounce of prevention is worth a pound of cure. In primary care, we need to focus on prevention. Vaccination is often one of our best tools against the myriad of infections we are hoping to help patients prevent during cold and flu season. Most recently, we have fall vaccinations aimed to prevent COVID-19, influenza, and respiratory syncytial virus (RSV).
The number and timing of each of these vaccinations has different recommendations based on a variety of factors including age, pregnancy status, and whether or not the patient is immunocompromised. For the 2024-2025 season, the Centers for Disease Control and Prevention has recommended updated vaccines for both influenza and COVID-19.1
They have also updated the RSV vaccine recommendations to “People 75 or older, or between 60-74 with certain chronic health conditions or living in a nursing home should get one dose of the RSV vaccine to provide an extra layer of protection.”2
In addition to vaccines as prevention, there is also hygiene, staying home when sick and away from others who are sick, following guidelines for where and when to wear a face mask, and the general tools of eating well, and getting sufficient sleep and exercise to help maintain the healthiest immune system.
Despite the best of intentions, there will still be many who experience viral infections in this upcoming season. The CDC is currently recommending persons to stay away from others for at least 24 hours after their symptoms improve and they are fever-free without antipyretics. In addition to isolation while sick, general symptom management is something that we can recommend for all of these illnesses.
There is more to consider, though, as our patients face these illnesses. The first question is how to determine the diagnosis — and if that diagnosis is even necessary. Unfortunately, many of these viral illnesses can look the same. They can all cause fevers, chills, and other upper respiratory symptoms. They are all fairly contagious. All of these viruses can cause serious illness associated with additional complications. It is not truly possible to determine which virus someone has by symptoms alone, our patients can have multiple viruses at the same time and diagnosis of one does not preclude having another.3
Instead, we truly do need a test for diagnosis. In-office testing is available for RSV, influenza, and COVID-19. Additionally, despite not being as freely available as they were during the pandemic, patients are able to do home COVID tests and then call in with their results. At the time of writing this, at-home rapid influenza tests have also been approved by the FDA but are not yet readily available to the public. These tests are important for determining if the patient is eligible for treatment. Both influenza and COVID-19 have antiviral treatments available to help decrease the severity of the illness and potentially the length of illness and time contagious. According to the CDC, both treatments are underutilized.
This could be because of a lack of testing and diagnosis. It may also be because of a lack of familiarity with the available treatments.4,5
Influenza treatment is recommended as soon as possible for those with suspected or confirmed diagnosis, immediately for anyone hospitalized, anyone with severe, complicated, or progressing illness, and for those at high risk of severe illness including but not limited to those under 2 years old, those over 65, those who are pregnant, and those with many chronic conditions.
Treatment can also be used for those who are not high risk when diagnosed within 48 hours. In the United States, four antivirals are recommended to treat influenza: oseltamivir phosphate, zanamivir, peramivir, and baloxavir marboxil. For COVID-19, treatments are also available for mild or moderate disease in those at risk for severe disease. Both remdesivir and nimatrelvir with ritonavir are treatment options that can be used for COVID-19 infection. Unfortunately, no specific antiviral is available for the other viral illnesses we see often during this season.
In primary care, we have some important roles to play. We need to continue to discuss all methods of prevention. Not only do vaccine recommendations change at least annually, our patients’ situations change and we have to reassess them. Additionally, people often need to hear things more than once before committing — so it never hurts to continue having those conversations. Combining the conversation about vaccines with other prevention measures is also important so that it does not seem like we are only recommending one thing. We should also start talking about treatment options before our patients are sick. We can communicate what is available as long as they let us know they are sick early. We can also be there to help our patients determine when they are at risk for severe illness and when they should consider a higher level of care.
The availability of home testing gives us the opportunity to provide these treatments via telehealth and even potentially in times when these illnesses are everywhere — with standing orders with our clinical teams. Although it is a busy time for us in the clinic, “cold and flu” season is definitely one of those times when our primary care relationship can truly help our patients.
References
1. CDC Recommends Updated 2024-2025 COVID-19 and Flu Vaccines for Fall/Winter Virus Season. https://www.cdc.gov/media/releases/2024/s-t0627-vaccine-recommendations.html. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention.
2. CDC Updates RSV Vaccination Recommendation for Adults. https://www.cdc.gov/media/releases/2024/s-0626-vaccination-adults.html. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention.
3. Similarities and Differences between Flu and COVID-19. https://www.cdc.gov/flu/symptoms/flu-vs-covid19.htm. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention, National Center for Immunization and Respiratory Diseases.
4. Respiratory Virus Guidance. https://www.cdc.gov/respiratory-viruses/guidance/index.html. Accessed August 9, 2024. Source: National Center for Immunization and Respiratory Diseases.
5. Provider Toolkit: Preparing Patients for the Fall and Winter Virus Season. https://www.cdc.gov/respiratory-viruses/hcp/tools-resources/index.html. Accessed August 9, 2024. Source: Centers for Disease Control and Prevention.
We are quickly approaching the typical cold and flu season. But can we call anything typical since 2020? Since 2020, there have been different recommendations for prevention, testing, return to work, and treatment since our world was rocked by the pandemic. Now that we are in the “post-pandemic” era, family physicians and other primary care professionals are the front line for discussions on prevention, evaluation, and treatment of the typical upper-respiratory infections, influenza, and COVID-19.
Let’s start with prevention. We have all heard the old adage, an ounce of prevention is worth a pound of cure. In primary care, we need to focus on prevention. Vaccination is often one of our best tools against the myriad of infections we are hoping to help patients prevent during cold and flu season. Most recently, we have fall vaccinations aimed to prevent COVID-19, influenza, and respiratory syncytial virus (RSV).
The number and timing of each of these vaccinations has different recommendations based on a variety of factors including age, pregnancy status, and whether or not the patient is immunocompromised. For the 2024-2025 season, the Centers for Disease Control and Prevention has recommended updated vaccines for both influenza and COVID-19.1
They have also updated the RSV vaccine recommendations to “People 75 or older, or between 60-74 with certain chronic health conditions or living in a nursing home should get one dose of the RSV vaccine to provide an extra layer of protection.”2
In addition to vaccines as prevention, there is also hygiene, staying home when sick and away from others who are sick, following guidelines for where and when to wear a face mask, and the general tools of eating well, and getting sufficient sleep and exercise to help maintain the healthiest immune system.
Despite the best of intentions, there will still be many who experience viral infections in this upcoming season. The CDC is currently recommending persons to stay away from others for at least 24 hours after their symptoms improve and they are fever-free without antipyretics. In addition to isolation while sick, general symptom management is something that we can recommend for all of these illnesses.
There is more to consider, though, as our patients face these illnesses. The first question is how to determine the diagnosis — and if that diagnosis is even necessary. Unfortunately, many of these viral illnesses can look the same. They can all cause fevers, chills, and other upper respiratory symptoms. They are all fairly contagious. All of these viruses can cause serious illness associated with additional complications. It is not truly possible to determine which virus someone has by symptoms alone, our patients can have multiple viruses at the same time and diagnosis of one does not preclude having another.3
Instead, we truly do need a test for diagnosis. In-office testing is available for RSV, influenza, and COVID-19. Additionally, despite not being as freely available as they were during the pandemic, patients are able to do home COVID tests and then call in with their results. At the time of writing this, at-home rapid influenza tests have also been approved by the FDA but are not yet readily available to the public. These tests are important for determining if the patient is eligible for treatment. Both influenza and COVID-19 have antiviral treatments available to help decrease the severity of the illness and potentially the length of illness and time contagious. According to the CDC, both treatments are underutilized.
This could be because of a lack of testing and diagnosis. It may also be because of a lack of familiarity with the available treatments.4,5
Influenza treatment is recommended as soon as possible for those with suspected or confirmed diagnosis, immediately for anyone hospitalized, anyone with severe, complicated, or progressing illness, and for those at high risk of severe illness including but not limited to those under 2 years old, those over 65, those who are pregnant, and those with many chronic conditions.
Treatment can also be used for those who are not high risk when diagnosed within 48 hours. In the United States, four antivirals are recommended to treat influenza: oseltamivir phosphate, zanamivir, peramivir, and baloxavir marboxil. For COVID-19, treatments are also available for mild or moderate disease in those at risk for severe disease. Both remdesivir and nimatrelvir with ritonavir are treatment options that can be used for COVID-19 infection. Unfortunately, no specific antiviral is available for the other viral illnesses we see often during this season.
In primary care, we have some important roles to play. We need to continue to discuss all methods of prevention. Not only do vaccine recommendations change at least annually, our patients’ situations change and we have to reassess them. Additionally, people often need to hear things more than once before committing — so it never hurts to continue having those conversations. Combining the conversation about vaccines with other prevention measures is also important so that it does not seem like we are only recommending one thing. We should also start talking about treatment options before our patients are sick. We can communicate what is available as long as they let us know they are sick early. We can also be there to help our patients determine when they are at risk for severe illness and when they should consider a higher level of care.
The availability of home testing gives us the opportunity to provide these treatments via telehealth and even potentially in times when these illnesses are everywhere — with standing orders with our clinical teams. Although it is a busy time for us in the clinic, “cold and flu” season is definitely one of those times when our primary care relationship can truly help our patients.
References
1. CDC Recommends Updated 2024-2025 COVID-19 and Flu Vaccines for Fall/Winter Virus Season. https://www.cdc.gov/media/releases/2024/s-t0627-vaccine-recommendations.html. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention.
2. CDC Updates RSV Vaccination Recommendation for Adults. https://www.cdc.gov/media/releases/2024/s-0626-vaccination-adults.html. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention.
3. Similarities and Differences between Flu and COVID-19. https://www.cdc.gov/flu/symptoms/flu-vs-covid19.htm. Accessed August 8, 2024. Source: Centers for Disease Control and Prevention, National Center for Immunization and Respiratory Diseases.
4. Respiratory Virus Guidance. https://www.cdc.gov/respiratory-viruses/guidance/index.html. Accessed August 9, 2024. Source: National Center for Immunization and Respiratory Diseases.
5. Provider Toolkit: Preparing Patients for the Fall and Winter Virus Season. https://www.cdc.gov/respiratory-viruses/hcp/tools-resources/index.html. Accessed August 9, 2024. Source: Centers for Disease Control and Prevention.
Stool-Based Methylation Test May Improve CRC Screening
based on a prospective, real-world study.
These findings suggest that the mSDC2 assay could improve the efficacy and resource utilization of existing screening programs, reported co–lead authors Shengbing Zhao, MD and Zixuan He, MD, of Naval Medical University, Shanghai, China, and colleagues.
“Conventional risk-stratification strategies, such as fecal immunochemical test (FIT) and life risk factors, are still criticized for being inferior at identifying early-stage CRC and ACN, and their real-world performance is probably further weakened by the low annual participation rate and compliance of subsequent colonoscopy,” the investigators wrote in Gastroenterology. Recent case studies have reported “high diagnostic performance” using stool-based testing for mSDC2, which is “the most accurate single-targeted gene” for colorectal neoplasia, according to the investigators; however, real-world outcomes have yet to be demonstrated, prompting the present study. The prospective, multicenter, community-based trial compared the diagnostic performance of the mSDC2 test against FIT and Asia-Pacific Colorectal Screening (APCS) scores.
The primary outcome was detection of ACN. Secondary outcomes included detection of CRC, early-stage CRC, ACN, colorectal neoplasia (CN), and clinically relevant serrated polyp (CRSP). Screening strategies were also compared in terms of cost-effectiveness and impact on colonoscopy workload.The final dataset included 10,360 participants aged 45-75 years who underwent screening between 2020 and 2022.
After determining APCS scores, stool samples were analyzed for mSDC2 and FIT markers. Based on risk stratification results, participants were invited to undergo colonoscopy. A total of 3,381 participants completed colonoscopy, with 1914 from the increased-risk population and 1467 from the average-risk population. Participants who tested positive for mSDC2 had significantly higher detection rates for all measured outcomes than those who tested negative (all, P < .05). For example, the detection rate for ACN was 26.6% in mSDC2-positive participants, compared with 9.3% in mSDC2-negative participants, with a relative risk of 2.87 (95% CI, 2.39-3.44). For CRC, the detection rate was 4.2% in mSDC2-positive participants vs 0.1% in mSDC2-negative participants, yielding a relative risk of 29.73 (95% CI, 10.29-85.91). Performance held steady across subgroups.The mSDC2 test demonstrated cost-effectiveness by significantly reducing the number of colonoscopies needed to detect one case of ACN or CRC. Specifically, the number of colonoscopies needed to screen for ACN and CRC was reduced by 56.2% and 81.5%, respectively. Parallel combinations of mSDC2 with APCS or FIT enhanced both diagnostic performance and cost-effectiveness.
“This study further illustrates that the mSDC2 test consistently improves predictive abilities for CN, CRSP, ACN, and CRC, which is not influenced by subgroups of lesion location or risk factors, even under the risk stratification by FIT or APCS,” the investigators wrote. “The excellent diagnostic ability of mSDC2 in premalignant lesions, early-stage CRC, and early-onset CRC indicates a promising value in early detection and prevention of CRC ... the mSDC2 test or a parallel combination of multiple screening methods might be promising to improve real-world CRC screening performance and reduce colonoscopy workload in community practice.”The study was supported by the National Key Research and Development Program of China, Deep Blue Project of Naval Medical University, the Creative Biosciences, and others. The investigators reported no conflicts of interest.
based on a prospective, real-world study.
These findings suggest that the mSDC2 assay could improve the efficacy and resource utilization of existing screening programs, reported co–lead authors Shengbing Zhao, MD and Zixuan He, MD, of Naval Medical University, Shanghai, China, and colleagues.
“Conventional risk-stratification strategies, such as fecal immunochemical test (FIT) and life risk factors, are still criticized for being inferior at identifying early-stage CRC and ACN, and their real-world performance is probably further weakened by the low annual participation rate and compliance of subsequent colonoscopy,” the investigators wrote in Gastroenterology. Recent case studies have reported “high diagnostic performance” using stool-based testing for mSDC2, which is “the most accurate single-targeted gene” for colorectal neoplasia, according to the investigators; however, real-world outcomes have yet to be demonstrated, prompting the present study. The prospective, multicenter, community-based trial compared the diagnostic performance of the mSDC2 test against FIT and Asia-Pacific Colorectal Screening (APCS) scores.
The primary outcome was detection of ACN. Secondary outcomes included detection of CRC, early-stage CRC, ACN, colorectal neoplasia (CN), and clinically relevant serrated polyp (CRSP). Screening strategies were also compared in terms of cost-effectiveness and impact on colonoscopy workload.The final dataset included 10,360 participants aged 45-75 years who underwent screening between 2020 and 2022.
After determining APCS scores, stool samples were analyzed for mSDC2 and FIT markers. Based on risk stratification results, participants were invited to undergo colonoscopy. A total of 3,381 participants completed colonoscopy, with 1914 from the increased-risk population and 1467 from the average-risk population. Participants who tested positive for mSDC2 had significantly higher detection rates for all measured outcomes than those who tested negative (all, P < .05). For example, the detection rate for ACN was 26.6% in mSDC2-positive participants, compared with 9.3% in mSDC2-negative participants, with a relative risk of 2.87 (95% CI, 2.39-3.44). For CRC, the detection rate was 4.2% in mSDC2-positive participants vs 0.1% in mSDC2-negative participants, yielding a relative risk of 29.73 (95% CI, 10.29-85.91). Performance held steady across subgroups.The mSDC2 test demonstrated cost-effectiveness by significantly reducing the number of colonoscopies needed to detect one case of ACN or CRC. Specifically, the number of colonoscopies needed to screen for ACN and CRC was reduced by 56.2% and 81.5%, respectively. Parallel combinations of mSDC2 with APCS or FIT enhanced both diagnostic performance and cost-effectiveness.
“This study further illustrates that the mSDC2 test consistently improves predictive abilities for CN, CRSP, ACN, and CRC, which is not influenced by subgroups of lesion location or risk factors, even under the risk stratification by FIT or APCS,” the investigators wrote. “The excellent diagnostic ability of mSDC2 in premalignant lesions, early-stage CRC, and early-onset CRC indicates a promising value in early detection and prevention of CRC ... the mSDC2 test or a parallel combination of multiple screening methods might be promising to improve real-world CRC screening performance and reduce colonoscopy workload in community practice.”The study was supported by the National Key Research and Development Program of China, Deep Blue Project of Naval Medical University, the Creative Biosciences, and others. The investigators reported no conflicts of interest.
based on a prospective, real-world study.
These findings suggest that the mSDC2 assay could improve the efficacy and resource utilization of existing screening programs, reported co–lead authors Shengbing Zhao, MD and Zixuan He, MD, of Naval Medical University, Shanghai, China, and colleagues.
“Conventional risk-stratification strategies, such as fecal immunochemical test (FIT) and life risk factors, are still criticized for being inferior at identifying early-stage CRC and ACN, and their real-world performance is probably further weakened by the low annual participation rate and compliance of subsequent colonoscopy,” the investigators wrote in Gastroenterology. Recent case studies have reported “high diagnostic performance” using stool-based testing for mSDC2, which is “the most accurate single-targeted gene” for colorectal neoplasia, according to the investigators; however, real-world outcomes have yet to be demonstrated, prompting the present study. The prospective, multicenter, community-based trial compared the diagnostic performance of the mSDC2 test against FIT and Asia-Pacific Colorectal Screening (APCS) scores.
The primary outcome was detection of ACN. Secondary outcomes included detection of CRC, early-stage CRC, ACN, colorectal neoplasia (CN), and clinically relevant serrated polyp (CRSP). Screening strategies were also compared in terms of cost-effectiveness and impact on colonoscopy workload.The final dataset included 10,360 participants aged 45-75 years who underwent screening between 2020 and 2022.
After determining APCS scores, stool samples were analyzed for mSDC2 and FIT markers. Based on risk stratification results, participants were invited to undergo colonoscopy. A total of 3,381 participants completed colonoscopy, with 1914 from the increased-risk population and 1467 from the average-risk population. Participants who tested positive for mSDC2 had significantly higher detection rates for all measured outcomes than those who tested negative (all, P < .05). For example, the detection rate for ACN was 26.6% in mSDC2-positive participants, compared with 9.3% in mSDC2-negative participants, with a relative risk of 2.87 (95% CI, 2.39-3.44). For CRC, the detection rate was 4.2% in mSDC2-positive participants vs 0.1% in mSDC2-negative participants, yielding a relative risk of 29.73 (95% CI, 10.29-85.91). Performance held steady across subgroups.The mSDC2 test demonstrated cost-effectiveness by significantly reducing the number of colonoscopies needed to detect one case of ACN or CRC. Specifically, the number of colonoscopies needed to screen for ACN and CRC was reduced by 56.2% and 81.5%, respectively. Parallel combinations of mSDC2 with APCS or FIT enhanced both diagnostic performance and cost-effectiveness.
“This study further illustrates that the mSDC2 test consistently improves predictive abilities for CN, CRSP, ACN, and CRC, which is not influenced by subgroups of lesion location or risk factors, even under the risk stratification by FIT or APCS,” the investigators wrote. “The excellent diagnostic ability of mSDC2 in premalignant lesions, early-stage CRC, and early-onset CRC indicates a promising value in early detection and prevention of CRC ... the mSDC2 test or a parallel combination of multiple screening methods might be promising to improve real-world CRC screening performance and reduce colonoscopy workload in community practice.”The study was supported by the National Key Research and Development Program of China, Deep Blue Project of Naval Medical University, the Creative Biosciences, and others. The investigators reported no conflicts of interest.
FROM GASTROENTEROLOGY
Sexual Arousal Cream Promising in Some Subsets of Women
Topical sildenafil (citrate) cream 3.6% used by healthy premenopausal women with a primary symptom of female sexual arousal disorder did not show statistically significant improvement over placebo in the coprimary or secondary endpoints over a 3-month period in new preliminary study data published in Obstetrics & Gynecology.
Topical sildenafil cream is currently used for erectile dysfunction in men. There are no US Food and Drug Administration–approved treatments for female sexual arousal disorder, which affects up to 26% of women in the United States by some estimates.
Isabella Johnson, senior manager of product development at Daré Bioscience, San Diego, California, led a phase 2b, exploratory, randomized, placebo-controlled, double-blind study of sildenafil cream’s potential to help women improve their sexual experiences.
The study included 200 women with female sexual arousal disorder randomized to sildenafil cream (n = 101) or placebo cream (n = 99); 177 completed the trial and made up the intention-to-treat group. Healthy premenopausal women at least 18 years old and their sexual partners were screened for the study.
The authors report that the primary endpoints were scores on Sexual Function Questionnaire (SFQ28) arousal sensation domain and question 14 on the Female Sexual Distress Scale — Desire/Arousal/Orgasm (FSD-DAO), which asks “How often in the past 30 days did you feel concerned by difficulties with sexual arousal?” The secondary endpoint was the average number and average proportion of satisfactory sexual events. Topical sildenafil was not more effective than placebo with these primary or secondary endpoints.
Some Subgroups Benefited
However, a post hoc analysis told a different story. “[A]mong a subset of women with female sexual arousal disorder only or female sexual arousal disorder with concomitant decreased desire, we found either trends or significant improvements in sexual functioning with sildenafil cream compared with placebo cream across multiple aspects of sexual function,” the authors write.
The researchers also noted that several FSDS-DAO questions, other than question 14, asked about generalized feelings related to sexual distress and interpersonal difficulties and scores on those questions showed significant improvement with sildenafil cream compared with placebo in the exploratory subset.
“The total FSDS-DAO score decreased by about 7 points for sildenafil cream users in the subset population (a clinically meaningful decrease in sexual distress) compared with a two-point decrease for placebo cream users (P = .10),” they write.
Post Hoc Analysis Is Exploratory
JoAnn V. Pinkerton, MD, with the Department of Obstetrics and Gynecology, University of Virginia Health in Charlottesville, writes in an editorial that because the authors did not adjust for multiple hypothesis testing, the post hoc subset analyses should be considered only exploratory.
She notes that the trial was underpowered partly because it was halted after recruitment challenges during the COVID-19 pandemic. The small sample size and the varied reasons for arousal disorder among the women “may have limited the ability to find a positive outcome.”
, Dr. Pinkerton writes.
“Because improvement in genital arousal is thought to be due to the increased genital blood flow from sildenafil citrate, the subset of participants found least likely to benefit from sildenafil citrate cream were those with concomitant orgasmic dysfunction with or without genital pain,” she writes.
Data May Inform Phase 3 Trial
This phase 2b trial sets the stage for a phase 3 trial, she writes, to evaluate sildenafil topical cream in women with female sexual arousal disorder in the subsets where there were positive findings (those with or without a secondary diagnosis of decreased desire) but not among women having difficulty reaching orgasm.
“If positive, it could lead to a new therapeutic area for the unmet treatment needs of premenopausal and postmenopausal women with female sexual arousal disorder,” Dr. Pinkerton writes.
A study coauthor, Clint Dart, reports money was paid to his institution from Daré Bioscience, he provided independent data verification, and he is an employee of Premier Research. Isabella Johnson, Andrea Ries Thurman, MD, Jessica Hatheway, MBA, David R. Friend, PhD, and Andrew Goldstein, MD, are employees of Daré Bioscience. Katherine A. Cornell is an employee of Strategic Science & Technologies, LLC. C. Paige Brainard, MD, was financially compensated by Del Sol Research Management and her practice received funding from Daré Bioscience for study-specific activities. Dr. Goldstein also reported receiving payments from Nuvig, Ipsen, and AbbVie. Dr. Pinkerton’s institution received funds from Bayer Pharmaceuticals as she served as PI for a multinational clinical trial.
Topical sildenafil (citrate) cream 3.6% used by healthy premenopausal women with a primary symptom of female sexual arousal disorder did not show statistically significant improvement over placebo in the coprimary or secondary endpoints over a 3-month period in new preliminary study data published in Obstetrics & Gynecology.
Topical sildenafil cream is currently used for erectile dysfunction in men. There are no US Food and Drug Administration–approved treatments for female sexual arousal disorder, which affects up to 26% of women in the United States by some estimates.
Isabella Johnson, senior manager of product development at Daré Bioscience, San Diego, California, led a phase 2b, exploratory, randomized, placebo-controlled, double-blind study of sildenafil cream’s potential to help women improve their sexual experiences.
The study included 200 women with female sexual arousal disorder randomized to sildenafil cream (n = 101) or placebo cream (n = 99); 177 completed the trial and made up the intention-to-treat group. Healthy premenopausal women at least 18 years old and their sexual partners were screened for the study.
The authors report that the primary endpoints were scores on Sexual Function Questionnaire (SFQ28) arousal sensation domain and question 14 on the Female Sexual Distress Scale — Desire/Arousal/Orgasm (FSD-DAO), which asks “How often in the past 30 days did you feel concerned by difficulties with sexual arousal?” The secondary endpoint was the average number and average proportion of satisfactory sexual events. Topical sildenafil was not more effective than placebo with these primary or secondary endpoints.
Some Subgroups Benefited
However, a post hoc analysis told a different story. “[A]mong a subset of women with female sexual arousal disorder only or female sexual arousal disorder with concomitant decreased desire, we found either trends or significant improvements in sexual functioning with sildenafil cream compared with placebo cream across multiple aspects of sexual function,” the authors write.
The researchers also noted that several FSDS-DAO questions, other than question 14, asked about generalized feelings related to sexual distress and interpersonal difficulties and scores on those questions showed significant improvement with sildenafil cream compared with placebo in the exploratory subset.
“The total FSDS-DAO score decreased by about 7 points for sildenafil cream users in the subset population (a clinically meaningful decrease in sexual distress) compared with a two-point decrease for placebo cream users (P = .10),” they write.
Post Hoc Analysis Is Exploratory
JoAnn V. Pinkerton, MD, with the Department of Obstetrics and Gynecology, University of Virginia Health in Charlottesville, writes in an editorial that because the authors did not adjust for multiple hypothesis testing, the post hoc subset analyses should be considered only exploratory.
She notes that the trial was underpowered partly because it was halted after recruitment challenges during the COVID-19 pandemic. The small sample size and the varied reasons for arousal disorder among the women “may have limited the ability to find a positive outcome.”
, Dr. Pinkerton writes.
“Because improvement in genital arousal is thought to be due to the increased genital blood flow from sildenafil citrate, the subset of participants found least likely to benefit from sildenafil citrate cream were those with concomitant orgasmic dysfunction with or without genital pain,” she writes.
Data May Inform Phase 3 Trial
This phase 2b trial sets the stage for a phase 3 trial, she writes, to evaluate sildenafil topical cream in women with female sexual arousal disorder in the subsets where there were positive findings (those with or without a secondary diagnosis of decreased desire) but not among women having difficulty reaching orgasm.
“If positive, it could lead to a new therapeutic area for the unmet treatment needs of premenopausal and postmenopausal women with female sexual arousal disorder,” Dr. Pinkerton writes.
A study coauthor, Clint Dart, reports money was paid to his institution from Daré Bioscience, he provided independent data verification, and he is an employee of Premier Research. Isabella Johnson, Andrea Ries Thurman, MD, Jessica Hatheway, MBA, David R. Friend, PhD, and Andrew Goldstein, MD, are employees of Daré Bioscience. Katherine A. Cornell is an employee of Strategic Science & Technologies, LLC. C. Paige Brainard, MD, was financially compensated by Del Sol Research Management and her practice received funding from Daré Bioscience for study-specific activities. Dr. Goldstein also reported receiving payments from Nuvig, Ipsen, and AbbVie. Dr. Pinkerton’s institution received funds from Bayer Pharmaceuticals as she served as PI for a multinational clinical trial.
Topical sildenafil (citrate) cream 3.6% used by healthy premenopausal women with a primary symptom of female sexual arousal disorder did not show statistically significant improvement over placebo in the coprimary or secondary endpoints over a 3-month period in new preliminary study data published in Obstetrics & Gynecology.
Topical sildenafil cream is currently used for erectile dysfunction in men. There are no US Food and Drug Administration–approved treatments for female sexual arousal disorder, which affects up to 26% of women in the United States by some estimates.
Isabella Johnson, senior manager of product development at Daré Bioscience, San Diego, California, led a phase 2b, exploratory, randomized, placebo-controlled, double-blind study of sildenafil cream’s potential to help women improve their sexual experiences.
The study included 200 women with female sexual arousal disorder randomized to sildenafil cream (n = 101) or placebo cream (n = 99); 177 completed the trial and made up the intention-to-treat group. Healthy premenopausal women at least 18 years old and their sexual partners were screened for the study.
The authors report that the primary endpoints were scores on Sexual Function Questionnaire (SFQ28) arousal sensation domain and question 14 on the Female Sexual Distress Scale — Desire/Arousal/Orgasm (FSD-DAO), which asks “How often in the past 30 days did you feel concerned by difficulties with sexual arousal?” The secondary endpoint was the average number and average proportion of satisfactory sexual events. Topical sildenafil was not more effective than placebo with these primary or secondary endpoints.
Some Subgroups Benefited
However, a post hoc analysis told a different story. “[A]mong a subset of women with female sexual arousal disorder only or female sexual arousal disorder with concomitant decreased desire, we found either trends or significant improvements in sexual functioning with sildenafil cream compared with placebo cream across multiple aspects of sexual function,” the authors write.
The researchers also noted that several FSDS-DAO questions, other than question 14, asked about generalized feelings related to sexual distress and interpersonal difficulties and scores on those questions showed significant improvement with sildenafil cream compared with placebo in the exploratory subset.
“The total FSDS-DAO score decreased by about 7 points for sildenafil cream users in the subset population (a clinically meaningful decrease in sexual distress) compared with a two-point decrease for placebo cream users (P = .10),” they write.
Post Hoc Analysis Is Exploratory
JoAnn V. Pinkerton, MD, with the Department of Obstetrics and Gynecology, University of Virginia Health in Charlottesville, writes in an editorial that because the authors did not adjust for multiple hypothesis testing, the post hoc subset analyses should be considered only exploratory.
She notes that the trial was underpowered partly because it was halted after recruitment challenges during the COVID-19 pandemic. The small sample size and the varied reasons for arousal disorder among the women “may have limited the ability to find a positive outcome.”
, Dr. Pinkerton writes.
“Because improvement in genital arousal is thought to be due to the increased genital blood flow from sildenafil citrate, the subset of participants found least likely to benefit from sildenafil citrate cream were those with concomitant orgasmic dysfunction with or without genital pain,” she writes.
Data May Inform Phase 3 Trial
This phase 2b trial sets the stage for a phase 3 trial, she writes, to evaluate sildenafil topical cream in women with female sexual arousal disorder in the subsets where there were positive findings (those with or without a secondary diagnosis of decreased desire) but not among women having difficulty reaching orgasm.
“If positive, it could lead to a new therapeutic area for the unmet treatment needs of premenopausal and postmenopausal women with female sexual arousal disorder,” Dr. Pinkerton writes.
A study coauthor, Clint Dart, reports money was paid to his institution from Daré Bioscience, he provided independent data verification, and he is an employee of Premier Research. Isabella Johnson, Andrea Ries Thurman, MD, Jessica Hatheway, MBA, David R. Friend, PhD, and Andrew Goldstein, MD, are employees of Daré Bioscience. Katherine A. Cornell is an employee of Strategic Science & Technologies, LLC. C. Paige Brainard, MD, was financially compensated by Del Sol Research Management and her practice received funding from Daré Bioscience for study-specific activities. Dr. Goldstein also reported receiving payments from Nuvig, Ipsen, and AbbVie. Dr. Pinkerton’s institution received funds from Bayer Pharmaceuticals as she served as PI for a multinational clinical trial.
FROM OBSTETRICS & GYNECOLOGY
Doctor I-Don’t-Know
Many, many years ago there was a Thanksgiving when as I was just beginning to earn a reputation in my wife’s family. There were no place cards on the table and the usual hovering and jockeying seats was well underway. From behind me I heard one of my young nieces pipe up: “I want to sit next to Doctor I-don’t-know.”
After a few words of negotiation we were all settled in our places and ready to enjoy our meal. It took only a few seconds of introspection for me to grasp how I had received that moniker, which some physicians might consider disrespectful.
I was the only physician within several generations of that family and, as such, my in-laws thought it only appropriate to ask me medical questions. They courteously seemed to avoid personal questions about their own health and were particularly careful not to roll up their sleeves or unbutton their shirts to show me a lesion or a recently acquired surgical scar. No, my wife’s family members were curious. They wanted answers to deeper questions, the hard science so to speak. “How does aspirin work?” was a typical and painful example. Maybe pharmacologists today have better answers but 40 years ago I’m not so sure; I certainly didn’t know back then and would reply, “I don’t know.” Probably for the third or fourth time that day.
Usually I genuinely didn’t know the answer. However, sometimes my answer was going to be so different from the beliefs and biases of my inquisitor that, in the interest of expediency, “I don’t know” seemed the most appropriate response.
If you were reading Letters from Maine 25 years ago, that scenario might sound familiar. I have chosen to pull it out of the archives as a jumping-off point for a consideration of the unfortunate example some of us set when the COVID pandemic threw a tsunami of unknowns at us. Too many physician-“experts” were afraid to say, “I don’t know.” Instead, and maybe because, they themselves were afraid that the patients couldn’t handle the truth that none of us in the profession knew the correct answers. When so many initial pronouncements proved incorrect, it was too late to undo the damage that had been done to the community’s trust in the rest of us.
It turns out that my in-laws were not the only folks who thought of me as Doctor I-don’t-know. One of the perks of remaining in the same community after one retires is that encounters with former patients and their parents happen frequently. On more than one occasion a parent has thanked me for admitting my ignorance. Some have even claimed that my candid approach was what they remembered most fondly. And, that quality increased their trust when I finally provided an answer.
There is an art to delivering “I don’t know.” Thirty years ago I would excuse myself and tell the family I was going to my office to pull a book off the shelf or call a previous mentor. Now one only needs to ask Dr. Google. No need to leave the room. If appropriate, the provider can swing the computer screen so that the patient can share in the search for the answer.
That strategy only works when the provider merely needs to update or expand his/her knowledge. However, there are those difficult situations when no one could know the answer given the current parameters of the patient’s situation. More lab work might be needed. It may be too early in the trajectory of the patient’s illness for the illnesses signs and symptoms to declare themselves.
In these situations “I don’t know” must be followed by a “but.” It is what comes after that “but” and how it is delivered that can convert the provider’s admission of ignorance into a demonstration of his or her character. Is he/she a caring person trying to understand the patient’s concerns? Willing to enter into a cooperative relationship as together they search for the cause and hopefully for a cure for the patient’s currently mysterious illness?
I recently read about a physician who is encouraging medical educators to incorporate more discussions of “humility” and its role in patient care into the medical school and postgraduate training curricula. He feels, as do I, that
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
Many, many years ago there was a Thanksgiving when as I was just beginning to earn a reputation in my wife’s family. There were no place cards on the table and the usual hovering and jockeying seats was well underway. From behind me I heard one of my young nieces pipe up: “I want to sit next to Doctor I-don’t-know.”
After a few words of negotiation we were all settled in our places and ready to enjoy our meal. It took only a few seconds of introspection for me to grasp how I had received that moniker, which some physicians might consider disrespectful.
I was the only physician within several generations of that family and, as such, my in-laws thought it only appropriate to ask me medical questions. They courteously seemed to avoid personal questions about their own health and were particularly careful not to roll up their sleeves or unbutton their shirts to show me a lesion or a recently acquired surgical scar. No, my wife’s family members were curious. They wanted answers to deeper questions, the hard science so to speak. “How does aspirin work?” was a typical and painful example. Maybe pharmacologists today have better answers but 40 years ago I’m not so sure; I certainly didn’t know back then and would reply, “I don’t know.” Probably for the third or fourth time that day.
Usually I genuinely didn’t know the answer. However, sometimes my answer was going to be so different from the beliefs and biases of my inquisitor that, in the interest of expediency, “I don’t know” seemed the most appropriate response.
If you were reading Letters from Maine 25 years ago, that scenario might sound familiar. I have chosen to pull it out of the archives as a jumping-off point for a consideration of the unfortunate example some of us set when the COVID pandemic threw a tsunami of unknowns at us. Too many physician-“experts” were afraid to say, “I don’t know.” Instead, and maybe because, they themselves were afraid that the patients couldn’t handle the truth that none of us in the profession knew the correct answers. When so many initial pronouncements proved incorrect, it was too late to undo the damage that had been done to the community’s trust in the rest of us.
It turns out that my in-laws were not the only folks who thought of me as Doctor I-don’t-know. One of the perks of remaining in the same community after one retires is that encounters with former patients and their parents happen frequently. On more than one occasion a parent has thanked me for admitting my ignorance. Some have even claimed that my candid approach was what they remembered most fondly. And, that quality increased their trust when I finally provided an answer.
There is an art to delivering “I don’t know.” Thirty years ago I would excuse myself and tell the family I was going to my office to pull a book off the shelf or call a previous mentor. Now one only needs to ask Dr. Google. No need to leave the room. If appropriate, the provider can swing the computer screen so that the patient can share in the search for the answer.
That strategy only works when the provider merely needs to update or expand his/her knowledge. However, there are those difficult situations when no one could know the answer given the current parameters of the patient’s situation. More lab work might be needed. It may be too early in the trajectory of the patient’s illness for the illnesses signs and symptoms to declare themselves.
In these situations “I don’t know” must be followed by a “but.” It is what comes after that “but” and how it is delivered that can convert the provider’s admission of ignorance into a demonstration of his or her character. Is he/she a caring person trying to understand the patient’s concerns? Willing to enter into a cooperative relationship as together they search for the cause and hopefully for a cure for the patient’s currently mysterious illness?
I recently read about a physician who is encouraging medical educators to incorporate more discussions of “humility” and its role in patient care into the medical school and postgraduate training curricula. He feels, as do I, that
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
Many, many years ago there was a Thanksgiving when as I was just beginning to earn a reputation in my wife’s family. There were no place cards on the table and the usual hovering and jockeying seats was well underway. From behind me I heard one of my young nieces pipe up: “I want to sit next to Doctor I-don’t-know.”
After a few words of negotiation we were all settled in our places and ready to enjoy our meal. It took only a few seconds of introspection for me to grasp how I had received that moniker, which some physicians might consider disrespectful.
I was the only physician within several generations of that family and, as such, my in-laws thought it only appropriate to ask me medical questions. They courteously seemed to avoid personal questions about their own health and were particularly careful not to roll up their sleeves or unbutton their shirts to show me a lesion or a recently acquired surgical scar. No, my wife’s family members were curious. They wanted answers to deeper questions, the hard science so to speak. “How does aspirin work?” was a typical and painful example. Maybe pharmacologists today have better answers but 40 years ago I’m not so sure; I certainly didn’t know back then and would reply, “I don’t know.” Probably for the third or fourth time that day.
Usually I genuinely didn’t know the answer. However, sometimes my answer was going to be so different from the beliefs and biases of my inquisitor that, in the interest of expediency, “I don’t know” seemed the most appropriate response.
If you were reading Letters from Maine 25 years ago, that scenario might sound familiar. I have chosen to pull it out of the archives as a jumping-off point for a consideration of the unfortunate example some of us set when the COVID pandemic threw a tsunami of unknowns at us. Too many physician-“experts” were afraid to say, “I don’t know.” Instead, and maybe because, they themselves were afraid that the patients couldn’t handle the truth that none of us in the profession knew the correct answers. When so many initial pronouncements proved incorrect, it was too late to undo the damage that had been done to the community’s trust in the rest of us.
It turns out that my in-laws were not the only folks who thought of me as Doctor I-don’t-know. One of the perks of remaining in the same community after one retires is that encounters with former patients and their parents happen frequently. On more than one occasion a parent has thanked me for admitting my ignorance. Some have even claimed that my candid approach was what they remembered most fondly. And, that quality increased their trust when I finally provided an answer.
There is an art to delivering “I don’t know.” Thirty years ago I would excuse myself and tell the family I was going to my office to pull a book off the shelf or call a previous mentor. Now one only needs to ask Dr. Google. No need to leave the room. If appropriate, the provider can swing the computer screen so that the patient can share in the search for the answer.
That strategy only works when the provider merely needs to update or expand his/her knowledge. However, there are those difficult situations when no one could know the answer given the current parameters of the patient’s situation. More lab work might be needed. It may be too early in the trajectory of the patient’s illness for the illnesses signs and symptoms to declare themselves.
In these situations “I don’t know” must be followed by a “but.” It is what comes after that “but” and how it is delivered that can convert the provider’s admission of ignorance into a demonstration of his or her character. Is he/she a caring person trying to understand the patient’s concerns? Willing to enter into a cooperative relationship as together they search for the cause and hopefully for a cure for the patient’s currently mysterious illness?
I recently read about a physician who is encouraging medical educators to incorporate more discussions of “humility” and its role in patient care into the medical school and postgraduate training curricula. He feels, as do I, that
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.