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2019-nCoV: Structure, characteristics of key potential therapy target determined
Researchers have identified the structure of a protein that could turn out to be a potential vaccine target for the 2019-nCoV.
As is typical of other coronaviruses, 2019-nCoV makes use of a densely glycosylated spike protein to gain entry into host cells. The spike protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a dramatic structural rearrangement to fuse the viral membrane with the host-cell membrane, according to Daniel Wrapp of the University of Texas at Austin and colleagues.
The researchers performed a study to synthesize and determine the 3-D structure of the spike protein because it is a logical target for vaccine development and for the development of targeted therapeutics for COVID-19, the disease caused by the virus.
“As soon as we knew this was a coronavirus, we felt we had to jump at it,” senior author Jason S. McLellan, PhD, associate professor of molecular science, said in a press release from the University, “because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this because we’ve already shown these mutations work for a bunch of other coronaviruses.”
Because recent reports by other researchers demonstrated that 2019-nCoV and SARS-CoV spike proteins share the same functional host-cell receptor–angiotensin-converting enzyme 2 (ACE2), Dr. McLellan and his colleagues examined the relation between the two viruses. They found biophysical and structural evidence that the 2019-nCoV spike protein binds ACE2 with higher affinity than the closely related SARS-CoV spike protein. “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human; however, additional studies are needed to investigate this possibility,” the researchers wrote.
Focusing their attention on the receptor-binding domain (RBD) of the 2019-nCoV spike protein, they tested several published SARS-CoV RBD-specific monoclonal antibodies against it and found that these antibodies showed no appreciable binding to 2019-nCoV spike protein, which suggests limited antibody cross-reactivity. For this reason, they suggested that future antibody isolation and therapeutic design efforts will benefit from specifically using 2019-nCoV spike proteins as probes.
“This information will support precision vaccine design and discovery of anti-viral therapeutics, accelerating medical countermeasure development,” they concluded.
The research was supported in part by an National Institutes of Health/National Institute of Allergy and Infectious Diseases grant and by intramural funding from the National Institute of Allergy and Infectious Diseases. Four authors are inventors on US patent application No. 62/412,703 (Prefusion Coronavirus Spike Proteins and Their Use) and all are inventors on US patent application No. 62/972,886 (2019-nCoV Vaccine).
SOURCE: Wrapp D et al. Science. 2020 Feb 19. doi: 10.1126/science.abb2507.
Researchers have identified the structure of a protein that could turn out to be a potential vaccine target for the 2019-nCoV.
As is typical of other coronaviruses, 2019-nCoV makes use of a densely glycosylated spike protein to gain entry into host cells. The spike protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a dramatic structural rearrangement to fuse the viral membrane with the host-cell membrane, according to Daniel Wrapp of the University of Texas at Austin and colleagues.
The researchers performed a study to synthesize and determine the 3-D structure of the spike protein because it is a logical target for vaccine development and for the development of targeted therapeutics for COVID-19, the disease caused by the virus.
“As soon as we knew this was a coronavirus, we felt we had to jump at it,” senior author Jason S. McLellan, PhD, associate professor of molecular science, said in a press release from the University, “because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this because we’ve already shown these mutations work for a bunch of other coronaviruses.”
Because recent reports by other researchers demonstrated that 2019-nCoV and SARS-CoV spike proteins share the same functional host-cell receptor–angiotensin-converting enzyme 2 (ACE2), Dr. McLellan and his colleagues examined the relation between the two viruses. They found biophysical and structural evidence that the 2019-nCoV spike protein binds ACE2 with higher affinity than the closely related SARS-CoV spike protein. “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human; however, additional studies are needed to investigate this possibility,” the researchers wrote.
Focusing their attention on the receptor-binding domain (RBD) of the 2019-nCoV spike protein, they tested several published SARS-CoV RBD-specific monoclonal antibodies against it and found that these antibodies showed no appreciable binding to 2019-nCoV spike protein, which suggests limited antibody cross-reactivity. For this reason, they suggested that future antibody isolation and therapeutic design efforts will benefit from specifically using 2019-nCoV spike proteins as probes.
“This information will support precision vaccine design and discovery of anti-viral therapeutics, accelerating medical countermeasure development,” they concluded.
The research was supported in part by an National Institutes of Health/National Institute of Allergy and Infectious Diseases grant and by intramural funding from the National Institute of Allergy and Infectious Diseases. Four authors are inventors on US patent application No. 62/412,703 (Prefusion Coronavirus Spike Proteins and Their Use) and all are inventors on US patent application No. 62/972,886 (2019-nCoV Vaccine).
SOURCE: Wrapp D et al. Science. 2020 Feb 19. doi: 10.1126/science.abb2507.
Researchers have identified the structure of a protein that could turn out to be a potential vaccine target for the 2019-nCoV.
As is typical of other coronaviruses, 2019-nCoV makes use of a densely glycosylated spike protein to gain entry into host cells. The spike protein is a trimeric class I fusion protein that exists in a metastable prefusion conformation that undergoes a dramatic structural rearrangement to fuse the viral membrane with the host-cell membrane, according to Daniel Wrapp of the University of Texas at Austin and colleagues.
The researchers performed a study to synthesize and determine the 3-D structure of the spike protein because it is a logical target for vaccine development and for the development of targeted therapeutics for COVID-19, the disease caused by the virus.
“As soon as we knew this was a coronavirus, we felt we had to jump at it,” senior author Jason S. McLellan, PhD, associate professor of molecular science, said in a press release from the University, “because we could be one of the first ones to get this structure. We knew exactly what mutations to put into this because we’ve already shown these mutations work for a bunch of other coronaviruses.”
Because recent reports by other researchers demonstrated that 2019-nCoV and SARS-CoV spike proteins share the same functional host-cell receptor–angiotensin-converting enzyme 2 (ACE2), Dr. McLellan and his colleagues examined the relation between the two viruses. They found biophysical and structural evidence that the 2019-nCoV spike protein binds ACE2 with higher affinity than the closely related SARS-CoV spike protein. “The high affinity of 2019-nCoV S for human ACE2 may contribute to the apparent ease with which 2019-nCoV can spread from human-to-human; however, additional studies are needed to investigate this possibility,” the researchers wrote.
Focusing their attention on the receptor-binding domain (RBD) of the 2019-nCoV spike protein, they tested several published SARS-CoV RBD-specific monoclonal antibodies against it and found that these antibodies showed no appreciable binding to 2019-nCoV spike protein, which suggests limited antibody cross-reactivity. For this reason, they suggested that future antibody isolation and therapeutic design efforts will benefit from specifically using 2019-nCoV spike proteins as probes.
“This information will support precision vaccine design and discovery of anti-viral therapeutics, accelerating medical countermeasure development,” they concluded.
The research was supported in part by an National Institutes of Health/National Institute of Allergy and Infectious Diseases grant and by intramural funding from the National Institute of Allergy and Infectious Diseases. Four authors are inventors on US patent application No. 62/412,703 (Prefusion Coronavirus Spike Proteins and Their Use) and all are inventors on US patent application No. 62/972,886 (2019-nCoV Vaccine).
SOURCE: Wrapp D et al. Science. 2020 Feb 19. doi: 10.1126/science.abb2507.
FROM SCIENCE
Risk factors found for respiratory AEs in children following OSA surgery
Underlying cardiac disease, airway anomalies, and younger age each independently boosted the risk of severe perioperative respiratory adverse events (PRAE) in children undergoing adenotonsillectomy to treat obstructive sleep apnea, in a review of 374 patients treated at a single Canadian tertiary-referral center.
In contrast, the analysis failed to show independent, significant effects from any assessed polysomnography or oximetry parameters on the rate of postoperative respiratory complications. The utility of preoperative polysomnography or oximetry for risk stratification is questionable for pediatric patients scheduled to adenotonsillectomy to treat obstructive sleep apnea, wrote Sherri L. Katz, MD, of the University of Ottawa, and associates in a recent report published in the Journal of Clinical Sleep Medicine, although they also added that making these assessments may be “unavoidable” because of their need for diagnosing obstructive sleep apnea and determining the need for surgery.
Despite this caveat, “overall our study results highlight the need to better define the complex interaction between comorbidities, age, nocturnal respiratory events, and gas exchange abnormalities in predicting risk for PRAE” after adenotonsillectomy, the researchers wrote. These findings “are consistent with existing clinical care guidelines,” and “cardiac and craniofacial conditions have been associated with risk of postoperative complications in other studies.”
The analysis used data collected from all children aged 0-18 years who underwent polysomnography assessment followed by adenotonsillectomy at one Canadian tertiary-referral center, Children’s Hospital of Eastern Ontario in Ottawa, during 2010-2016. Their median age was just over 6 years, and 39 patients (10%) were younger than 3 years at the time of their surgery. More than three-quarters of the patients, 286, had at least one identified comorbidity, and nearly half had at least two comorbidities. Polysomnography identified sleep-disordered breathing in 344 of the children (92%), and diagnosed obstructive sleep apnea in 256 (68%), including 148 (43% of the full cohort) with a severe apnea-hypopnea index.
Sixty-six of the children (18%) had at least one severe PRAE that required intervention. Specifically these were either oxygen desaturations requiring intervention or need for airway or ventilatory support with interventions such as jaw thrust, oral or nasal airway placement, bag and mask ventilation, or endotracheal intubation.
A multivariate regression analysis of the measured comorbidity, polysomnography, and oximetry parameters, as well as age, identified three factors that independently linked with a statistically significant increase in the rate of severe PRAE: airway anomaly, underlying cardiac disease, and young age. Patients with an airway anomaly had a 219% increased rate of PRAE, compared with those with no anomaly; patients with underlying cardiac disease had a 109% increased rate, compared with those without cardiac disease; and patients aged younger than 3 years had a 310% higher rate of PRAE, compared with the children aged 6 years or older, while children aged 3-5 years had a 121% higher rate of PRAE, compared with older children.
The study received no commercial funding. Dr. Katz has received honoraria for speaking from Biogen that had no relevance to the study.
SOURCE: Katz SL et al. J Clin Sleep Med. 2020 Jan 15;16(1):41-8.
This well-conducted, retrospective, chart-review study adds important information to the published literature about risk stratification for children in a tertiary-referral population undergoing adenotonsillectomy. Their findings indicate that younger children remain at higher risk as well as those children with complex comorbid medical disease. They also show that children with severe sleep apnea or significant oxyhemoglobin desaturation are likewise at higher risk of postoperative respiratory compromise – emphasizing the need for preoperative polysomnography – particularly in a tertiary setting where many patients have medical comorbidities.
Despite the strengths of this study in assessing perioperative risk for respiratory compromise in a referral population with highly prevalent medical comorbidities, this study does not provide significant insight into the management of otherwise healthy children in a community setting who are undergoing adenotonsillectomy. This is important because a large number of adenotonsillectomies are performed outside of a tertiary-referral center and many of these children may not have undergone preoperative polysomnography to stratify risk. The utility of preoperative polysomnography in the evaluation of all children undergoing adenotonsillectomy remains controversial, with diverging recommendations from two major U.S. medical groups.
This study does not address the utility of polysomnography in community-based populations of otherwise healthy children. It is imperative to accurately ascertain risk so perioperative planning can ensure the safety of children at higher risk following adenotonsillectomy; however, there remains a paucity of studies assessing the cost-effectiveness as well as the positive and negative predictive value of polysomnographic findings. This study highlights the need for community-based studies of otherwise healthy children undergoing adenotonsillectomy to ensure that children at risk receive appropriate monitoring in an inpatient setting whereas those at lesser risk are not unnecessarily hospitalized postoperatively.
Heidi V. Connolly, MD, and Laura E. Tomaselli, MD, are pediatric sleep medicine physicians, and Margo K. McKenna Benoit, MD, is an otolaryngologist at the University of Rochester (N.Y.). They made these comments in a commentary that accompanied the published report ( J Clin Sleep Med. 2020 Jan 15;16[1]:3-4 ). They had no disclosures.
This well-conducted, retrospective, chart-review study adds important information to the published literature about risk stratification for children in a tertiary-referral population undergoing adenotonsillectomy. Their findings indicate that younger children remain at higher risk as well as those children with complex comorbid medical disease. They also show that children with severe sleep apnea or significant oxyhemoglobin desaturation are likewise at higher risk of postoperative respiratory compromise – emphasizing the need for preoperative polysomnography – particularly in a tertiary setting where many patients have medical comorbidities.
Despite the strengths of this study in assessing perioperative risk for respiratory compromise in a referral population with highly prevalent medical comorbidities, this study does not provide significant insight into the management of otherwise healthy children in a community setting who are undergoing adenotonsillectomy. This is important because a large number of adenotonsillectomies are performed outside of a tertiary-referral center and many of these children may not have undergone preoperative polysomnography to stratify risk. The utility of preoperative polysomnography in the evaluation of all children undergoing adenotonsillectomy remains controversial, with diverging recommendations from two major U.S. medical groups.
This study does not address the utility of polysomnography in community-based populations of otherwise healthy children. It is imperative to accurately ascertain risk so perioperative planning can ensure the safety of children at higher risk following adenotonsillectomy; however, there remains a paucity of studies assessing the cost-effectiveness as well as the positive and negative predictive value of polysomnographic findings. This study highlights the need for community-based studies of otherwise healthy children undergoing adenotonsillectomy to ensure that children at risk receive appropriate monitoring in an inpatient setting whereas those at lesser risk are not unnecessarily hospitalized postoperatively.
Heidi V. Connolly, MD, and Laura E. Tomaselli, MD, are pediatric sleep medicine physicians, and Margo K. McKenna Benoit, MD, is an otolaryngologist at the University of Rochester (N.Y.). They made these comments in a commentary that accompanied the published report ( J Clin Sleep Med. 2020 Jan 15;16[1]:3-4 ). They had no disclosures.
This well-conducted, retrospective, chart-review study adds important information to the published literature about risk stratification for children in a tertiary-referral population undergoing adenotonsillectomy. Their findings indicate that younger children remain at higher risk as well as those children with complex comorbid medical disease. They also show that children with severe sleep apnea or significant oxyhemoglobin desaturation are likewise at higher risk of postoperative respiratory compromise – emphasizing the need for preoperative polysomnography – particularly in a tertiary setting where many patients have medical comorbidities.
Despite the strengths of this study in assessing perioperative risk for respiratory compromise in a referral population with highly prevalent medical comorbidities, this study does not provide significant insight into the management of otherwise healthy children in a community setting who are undergoing adenotonsillectomy. This is important because a large number of adenotonsillectomies are performed outside of a tertiary-referral center and many of these children may not have undergone preoperative polysomnography to stratify risk. The utility of preoperative polysomnography in the evaluation of all children undergoing adenotonsillectomy remains controversial, with diverging recommendations from two major U.S. medical groups.
This study does not address the utility of polysomnography in community-based populations of otherwise healthy children. It is imperative to accurately ascertain risk so perioperative planning can ensure the safety of children at higher risk following adenotonsillectomy; however, there remains a paucity of studies assessing the cost-effectiveness as well as the positive and negative predictive value of polysomnographic findings. This study highlights the need for community-based studies of otherwise healthy children undergoing adenotonsillectomy to ensure that children at risk receive appropriate monitoring in an inpatient setting whereas those at lesser risk are not unnecessarily hospitalized postoperatively.
Heidi V. Connolly, MD, and Laura E. Tomaselli, MD, are pediatric sleep medicine physicians, and Margo K. McKenna Benoit, MD, is an otolaryngologist at the University of Rochester (N.Y.). They made these comments in a commentary that accompanied the published report ( J Clin Sleep Med. 2020 Jan 15;16[1]:3-4 ). They had no disclosures.
Underlying cardiac disease, airway anomalies, and younger age each independently boosted the risk of severe perioperative respiratory adverse events (PRAE) in children undergoing adenotonsillectomy to treat obstructive sleep apnea, in a review of 374 patients treated at a single Canadian tertiary-referral center.
In contrast, the analysis failed to show independent, significant effects from any assessed polysomnography or oximetry parameters on the rate of postoperative respiratory complications. The utility of preoperative polysomnography or oximetry for risk stratification is questionable for pediatric patients scheduled to adenotonsillectomy to treat obstructive sleep apnea, wrote Sherri L. Katz, MD, of the University of Ottawa, and associates in a recent report published in the Journal of Clinical Sleep Medicine, although they also added that making these assessments may be “unavoidable” because of their need for diagnosing obstructive sleep apnea and determining the need for surgery.
Despite this caveat, “overall our study results highlight the need to better define the complex interaction between comorbidities, age, nocturnal respiratory events, and gas exchange abnormalities in predicting risk for PRAE” after adenotonsillectomy, the researchers wrote. These findings “are consistent with existing clinical care guidelines,” and “cardiac and craniofacial conditions have been associated with risk of postoperative complications in other studies.”
The analysis used data collected from all children aged 0-18 years who underwent polysomnography assessment followed by adenotonsillectomy at one Canadian tertiary-referral center, Children’s Hospital of Eastern Ontario in Ottawa, during 2010-2016. Their median age was just over 6 years, and 39 patients (10%) were younger than 3 years at the time of their surgery. More than three-quarters of the patients, 286, had at least one identified comorbidity, and nearly half had at least two comorbidities. Polysomnography identified sleep-disordered breathing in 344 of the children (92%), and diagnosed obstructive sleep apnea in 256 (68%), including 148 (43% of the full cohort) with a severe apnea-hypopnea index.
Sixty-six of the children (18%) had at least one severe PRAE that required intervention. Specifically these were either oxygen desaturations requiring intervention or need for airway or ventilatory support with interventions such as jaw thrust, oral or nasal airway placement, bag and mask ventilation, or endotracheal intubation.
A multivariate regression analysis of the measured comorbidity, polysomnography, and oximetry parameters, as well as age, identified three factors that independently linked with a statistically significant increase in the rate of severe PRAE: airway anomaly, underlying cardiac disease, and young age. Patients with an airway anomaly had a 219% increased rate of PRAE, compared with those with no anomaly; patients with underlying cardiac disease had a 109% increased rate, compared with those without cardiac disease; and patients aged younger than 3 years had a 310% higher rate of PRAE, compared with the children aged 6 years or older, while children aged 3-5 years had a 121% higher rate of PRAE, compared with older children.
The study received no commercial funding. Dr. Katz has received honoraria for speaking from Biogen that had no relevance to the study.
SOURCE: Katz SL et al. J Clin Sleep Med. 2020 Jan 15;16(1):41-8.
Underlying cardiac disease, airway anomalies, and younger age each independently boosted the risk of severe perioperative respiratory adverse events (PRAE) in children undergoing adenotonsillectomy to treat obstructive sleep apnea, in a review of 374 patients treated at a single Canadian tertiary-referral center.
In contrast, the analysis failed to show independent, significant effects from any assessed polysomnography or oximetry parameters on the rate of postoperative respiratory complications. The utility of preoperative polysomnography or oximetry for risk stratification is questionable for pediatric patients scheduled to adenotonsillectomy to treat obstructive sleep apnea, wrote Sherri L. Katz, MD, of the University of Ottawa, and associates in a recent report published in the Journal of Clinical Sleep Medicine, although they also added that making these assessments may be “unavoidable” because of their need for diagnosing obstructive sleep apnea and determining the need for surgery.
Despite this caveat, “overall our study results highlight the need to better define the complex interaction between comorbidities, age, nocturnal respiratory events, and gas exchange abnormalities in predicting risk for PRAE” after adenotonsillectomy, the researchers wrote. These findings “are consistent with existing clinical care guidelines,” and “cardiac and craniofacial conditions have been associated with risk of postoperative complications in other studies.”
The analysis used data collected from all children aged 0-18 years who underwent polysomnography assessment followed by adenotonsillectomy at one Canadian tertiary-referral center, Children’s Hospital of Eastern Ontario in Ottawa, during 2010-2016. Their median age was just over 6 years, and 39 patients (10%) were younger than 3 years at the time of their surgery. More than three-quarters of the patients, 286, had at least one identified comorbidity, and nearly half had at least two comorbidities. Polysomnography identified sleep-disordered breathing in 344 of the children (92%), and diagnosed obstructive sleep apnea in 256 (68%), including 148 (43% of the full cohort) with a severe apnea-hypopnea index.
Sixty-six of the children (18%) had at least one severe PRAE that required intervention. Specifically these were either oxygen desaturations requiring intervention or need for airway or ventilatory support with interventions such as jaw thrust, oral or nasal airway placement, bag and mask ventilation, or endotracheal intubation.
A multivariate regression analysis of the measured comorbidity, polysomnography, and oximetry parameters, as well as age, identified three factors that independently linked with a statistically significant increase in the rate of severe PRAE: airway anomaly, underlying cardiac disease, and young age. Patients with an airway anomaly had a 219% increased rate of PRAE, compared with those with no anomaly; patients with underlying cardiac disease had a 109% increased rate, compared with those without cardiac disease; and patients aged younger than 3 years had a 310% higher rate of PRAE, compared with the children aged 6 years or older, while children aged 3-5 years had a 121% higher rate of PRAE, compared with older children.
The study received no commercial funding. Dr. Katz has received honoraria for speaking from Biogen that had no relevance to the study.
SOURCE: Katz SL et al. J Clin Sleep Med. 2020 Jan 15;16(1):41-8.
FROM THE JOURNAL OF CLINICAL SLEEP MEDICINE
Nail dystrophy and nail plate thinning
At a follow-up visit, a biopsy of the skin on the fingertips was performed, which showed lichenoid lymphocytic inflammatory infiltrate with associated hyperkeratosis, hypergranulosis, and acanthosis.
No fungal elements were seen. The findings were consistent with lichen planus.
The patient was started on hydroxychloroquine. It was recommended she start a 6-week course of oral prednisone, but the mother was opposed to systemic treatment because of potential side effects.
She continued topical betamethasone without much change. Topical tacrolimus later was recommended to use on off days of betamethasone, which led to no improvement. Narrow-band UVB also was started with minimal improvement. Unfortunately,
Nail lichen planus (NLP) in children is not a common condition.1 In a recent series from Chiheb et al., NLP was reported in 90 patients, of which 40% were children; a quarter of the patients reported having extracutaneous involvement as well.2 In another childhood LP series,14 % of the children presented with nail disease.3 It can be a severe disease that, if not treated aggressively, may lead to destruction of the nail bed. This condition seems to be more prevalent in boys than girls and more prevalent in African American children.3 Unfortunately, in this patient’s case, the mother was hesitant to use systemic therapy and aggressive treatment was delayed.
Possible but not clear associations with autoimmune conditions such as vitiligo, autoimmune thyroiditis, myasthenia gravis, alopecia areata, thymoma, autoimmune polyendocrinopathy, atopic dermatitis, and lichen nitidus have been described in children with LP.
The clinical characteristics of NLP include nail plate thinning with longitudinal ridging and fissuring, with or without pterygium; trachyonychia; and erythema of the lunula when the nail matrix is involved. When the nail bed is affected, the patient can present with onycholysis with or without subungual hyperkeratosis and violaceous hue of the nail bed.4 NLP can have three different clinical presentations described by Tosti et al., which include typical NLP, 20‐nail dystrophy (trachyonychia), and idiopathic nail atrophy. Idiopathic nail atrophy is described solely in children as an acute and rapid progression that leads to destruction of the nail within months, which appears to be the clinical presentation in our patient.
The differential diagnosis of nail dystrophy in children includes infectious processes such as onychomycosis, especially when children present with onycholysis and subungual hyperkeratosis. Because of this, it is recommended to perform a nail culture or submit a sample of nail clippings for microscopic evaluation to confirm the diagnosis of onychomycosis prior to starting systemic therapy in children. Fingernail involvement without toenail involvement is an unusual presentation of onychomycosis.
Twenty-nail dystrophy – also known as trachyonychia – can be caused by several inflammatory skin conditions such as lichen planus, psoriasis, eczema, pemphigus vulgaris, and alopecia areata. Clinically, there is uniformly monomorphic thinning of the nail plate with longitudinal ridging without splitting or pterygium.1 This is a benign condition and should not cause scarring. About 10% of the cases of 20-nail dystrophy are caused by lichen planus.
Nail psoriasis is characterized by nail pitting, oil spots on the nail plate, leukonychia, subungual hyperkeratosis, and onycholysis, as well as nail crumbling, which were not seen in our patient. Although her initial presentation was of 20-nail dystrophy, which also can be a presentation of nail psoriasis, its rapid evolution with associated nail atrophy and pterygium make it unlikely to be psoriasis in this particular patient.
Patients with pachyonychia congenita – which is a genetic disorder or keratinization caused by mutations on several genes encoding keratin such as K6a, K16, K17, K6b, and possibly K6c – present with nail thickening (pachyonychia) and discoloration of the nails, as well as pincer nails. These patients also present with oral leukokeratosis and focal palmoplantar keratoderma.
The main treatment of lichen planus is potent topical corticosteroids.
For nail disease, topical treatment may not be effective and systemic treatment may be necessary. Systemic corticosteroids have been used in several pediatric series varying from a short course given at a dose of 1- 2 mg/kg per day for 2 weeks to a longer 3-month course followed by tapering.3 There are several protocols of intramuscular triamcinolone at a dose of 0.5 mg/kg in children in once a month injections for about 3 months that have been reported successful with minimal side effects.1 Other medications reported useful in patients with NLP include dapsone and acitretin. Other treatment options include narrow-band UVB and PUVA.3
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at pdnews@mdedge.com.
References
1. Arch Dermatol. 2001 Aug;137(8):1027-32.
2. Ann Dermatol Venereol. 2015 Jan;142(1):21-5.
3. Pediatr Dermatol. 2014 Jan-Feb;31(1):59-67.
4. Dermatological diseases, in “Nails: Diagnosis, Therapy, and Surgery,” 3rd ed. (Oxford: Elsevier Saunders, 2005, p. 105).
At a follow-up visit, a biopsy of the skin on the fingertips was performed, which showed lichenoid lymphocytic inflammatory infiltrate with associated hyperkeratosis, hypergranulosis, and acanthosis.
No fungal elements were seen. The findings were consistent with lichen planus.
The patient was started on hydroxychloroquine. It was recommended she start a 6-week course of oral prednisone, but the mother was opposed to systemic treatment because of potential side effects.
She continued topical betamethasone without much change. Topical tacrolimus later was recommended to use on off days of betamethasone, which led to no improvement. Narrow-band UVB also was started with minimal improvement. Unfortunately,
Nail lichen planus (NLP) in children is not a common condition.1 In a recent series from Chiheb et al., NLP was reported in 90 patients, of which 40% were children; a quarter of the patients reported having extracutaneous involvement as well.2 In another childhood LP series,14 % of the children presented with nail disease.3 It can be a severe disease that, if not treated aggressively, may lead to destruction of the nail bed. This condition seems to be more prevalent in boys than girls and more prevalent in African American children.3 Unfortunately, in this patient’s case, the mother was hesitant to use systemic therapy and aggressive treatment was delayed.
Possible but not clear associations with autoimmune conditions such as vitiligo, autoimmune thyroiditis, myasthenia gravis, alopecia areata, thymoma, autoimmune polyendocrinopathy, atopic dermatitis, and lichen nitidus have been described in children with LP.
The clinical characteristics of NLP include nail plate thinning with longitudinal ridging and fissuring, with or without pterygium; trachyonychia; and erythema of the lunula when the nail matrix is involved. When the nail bed is affected, the patient can present with onycholysis with or without subungual hyperkeratosis and violaceous hue of the nail bed.4 NLP can have three different clinical presentations described by Tosti et al., which include typical NLP, 20‐nail dystrophy (trachyonychia), and idiopathic nail atrophy. Idiopathic nail atrophy is described solely in children as an acute and rapid progression that leads to destruction of the nail within months, which appears to be the clinical presentation in our patient.
The differential diagnosis of nail dystrophy in children includes infectious processes such as onychomycosis, especially when children present with onycholysis and subungual hyperkeratosis. Because of this, it is recommended to perform a nail culture or submit a sample of nail clippings for microscopic evaluation to confirm the diagnosis of onychomycosis prior to starting systemic therapy in children. Fingernail involvement without toenail involvement is an unusual presentation of onychomycosis.
Twenty-nail dystrophy – also known as trachyonychia – can be caused by several inflammatory skin conditions such as lichen planus, psoriasis, eczema, pemphigus vulgaris, and alopecia areata. Clinically, there is uniformly monomorphic thinning of the nail plate with longitudinal ridging without splitting or pterygium.1 This is a benign condition and should not cause scarring. About 10% of the cases of 20-nail dystrophy are caused by lichen planus.
Nail psoriasis is characterized by nail pitting, oil spots on the nail plate, leukonychia, subungual hyperkeratosis, and onycholysis, as well as nail crumbling, which were not seen in our patient. Although her initial presentation was of 20-nail dystrophy, which also can be a presentation of nail psoriasis, its rapid evolution with associated nail atrophy and pterygium make it unlikely to be psoriasis in this particular patient.
Patients with pachyonychia congenita – which is a genetic disorder or keratinization caused by mutations on several genes encoding keratin such as K6a, K16, K17, K6b, and possibly K6c – present with nail thickening (pachyonychia) and discoloration of the nails, as well as pincer nails. These patients also present with oral leukokeratosis and focal palmoplantar keratoderma.
The main treatment of lichen planus is potent topical corticosteroids.
For nail disease, topical treatment may not be effective and systemic treatment may be necessary. Systemic corticosteroids have been used in several pediatric series varying from a short course given at a dose of 1- 2 mg/kg per day for 2 weeks to a longer 3-month course followed by tapering.3 There are several protocols of intramuscular triamcinolone at a dose of 0.5 mg/kg in children in once a month injections for about 3 months that have been reported successful with minimal side effects.1 Other medications reported useful in patients with NLP include dapsone and acitretin. Other treatment options include narrow-band UVB and PUVA.3
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at pdnews@mdedge.com.
References
1. Arch Dermatol. 2001 Aug;137(8):1027-32.
2. Ann Dermatol Venereol. 2015 Jan;142(1):21-5.
3. Pediatr Dermatol. 2014 Jan-Feb;31(1):59-67.
4. Dermatological diseases, in “Nails: Diagnosis, Therapy, and Surgery,” 3rd ed. (Oxford: Elsevier Saunders, 2005, p. 105).
At a follow-up visit, a biopsy of the skin on the fingertips was performed, which showed lichenoid lymphocytic inflammatory infiltrate with associated hyperkeratosis, hypergranulosis, and acanthosis.
No fungal elements were seen. The findings were consistent with lichen planus.
The patient was started on hydroxychloroquine. It was recommended she start a 6-week course of oral prednisone, but the mother was opposed to systemic treatment because of potential side effects.
She continued topical betamethasone without much change. Topical tacrolimus later was recommended to use on off days of betamethasone, which led to no improvement. Narrow-band UVB also was started with minimal improvement. Unfortunately,
Nail lichen planus (NLP) in children is not a common condition.1 In a recent series from Chiheb et al., NLP was reported in 90 patients, of which 40% were children; a quarter of the patients reported having extracutaneous involvement as well.2 In another childhood LP series,14 % of the children presented with nail disease.3 It can be a severe disease that, if not treated aggressively, may lead to destruction of the nail bed. This condition seems to be more prevalent in boys than girls and more prevalent in African American children.3 Unfortunately, in this patient’s case, the mother was hesitant to use systemic therapy and aggressive treatment was delayed.
Possible but not clear associations with autoimmune conditions such as vitiligo, autoimmune thyroiditis, myasthenia gravis, alopecia areata, thymoma, autoimmune polyendocrinopathy, atopic dermatitis, and lichen nitidus have been described in children with LP.
The clinical characteristics of NLP include nail plate thinning with longitudinal ridging and fissuring, with or without pterygium; trachyonychia; and erythema of the lunula when the nail matrix is involved. When the nail bed is affected, the patient can present with onycholysis with or without subungual hyperkeratosis and violaceous hue of the nail bed.4 NLP can have three different clinical presentations described by Tosti et al., which include typical NLP, 20‐nail dystrophy (trachyonychia), and idiopathic nail atrophy. Idiopathic nail atrophy is described solely in children as an acute and rapid progression that leads to destruction of the nail within months, which appears to be the clinical presentation in our patient.
The differential diagnosis of nail dystrophy in children includes infectious processes such as onychomycosis, especially when children present with onycholysis and subungual hyperkeratosis. Because of this, it is recommended to perform a nail culture or submit a sample of nail clippings for microscopic evaluation to confirm the diagnosis of onychomycosis prior to starting systemic therapy in children. Fingernail involvement without toenail involvement is an unusual presentation of onychomycosis.
Twenty-nail dystrophy – also known as trachyonychia – can be caused by several inflammatory skin conditions such as lichen planus, psoriasis, eczema, pemphigus vulgaris, and alopecia areata. Clinically, there is uniformly monomorphic thinning of the nail plate with longitudinal ridging without splitting or pterygium.1 This is a benign condition and should not cause scarring. About 10% of the cases of 20-nail dystrophy are caused by lichen planus.
Nail psoriasis is characterized by nail pitting, oil spots on the nail plate, leukonychia, subungual hyperkeratosis, and onycholysis, as well as nail crumbling, which were not seen in our patient. Although her initial presentation was of 20-nail dystrophy, which also can be a presentation of nail psoriasis, its rapid evolution with associated nail atrophy and pterygium make it unlikely to be psoriasis in this particular patient.
Patients with pachyonychia congenita – which is a genetic disorder or keratinization caused by mutations on several genes encoding keratin such as K6a, K16, K17, K6b, and possibly K6c – present with nail thickening (pachyonychia) and discoloration of the nails, as well as pincer nails. These patients also present with oral leukokeratosis and focal palmoplantar keratoderma.
The main treatment of lichen planus is potent topical corticosteroids.
For nail disease, topical treatment may not be effective and systemic treatment may be necessary. Systemic corticosteroids have been used in several pediatric series varying from a short course given at a dose of 1- 2 mg/kg per day for 2 weeks to a longer 3-month course followed by tapering.3 There are several protocols of intramuscular triamcinolone at a dose of 0.5 mg/kg in children in once a month injections for about 3 months that have been reported successful with minimal side effects.1 Other medications reported useful in patients with NLP include dapsone and acitretin. Other treatment options include narrow-band UVB and PUVA.3
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at pdnews@mdedge.com.
References
1. Arch Dermatol. 2001 Aug;137(8):1027-32.
2. Ann Dermatol Venereol. 2015 Jan;142(1):21-5.
3. Pediatr Dermatol. 2014 Jan-Feb;31(1):59-67.
4. Dermatological diseases, in “Nails: Diagnosis, Therapy, and Surgery,” 3rd ed. (Oxford: Elsevier Saunders, 2005, p. 105).
An 8-year-old female child comes to our pediatric dermatology clinic for evaluation of onychomycosis on her fingernails. The mother stated the child started developing funny-looking nails 1 year prior to the visit. It started with only two fingernails affected and now has spread to all her fingernails. Her toenails are not involved.
She denied any pain or itching. She initially was treated with topical antifungal medications as well as tea tree oil, apple cider vinegar, and a 6-week course of oral griseofulvin without any improvement. Her nails progressively have gotten much worse. She has no history of atopic dermatitis or any other skin conditions. She denied any joint pain, sun sensitivity, hair loss, or any other symptoms. The mother denied any family history of nail fungus, ringworm, psoriasis, or eczema.
She likes to play basketball and enjoys arts and crafts. She has a cat and a dog; neither of them have any skin problems.
On physical examination, there is nail dystrophy with nail plate thinning and longitudinal fissuring of all fingernails but not of the toenails. She also has hyperpigmented violaceous plaques on the surrounding periungual skin. There are no other skin lesions, and there are no oral or genital lesions. There is no scalp involvement or hair loss. At follow-up several months later, she had complete destruction of the nail plate with scar formation.
A fungal culture was performed, as well as microscopic analysis of the nail with periodic acid fast and giemsa stains, which showed no fungal organisms.
She initially was treated with topical betamethasone twice a day for 6 weeks and then 2 weeks on and 2 weeks off without much change.
Doctors look to existing drugs in coronavirus fight
COVID-19, the infection caused by the newly identified coronavirus, is a currently a disease with no pharmaceutical weapons against it. There’s no vaccine to prevent it, and no drugs can treat it.
But researchers are racing to change that. A vaccine could be ready to test as soon as April. More than two dozen studies have already been registered on ClinicalTrials.gov, a website that tracks research. These studies aim to test everything from traditional Chinese medicine to vitamin C, stem cells, steroids, and medications that fight other viruses, like the flu and HIV. The hope is that something about how these repurposed remedies work will help patients who are desperately ill with no other prospects.
Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, says this is all part of the playbook for brand-new diseases. “There’s a lot of empiric guessing,” he says. “They’re going to propose a whole lot of drugs that already exist. They’re going to say, here’s the data that shows it blocks the virus” in a test tube. But test tubes aren’t people, and many drugs that seem to work in a lab won’t end up helping patients.
Coronaviruses are especially hard to stop once they invade the body. Unlike many other kinds of viruses, they have a fail-safe against tampering – a “proofreader” that constantly inspects their code, looking for errors, including the potentially life-saving errors that drugs could introduce.
Dr. Fauci said that researchers will be able to make better guesses about how to help people when they can try drugs in animals. “We don’t have an animal model yet of the new coronavirus. When we do get an animal model, that will be a big boon to drugs because then, you can clearly test them in a physiological way, whether they work,” he says.
Looking to drugs for HIV and flu
One of the drugs already under study is the combination of two HIV medications: lopinavir and ritonavir (Kaletra). Kaletra stops viruses by interfering with the enzymes they need to infect cells, called proteases.
One study being done at the Guangzhou Eighth People’s Hospital in China is testing Kaletra against Arbidol, an antiviral drug approved in China and Russia to treat the flu. Two groups of patients will take the medications along with standard care. A third group in the study will receive only standard care, typically supportive therapy with oxygen and IV fluids that are meant to support the body so the immune system can fight off a virus on its own.
An Ebola drug gets a second look
One repurposed drug generating a lot of buzz is an experimental infusion called remdesivir (Xembify). It was originally tested against the Ebola virus. While it didn’t work for that infection, it has been shown to shut down the new coronavirus, at least in test tubes. It’s been given to a small number of COVID-19 patients already, including one in Washington state.
In order to have better evidence of how well it may work in people, two studies in Beijing are comparing remdesivir to a dummy pill to see if the drug can help patients with both mild and severe symptoms recover from their illnesses. Viruses work by infecting cells, taking over their machinery, and getting them to crank out more copies of the virus, which then goes on to infect more cells. Remdesivir is a mimic that fools a virus into replacing one of its four building blocks with a chemical fake. Once in the virus’s blueprints, the imposter acts like a stop sign that keeps the virus from copying itself.
Other kinds of drugs in the same class – called nucleotide analogs – are used to attack cancer and other infectious viruses like hepatitis.
Last week, Chinese scientists published study showing remdesivir was effective against the new coronavirus, 2019-nCoV. Out of seven drugs tested, only remdesivir and an older drug called chloroquine (Aralen), which is used to treat malaria, worked, at least in test tubes. “It functions like a knife that just cuts off the RNA strand,” says Mark Denison, MD, a pediatric infectious disease specialist at Vanderbilt University in Nashville. “They can’t replicate any more. It stops them from doing that.” Dr. Denison is part of a team of researchers in Tennessee and North Carolina that discovered remdesivir could stop coronaviruses, like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), in test tubes and animals. He has studied coronaviruses in his lab for 30 years. He knew they would pose a threat again. “We’re shocked, but not surprised, that this has happened again,” he says of the China-based outbreak of 2019-nCoV.
After the SARS outbreak, which infected more than 8,000 people in 26 countries during 2002-2003, and MERS, which has infected nearly 2,500 people in 27 countries since 2012, researchers knew they had to start looking for treatments that would work against coronaviruses. Dr. Denison reached out to Gilead Sciences, a company best known for its antiviral medications that treat HIV and hepatitis C, and asked it to send drug candidates for him to test on coronaviruses. “The idea was that we didn’t want a drug that would just work against SARS or MERS,” he says. “We wanted drugs that worked against every coronavirus.”
Many of the agents he tried didn’t work until Dr. Denison and his team knocked out the virus’s pesky proofreader. Remdesivir seems to be able to defeat the proofreader, though Dr. Denison admits that he does not know how the drug gets around a virus’s defenses. He has a grant from the National Institutes of Health to study that. Gilead has been giving remdesivir to “a small number” of coronavirus patients in the United States and Europe on a compassionate basis.
One of those patients was a 35-year-old man in Everett, Wash., who had gotten pneumonia after being infected with the new coronavirus during a trip to see family in Wuhan, China, the epicenter of the outbreak. His doctors started IV remdesivir on the evening of his 7th day in the hospital. On the 8th day, he improved. He was well enough to stop using oxygen. Signs of pneumonia were gone. He got his appetite back. His case was recently published in the New England Journal of Medicine, igniting a firestorm of interest in the therapy.
Unfortunately, though, even Dr. Denison says a single person’s case isn’t enough proof that the medication can treat the new coronavirus. The patient, who has not been identified, was getting expert care. He may have improved on his own, despite getting the drug. He said the challenge in people will be to find out two things: whether the medication can block the spread of virus in the body and whether it can reverse the disease. “You can remove the source of injury, but you still have the injury,” he said. Other important questions include how soon the drug may need to be given after infection for it work and whether it may cause significant side effects.
A promising pill
Another drug, a nucleoside analog, that appears to be able to defeat the coronavirus proofreader, EIDD-2801, was developed by Emory University in Atlanta. It was originally intended to treat the flu but has shown some effectiveness against coronaviruses like SARS and MERS.
The FDA recently reached out to Emory asking if it had any drug candidates that might work against the new coronavirus. “It’s a good shot on goal here,” says George Painter, PhD, CEO of Drug Innovation Ventures at Emory. EIDD-2801 can be taken as a pill, which makes it easier to use outside of a hospital setting.
“The capsules for the trial are being made at the end of this month. So we’re close,” Painter says. “We’re right on the edge.”
While these early tests are just getting started, and it will be months until researchers have results, the World Health Organization has sounded a note of caution.
In new guidelines for the clinical management of COVID-19, the WHO reminded doctors and patients that there’s not enough evidence to recommend any specific treatment for infected patients.
Right now, the guidelines recommend that doctors offer supportive care to help the body fight off an infection on its own.
The organization says unlicensed treatments should be given only in the context of clinical trials that have been ethically reviewed or with strict clinical monitoring in emergencies.
This article first appeared on WebMD.com.
COVID-19, the infection caused by the newly identified coronavirus, is a currently a disease with no pharmaceutical weapons against it. There’s no vaccine to prevent it, and no drugs can treat it.
But researchers are racing to change that. A vaccine could be ready to test as soon as April. More than two dozen studies have already been registered on ClinicalTrials.gov, a website that tracks research. These studies aim to test everything from traditional Chinese medicine to vitamin C, stem cells, steroids, and medications that fight other viruses, like the flu and HIV. The hope is that something about how these repurposed remedies work will help patients who are desperately ill with no other prospects.
Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, says this is all part of the playbook for brand-new diseases. “There’s a lot of empiric guessing,” he says. “They’re going to propose a whole lot of drugs that already exist. They’re going to say, here’s the data that shows it blocks the virus” in a test tube. But test tubes aren’t people, and many drugs that seem to work in a lab won’t end up helping patients.
Coronaviruses are especially hard to stop once they invade the body. Unlike many other kinds of viruses, they have a fail-safe against tampering – a “proofreader” that constantly inspects their code, looking for errors, including the potentially life-saving errors that drugs could introduce.
Dr. Fauci said that researchers will be able to make better guesses about how to help people when they can try drugs in animals. “We don’t have an animal model yet of the new coronavirus. When we do get an animal model, that will be a big boon to drugs because then, you can clearly test them in a physiological way, whether they work,” he says.
Looking to drugs for HIV and flu
One of the drugs already under study is the combination of two HIV medications: lopinavir and ritonavir (Kaletra). Kaletra stops viruses by interfering with the enzymes they need to infect cells, called proteases.
One study being done at the Guangzhou Eighth People’s Hospital in China is testing Kaletra against Arbidol, an antiviral drug approved in China and Russia to treat the flu. Two groups of patients will take the medications along with standard care. A third group in the study will receive only standard care, typically supportive therapy with oxygen and IV fluids that are meant to support the body so the immune system can fight off a virus on its own.
An Ebola drug gets a second look
One repurposed drug generating a lot of buzz is an experimental infusion called remdesivir (Xembify). It was originally tested against the Ebola virus. While it didn’t work for that infection, it has been shown to shut down the new coronavirus, at least in test tubes. It’s been given to a small number of COVID-19 patients already, including one in Washington state.
In order to have better evidence of how well it may work in people, two studies in Beijing are comparing remdesivir to a dummy pill to see if the drug can help patients with both mild and severe symptoms recover from their illnesses. Viruses work by infecting cells, taking over their machinery, and getting them to crank out more copies of the virus, which then goes on to infect more cells. Remdesivir is a mimic that fools a virus into replacing one of its four building blocks with a chemical fake. Once in the virus’s blueprints, the imposter acts like a stop sign that keeps the virus from copying itself.
Other kinds of drugs in the same class – called nucleotide analogs – are used to attack cancer and other infectious viruses like hepatitis.
Last week, Chinese scientists published study showing remdesivir was effective against the new coronavirus, 2019-nCoV. Out of seven drugs tested, only remdesivir and an older drug called chloroquine (Aralen), which is used to treat malaria, worked, at least in test tubes. “It functions like a knife that just cuts off the RNA strand,” says Mark Denison, MD, a pediatric infectious disease specialist at Vanderbilt University in Nashville. “They can’t replicate any more. It stops them from doing that.” Dr. Denison is part of a team of researchers in Tennessee and North Carolina that discovered remdesivir could stop coronaviruses, like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), in test tubes and animals. He has studied coronaviruses in his lab for 30 years. He knew they would pose a threat again. “We’re shocked, but not surprised, that this has happened again,” he says of the China-based outbreak of 2019-nCoV.
After the SARS outbreak, which infected more than 8,000 people in 26 countries during 2002-2003, and MERS, which has infected nearly 2,500 people in 27 countries since 2012, researchers knew they had to start looking for treatments that would work against coronaviruses. Dr. Denison reached out to Gilead Sciences, a company best known for its antiviral medications that treat HIV and hepatitis C, and asked it to send drug candidates for him to test on coronaviruses. “The idea was that we didn’t want a drug that would just work against SARS or MERS,” he says. “We wanted drugs that worked against every coronavirus.”
Many of the agents he tried didn’t work until Dr. Denison and his team knocked out the virus’s pesky proofreader. Remdesivir seems to be able to defeat the proofreader, though Dr. Denison admits that he does not know how the drug gets around a virus’s defenses. He has a grant from the National Institutes of Health to study that. Gilead has been giving remdesivir to “a small number” of coronavirus patients in the United States and Europe on a compassionate basis.
One of those patients was a 35-year-old man in Everett, Wash., who had gotten pneumonia after being infected with the new coronavirus during a trip to see family in Wuhan, China, the epicenter of the outbreak. His doctors started IV remdesivir on the evening of his 7th day in the hospital. On the 8th day, he improved. He was well enough to stop using oxygen. Signs of pneumonia were gone. He got his appetite back. His case was recently published in the New England Journal of Medicine, igniting a firestorm of interest in the therapy.
Unfortunately, though, even Dr. Denison says a single person’s case isn’t enough proof that the medication can treat the new coronavirus. The patient, who has not been identified, was getting expert care. He may have improved on his own, despite getting the drug. He said the challenge in people will be to find out two things: whether the medication can block the spread of virus in the body and whether it can reverse the disease. “You can remove the source of injury, but you still have the injury,” he said. Other important questions include how soon the drug may need to be given after infection for it work and whether it may cause significant side effects.
A promising pill
Another drug, a nucleoside analog, that appears to be able to defeat the coronavirus proofreader, EIDD-2801, was developed by Emory University in Atlanta. It was originally intended to treat the flu but has shown some effectiveness against coronaviruses like SARS and MERS.
The FDA recently reached out to Emory asking if it had any drug candidates that might work against the new coronavirus. “It’s a good shot on goal here,” says George Painter, PhD, CEO of Drug Innovation Ventures at Emory. EIDD-2801 can be taken as a pill, which makes it easier to use outside of a hospital setting.
“The capsules for the trial are being made at the end of this month. So we’re close,” Painter says. “We’re right on the edge.”
While these early tests are just getting started, and it will be months until researchers have results, the World Health Organization has sounded a note of caution.
In new guidelines for the clinical management of COVID-19, the WHO reminded doctors and patients that there’s not enough evidence to recommend any specific treatment for infected patients.
Right now, the guidelines recommend that doctors offer supportive care to help the body fight off an infection on its own.
The organization says unlicensed treatments should be given only in the context of clinical trials that have been ethically reviewed or with strict clinical monitoring in emergencies.
This article first appeared on WebMD.com.
COVID-19, the infection caused by the newly identified coronavirus, is a currently a disease with no pharmaceutical weapons against it. There’s no vaccine to prevent it, and no drugs can treat it.
But researchers are racing to change that. A vaccine could be ready to test as soon as April. More than two dozen studies have already been registered on ClinicalTrials.gov, a website that tracks research. These studies aim to test everything from traditional Chinese medicine to vitamin C, stem cells, steroids, and medications that fight other viruses, like the flu and HIV. The hope is that something about how these repurposed remedies work will help patients who are desperately ill with no other prospects.
Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, says this is all part of the playbook for brand-new diseases. “There’s a lot of empiric guessing,” he says. “They’re going to propose a whole lot of drugs that already exist. They’re going to say, here’s the data that shows it blocks the virus” in a test tube. But test tubes aren’t people, and many drugs that seem to work in a lab won’t end up helping patients.
Coronaviruses are especially hard to stop once they invade the body. Unlike many other kinds of viruses, they have a fail-safe against tampering – a “proofreader” that constantly inspects their code, looking for errors, including the potentially life-saving errors that drugs could introduce.
Dr. Fauci said that researchers will be able to make better guesses about how to help people when they can try drugs in animals. “We don’t have an animal model yet of the new coronavirus. When we do get an animal model, that will be a big boon to drugs because then, you can clearly test them in a physiological way, whether they work,” he says.
Looking to drugs for HIV and flu
One of the drugs already under study is the combination of two HIV medications: lopinavir and ritonavir (Kaletra). Kaletra stops viruses by interfering with the enzymes they need to infect cells, called proteases.
One study being done at the Guangzhou Eighth People’s Hospital in China is testing Kaletra against Arbidol, an antiviral drug approved in China and Russia to treat the flu. Two groups of patients will take the medications along with standard care. A third group in the study will receive only standard care, typically supportive therapy with oxygen and IV fluids that are meant to support the body so the immune system can fight off a virus on its own.
An Ebola drug gets a second look
One repurposed drug generating a lot of buzz is an experimental infusion called remdesivir (Xembify). It was originally tested against the Ebola virus. While it didn’t work for that infection, it has been shown to shut down the new coronavirus, at least in test tubes. It’s been given to a small number of COVID-19 patients already, including one in Washington state.
In order to have better evidence of how well it may work in people, two studies in Beijing are comparing remdesivir to a dummy pill to see if the drug can help patients with both mild and severe symptoms recover from their illnesses. Viruses work by infecting cells, taking over their machinery, and getting them to crank out more copies of the virus, which then goes on to infect more cells. Remdesivir is a mimic that fools a virus into replacing one of its four building blocks with a chemical fake. Once in the virus’s blueprints, the imposter acts like a stop sign that keeps the virus from copying itself.
Other kinds of drugs in the same class – called nucleotide analogs – are used to attack cancer and other infectious viruses like hepatitis.
Last week, Chinese scientists published study showing remdesivir was effective against the new coronavirus, 2019-nCoV. Out of seven drugs tested, only remdesivir and an older drug called chloroquine (Aralen), which is used to treat malaria, worked, at least in test tubes. “It functions like a knife that just cuts off the RNA strand,” says Mark Denison, MD, a pediatric infectious disease specialist at Vanderbilt University in Nashville. “They can’t replicate any more. It stops them from doing that.” Dr. Denison is part of a team of researchers in Tennessee and North Carolina that discovered remdesivir could stop coronaviruses, like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), in test tubes and animals. He has studied coronaviruses in his lab for 30 years. He knew they would pose a threat again. “We’re shocked, but not surprised, that this has happened again,” he says of the China-based outbreak of 2019-nCoV.
After the SARS outbreak, which infected more than 8,000 people in 26 countries during 2002-2003, and MERS, which has infected nearly 2,500 people in 27 countries since 2012, researchers knew they had to start looking for treatments that would work against coronaviruses. Dr. Denison reached out to Gilead Sciences, a company best known for its antiviral medications that treat HIV and hepatitis C, and asked it to send drug candidates for him to test on coronaviruses. “The idea was that we didn’t want a drug that would just work against SARS or MERS,” he says. “We wanted drugs that worked against every coronavirus.”
Many of the agents he tried didn’t work until Dr. Denison and his team knocked out the virus’s pesky proofreader. Remdesivir seems to be able to defeat the proofreader, though Dr. Denison admits that he does not know how the drug gets around a virus’s defenses. He has a grant from the National Institutes of Health to study that. Gilead has been giving remdesivir to “a small number” of coronavirus patients in the United States and Europe on a compassionate basis.
One of those patients was a 35-year-old man in Everett, Wash., who had gotten pneumonia after being infected with the new coronavirus during a trip to see family in Wuhan, China, the epicenter of the outbreak. His doctors started IV remdesivir on the evening of his 7th day in the hospital. On the 8th day, he improved. He was well enough to stop using oxygen. Signs of pneumonia were gone. He got his appetite back. His case was recently published in the New England Journal of Medicine, igniting a firestorm of interest in the therapy.
Unfortunately, though, even Dr. Denison says a single person’s case isn’t enough proof that the medication can treat the new coronavirus. The patient, who has not been identified, was getting expert care. He may have improved on his own, despite getting the drug. He said the challenge in people will be to find out two things: whether the medication can block the spread of virus in the body and whether it can reverse the disease. “You can remove the source of injury, but you still have the injury,” he said. Other important questions include how soon the drug may need to be given after infection for it work and whether it may cause significant side effects.
A promising pill
Another drug, a nucleoside analog, that appears to be able to defeat the coronavirus proofreader, EIDD-2801, was developed by Emory University in Atlanta. It was originally intended to treat the flu but has shown some effectiveness against coronaviruses like SARS and MERS.
The FDA recently reached out to Emory asking if it had any drug candidates that might work against the new coronavirus. “It’s a good shot on goal here,” says George Painter, PhD, CEO of Drug Innovation Ventures at Emory. EIDD-2801 can be taken as a pill, which makes it easier to use outside of a hospital setting.
“The capsules for the trial are being made at the end of this month. So we’re close,” Painter says. “We’re right on the edge.”
While these early tests are just getting started, and it will be months until researchers have results, the World Health Organization has sounded a note of caution.
In new guidelines for the clinical management of COVID-19, the WHO reminded doctors and patients that there’s not enough evidence to recommend any specific treatment for infected patients.
Right now, the guidelines recommend that doctors offer supportive care to help the body fight off an infection on its own.
The organization says unlicensed treatments should be given only in the context of clinical trials that have been ethically reviewed or with strict clinical monitoring in emergencies.
This article first appeared on WebMD.com.
Play it as it lies: Handling lying by kids
“Not my son!” your patient’s parent rants. “If he lies to me, he will regret it for a long time.” While your first reaction may be to agree that a child lying to a parent crosses a kind of moral line in the sand, lying is a far more nuanced part of parenting worth a deeper understanding.
In order to lie, a child has to develop cognitive and social understanding. Typically developing children look to see what is interesting to others, called “joint attention,” at around 12-18 months. Failure to do this is one of the early signs of autism reflecting atypical social understanding. At around 3.5 years, children may attempt to deceive if they have broken a rule. The study demonstrating this may sound a lot like home: Children are left alone with a tempting toy but told not to touch it. Although they do touch it while the adult is out of sight, they say rather sweetly (and eventually convincingly) that they did not, even though the toy was clearly moved! While boys generally have more behavior problems, girls and children with better verbal skills achieve deceit at an earlier age, some as young as 2 years. At this stage, children become aware that the adult can’t know exactly what they know. If the parent shows high emotion to what they consider a lie, this can be a topic for testing! Children with ADHD often lack the inhibition needed for early mastery of deception, and children with autism later or not at all. They don’t see the social point to lying nor can they fake a facial expression. They have a case of intractable honesty!
The inability to refrain from telling the truth can result in social rejection, for example when a child rats on a peer for a trivial misdeed in class. Even though he is speaking the truth and “following the (teacher’s) rules,” he did not see that the cost of breaking the (peer) social rules was more important. By age 6 years, children typically figure out that what another person thinks may not be true – their belief may be incorrect or a “false belief.” This understanding is called Theory of Mind, missing or delayed in autism. Only 40% of high-functioning children with autism passed false belief testing at ages 6- to 13-years-old, compared with 95% of typical age-matched peers (Physiol Behav. 2010 Jun 1;100[3]:268-76). The percentage of children on the spectrum understanding false beliefs more closely matched that of preschoolers (39%). At a later age and given extra time to think, some children with autism can do better at this kind of perspective taking, but many continue having difficulty understanding thoughts of others, especially social expectations or motivations (such as flirting, status seeking, and making an excuse) even as adults. This can impair social relationships even when desire to fit in and IQ are otherwise high.
On the other hand, ADHD is a common condition in which “lying” comes from saying the first thing that comes to mind even if the child knows otherwise. A wise parent of one of my patients with ADHD told me about her “30 second rule” where she would give her child that extra time and walk away briefly to “be sure that is what you wanted to say,” with praise rather than give a consequence for changing the story to the truth. This is an important concept we pediatricians need to know: Punishing lying in children tends to result in more, not less, lying and more sneakiness. Instead, parents need to be advised to recall the origins of the word discipline as being “to teach.”
When children lie there are four basic scenarios: They may not know the rules, they may know but have something they want more, they may be impulsive, or they may have developed an attitude of seeking to con the adults whom they feel are mean as a way to have some power in the relationship and get back at them. Clearly, we do not want to push children to this fourth resort by harsh reactions to lying. We have seen particular difficulty with harsh reactions to lying in parents from strong, rule-oriented careers such as police officers, military, and ministers. Asking “How would your parent have handled this?” often will reveal reasons for their tough but backfiring stance.
Lying can work to get what one wants and nearly all children try it. As with other new milestones, children practice this “skill,” much to parents’ dismay. Parents generally can tell if children are lying; they see it on their faces, hear the story from siblings, or see evidence of what happened. Lying provides an important opportunity for the adult to stop, take some breaths, touch the child, and empathize: “It is hard to admit a mistake. I know you did not mean to do it. But you are young, and I know that you are good and honest inside, and will get stronger and braver at telling the truth as you get older. Will you promise to try harder?” In some cases a consequence may be appropriate, for example if something was broken. Usually, simply empathizing and focusing on the expectation for improvement will increase the child’s desire to please the parents rather than get back at them. Actual rewards for honesty improve truth telling by 1.5 times if the reward is big enough.
But it is important to recognize that we all make split second tactical decisions about our actions based on how safe we feel in the situation and our knowledge of social rules and costs. Children over time need to learn that it is safe to tell the truth among family members and that they will not be harshly dealt with. It is a subtle task, but important to learn that deception is a tool that can be important used judiciously when required socially (I have a curfew) or in dangerous situations (I did not see the thug), but can undermine relationships and should not be used with your allies (family and friends).
But parenting involves lying also, which can be a model for the child. Sarcasm is a peculiar form of problematic adult lying. The adults say the opposite or an exaggeration of what they really mean, usually with a smirk or other nonverbal cue to their intent. This is confusing, if not infuriating, to immature children or those who do not understand this twisted communication. It is best to avoid sarcasm with children, or at least be sure to explain it so the children gain understanding over time.
Parents need to “lie” to their children to some extent to reassure and allow for development of confidence. What adult hasn’t said “It’s going to be all right” about a looming storm, car crash, or illness, when actually there is uncertainty. Children count on adults to keep them safe emotionally and physically from things they can’t yet handle. To move forward developmentally, children need adults to be brave leaders, even when the adults don’t feel confident. Some parents think their children must know the “truth” in every instance. Those children are often painfully anxious and overwhelmed.
There is plenty of time for more facts later when the child has the thinking and emotional power to handle the truth.
Dr. Howard is assistant professor of pediatrics at Johns Hopkins University, Baltimore, and creator of CHADIS (www.CHADIS.com). She had no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to MDedge News. E-mail her at pdnews@mdedge.com.
“Not my son!” your patient’s parent rants. “If he lies to me, he will regret it for a long time.” While your first reaction may be to agree that a child lying to a parent crosses a kind of moral line in the sand, lying is a far more nuanced part of parenting worth a deeper understanding.
In order to lie, a child has to develop cognitive and social understanding. Typically developing children look to see what is interesting to others, called “joint attention,” at around 12-18 months. Failure to do this is one of the early signs of autism reflecting atypical social understanding. At around 3.5 years, children may attempt to deceive if they have broken a rule. The study demonstrating this may sound a lot like home: Children are left alone with a tempting toy but told not to touch it. Although they do touch it while the adult is out of sight, they say rather sweetly (and eventually convincingly) that they did not, even though the toy was clearly moved! While boys generally have more behavior problems, girls and children with better verbal skills achieve deceit at an earlier age, some as young as 2 years. At this stage, children become aware that the adult can’t know exactly what they know. If the parent shows high emotion to what they consider a lie, this can be a topic for testing! Children with ADHD often lack the inhibition needed for early mastery of deception, and children with autism later or not at all. They don’t see the social point to lying nor can they fake a facial expression. They have a case of intractable honesty!
The inability to refrain from telling the truth can result in social rejection, for example when a child rats on a peer for a trivial misdeed in class. Even though he is speaking the truth and “following the (teacher’s) rules,” he did not see that the cost of breaking the (peer) social rules was more important. By age 6 years, children typically figure out that what another person thinks may not be true – their belief may be incorrect or a “false belief.” This understanding is called Theory of Mind, missing or delayed in autism. Only 40% of high-functioning children with autism passed false belief testing at ages 6- to 13-years-old, compared with 95% of typical age-matched peers (Physiol Behav. 2010 Jun 1;100[3]:268-76). The percentage of children on the spectrum understanding false beliefs more closely matched that of preschoolers (39%). At a later age and given extra time to think, some children with autism can do better at this kind of perspective taking, but many continue having difficulty understanding thoughts of others, especially social expectations or motivations (such as flirting, status seeking, and making an excuse) even as adults. This can impair social relationships even when desire to fit in and IQ are otherwise high.
On the other hand, ADHD is a common condition in which “lying” comes from saying the first thing that comes to mind even if the child knows otherwise. A wise parent of one of my patients with ADHD told me about her “30 second rule” where she would give her child that extra time and walk away briefly to “be sure that is what you wanted to say,” with praise rather than give a consequence for changing the story to the truth. This is an important concept we pediatricians need to know: Punishing lying in children tends to result in more, not less, lying and more sneakiness. Instead, parents need to be advised to recall the origins of the word discipline as being “to teach.”
When children lie there are four basic scenarios: They may not know the rules, they may know but have something they want more, they may be impulsive, or they may have developed an attitude of seeking to con the adults whom they feel are mean as a way to have some power in the relationship and get back at them. Clearly, we do not want to push children to this fourth resort by harsh reactions to lying. We have seen particular difficulty with harsh reactions to lying in parents from strong, rule-oriented careers such as police officers, military, and ministers. Asking “How would your parent have handled this?” often will reveal reasons for their tough but backfiring stance.
Lying can work to get what one wants and nearly all children try it. As with other new milestones, children practice this “skill,” much to parents’ dismay. Parents generally can tell if children are lying; they see it on their faces, hear the story from siblings, or see evidence of what happened. Lying provides an important opportunity for the adult to stop, take some breaths, touch the child, and empathize: “It is hard to admit a mistake. I know you did not mean to do it. But you are young, and I know that you are good and honest inside, and will get stronger and braver at telling the truth as you get older. Will you promise to try harder?” In some cases a consequence may be appropriate, for example if something was broken. Usually, simply empathizing and focusing on the expectation for improvement will increase the child’s desire to please the parents rather than get back at them. Actual rewards for honesty improve truth telling by 1.5 times if the reward is big enough.
But it is important to recognize that we all make split second tactical decisions about our actions based on how safe we feel in the situation and our knowledge of social rules and costs. Children over time need to learn that it is safe to tell the truth among family members and that they will not be harshly dealt with. It is a subtle task, but important to learn that deception is a tool that can be important used judiciously when required socially (I have a curfew) or in dangerous situations (I did not see the thug), but can undermine relationships and should not be used with your allies (family and friends).
But parenting involves lying also, which can be a model for the child. Sarcasm is a peculiar form of problematic adult lying. The adults say the opposite or an exaggeration of what they really mean, usually with a smirk or other nonverbal cue to their intent. This is confusing, if not infuriating, to immature children or those who do not understand this twisted communication. It is best to avoid sarcasm with children, or at least be sure to explain it so the children gain understanding over time.
Parents need to “lie” to their children to some extent to reassure and allow for development of confidence. What adult hasn’t said “It’s going to be all right” about a looming storm, car crash, or illness, when actually there is uncertainty. Children count on adults to keep them safe emotionally and physically from things they can’t yet handle. To move forward developmentally, children need adults to be brave leaders, even when the adults don’t feel confident. Some parents think their children must know the “truth” in every instance. Those children are often painfully anxious and overwhelmed.
There is plenty of time for more facts later when the child has the thinking and emotional power to handle the truth.
Dr. Howard is assistant professor of pediatrics at Johns Hopkins University, Baltimore, and creator of CHADIS (www.CHADIS.com). She had no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to MDedge News. E-mail her at pdnews@mdedge.com.
“Not my son!” your patient’s parent rants. “If he lies to me, he will regret it for a long time.” While your first reaction may be to agree that a child lying to a parent crosses a kind of moral line in the sand, lying is a far more nuanced part of parenting worth a deeper understanding.
In order to lie, a child has to develop cognitive and social understanding. Typically developing children look to see what is interesting to others, called “joint attention,” at around 12-18 months. Failure to do this is one of the early signs of autism reflecting atypical social understanding. At around 3.5 years, children may attempt to deceive if they have broken a rule. The study demonstrating this may sound a lot like home: Children are left alone with a tempting toy but told not to touch it. Although they do touch it while the adult is out of sight, they say rather sweetly (and eventually convincingly) that they did not, even though the toy was clearly moved! While boys generally have more behavior problems, girls and children with better verbal skills achieve deceit at an earlier age, some as young as 2 years. At this stage, children become aware that the adult can’t know exactly what they know. If the parent shows high emotion to what they consider a lie, this can be a topic for testing! Children with ADHD often lack the inhibition needed for early mastery of deception, and children with autism later or not at all. They don’t see the social point to lying nor can they fake a facial expression. They have a case of intractable honesty!
The inability to refrain from telling the truth can result in social rejection, for example when a child rats on a peer for a trivial misdeed in class. Even though he is speaking the truth and “following the (teacher’s) rules,” he did not see that the cost of breaking the (peer) social rules was more important. By age 6 years, children typically figure out that what another person thinks may not be true – their belief may be incorrect or a “false belief.” This understanding is called Theory of Mind, missing or delayed in autism. Only 40% of high-functioning children with autism passed false belief testing at ages 6- to 13-years-old, compared with 95% of typical age-matched peers (Physiol Behav. 2010 Jun 1;100[3]:268-76). The percentage of children on the spectrum understanding false beliefs more closely matched that of preschoolers (39%). At a later age and given extra time to think, some children with autism can do better at this kind of perspective taking, but many continue having difficulty understanding thoughts of others, especially social expectations or motivations (such as flirting, status seeking, and making an excuse) even as adults. This can impair social relationships even when desire to fit in and IQ are otherwise high.
On the other hand, ADHD is a common condition in which “lying” comes from saying the first thing that comes to mind even if the child knows otherwise. A wise parent of one of my patients with ADHD told me about her “30 second rule” where she would give her child that extra time and walk away briefly to “be sure that is what you wanted to say,” with praise rather than give a consequence for changing the story to the truth. This is an important concept we pediatricians need to know: Punishing lying in children tends to result in more, not less, lying and more sneakiness. Instead, parents need to be advised to recall the origins of the word discipline as being “to teach.”
When children lie there are four basic scenarios: They may not know the rules, they may know but have something they want more, they may be impulsive, or they may have developed an attitude of seeking to con the adults whom they feel are mean as a way to have some power in the relationship and get back at them. Clearly, we do not want to push children to this fourth resort by harsh reactions to lying. We have seen particular difficulty with harsh reactions to lying in parents from strong, rule-oriented careers such as police officers, military, and ministers. Asking “How would your parent have handled this?” often will reveal reasons for their tough but backfiring stance.
Lying can work to get what one wants and nearly all children try it. As with other new milestones, children practice this “skill,” much to parents’ dismay. Parents generally can tell if children are lying; they see it on their faces, hear the story from siblings, or see evidence of what happened. Lying provides an important opportunity for the adult to stop, take some breaths, touch the child, and empathize: “It is hard to admit a mistake. I know you did not mean to do it. But you are young, and I know that you are good and honest inside, and will get stronger and braver at telling the truth as you get older. Will you promise to try harder?” In some cases a consequence may be appropriate, for example if something was broken. Usually, simply empathizing and focusing on the expectation for improvement will increase the child’s desire to please the parents rather than get back at them. Actual rewards for honesty improve truth telling by 1.5 times if the reward is big enough.
But it is important to recognize that we all make split second tactical decisions about our actions based on how safe we feel in the situation and our knowledge of social rules and costs. Children over time need to learn that it is safe to tell the truth among family members and that they will not be harshly dealt with. It is a subtle task, but important to learn that deception is a tool that can be important used judiciously when required socially (I have a curfew) or in dangerous situations (I did not see the thug), but can undermine relationships and should not be used with your allies (family and friends).
But parenting involves lying also, which can be a model for the child. Sarcasm is a peculiar form of problematic adult lying. The adults say the opposite or an exaggeration of what they really mean, usually with a smirk or other nonverbal cue to their intent. This is confusing, if not infuriating, to immature children or those who do not understand this twisted communication. It is best to avoid sarcasm with children, or at least be sure to explain it so the children gain understanding over time.
Parents need to “lie” to their children to some extent to reassure and allow for development of confidence. What adult hasn’t said “It’s going to be all right” about a looming storm, car crash, or illness, when actually there is uncertainty. Children count on adults to keep them safe emotionally and physically from things they can’t yet handle. To move forward developmentally, children need adults to be brave leaders, even when the adults don’t feel confident. Some parents think their children must know the “truth” in every instance. Those children are often painfully anxious and overwhelmed.
There is plenty of time for more facts later when the child has the thinking and emotional power to handle the truth.
Dr. Howard is assistant professor of pediatrics at Johns Hopkins University, Baltimore, and creator of CHADIS (www.CHADIS.com). She had no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to MDedge News. E-mail her at pdnews@mdedge.com.
‘Momentous’ USMLE change: New pass/fail format stuns medicine
News that the United States Medical Licensing Examination (USMLE) program will change its Step 1 scoring from a 3-digit number to pass/fail starting Jan. 1, 2022, has set off a flurry of shocked responses from students and physicians.
J. Bryan Carmody, MD, MPH, an assistant professor at Eastern Virginia Medical School in Norfolk, said in an interview that he was “stunned” when he heard the news on Wednesday and said the switch presents “the single biggest opportunity for medical school education reform since the Flexner Report,” which in 1910 established standards for modern medical education.
Numbers will continue for some tests
The USMLE cosponsors – the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME) – said that the Step 2 Clinical Knowledge (CK) exam and Step 3 will continue to be scored numerically. Step 2 Clinical Skills (CS) will continue its pass/fail system.
The change was made after Step 1 had been roundly criticized as playing too big a role in the process of becoming a physician and for causing students to study for the test instead of engaging fully in their medical education.
Ramie Fathy, a third-year medical student at the University of Pennsylvania, Philadelphia, currently studying for Step 1, said in an interview that it would have been nice personally to have the pass/fail choice, but he predicts both good and unintended consequences in the change.
The positive news, Mr. Fathy said, is that less emphasis will be put on the Step 1 test, which includes memorizing basic science details that may or not be relevant depending on later specialty choice.
“It’s not necessarily measuring what the test makers intended, which was whether or not a student can understand and apply basic science concepts to the practice of medicine,” he said.
“The current system encourages students to get as high a score as possible, which – after a certain point – translates to memorizing many little details that become increasingly less practically relevant,” Mr. Fathy said.
Pressure may move elsewhere?
However, Mr. Fathy worries that, without a scoring system to help decide who stands out in Step 1, residency program directors will depend more on the reputation of candidates’ medical school and the clout of the person writing a letter of recommendation – factors that are often influenced by family resources and social standing. That could wedge a further economic divide into the path to becoming a physician.
Mr. Fathy said he and fellow students are watching for information on what the passing bar will be and what happens with Step 2 Clinical Knowledge exam. USMLE has promised more information as soon as it is available.
“The question is whether that test will replace Step 1 as the standardized metric of student competency,” Mr. Fathy said, which would put more pressure on students further down the medical path.
Will Step 2 anxiety increase?
Dr. Carmody agreed that there is the danger that students now will spend their time studying for Step 2 CK at the expense of other parts of their education.
Meaningful reform will depend on the pass/fail move being coupled with other reforms, most importantly application caps, said Dr. Carmody, who teaches preclinical medical students and works with the residency program.
He has been blogging about Step 1 pass/fail for the past year.
Currently students can apply for as many residencies as they can pay for and Carmody said the number of applications per student has been rising over the past decade.
“That puts program directors under an impossible burden,” he said. “With our Step 1-based system, there’s significant inequality in the number of interviews people get. Programs end up overinviting the same group of people who look good on paper.”
People outside that group respond by sending more applications than they need to just to get a few interviews, Dr. Carmody added.
With caps, students would have an incentive to apply to only those programs in which they had a sincere interest, he said. Program directors also would then be better able to evaluate each application.
Switching Step 1 to pass/fail may have some effect on medical school burnout, Dr. Carmody said.
“It’s one thing to work hard when you’re on call and your patients depend on it,” he said. “But I would have a hard time staying up late every night studying something that I know in my heart is not going to help my patients, but I have to do it because I have to do better than the person who’s studying in the apartment next to me.”
Test has strayed from original purpose
Joseph Safdieh, MD, an assistant dean for clinical curriculum and director of the medical student neurology clerkship for the Weill Cornell Medicine, New York, sees the move as positive overall.
“We should not be using any single metric to define or describe our students’ overall profile,” he said in an interview.
“This has been a very significant anxiety point for our medical students for quite a number of years,” Dr. Safdieh said. “They were frustrated that their entire 4 years of medical school seemingly came down to one number.”
The test was created originally as one of three parts of licensure, he pointed out.
“Over the past 10 or 15 years, the exam has morphed to become a litmus test for very specific residency programs,” he said.
However, Dr. Safdieh has concerns that Step 2 will cultivate the same anxiety and may get too big a spotlight without the Step 1 metric, “although one could argue that test does more accurately reflect clinical material,” he said.
He also worries that students who have selected a specialty by the time they take Step 2 may find late in the game that they are less competitive in their field than they thought they were and may have to make a last-minute switch.
Dr. Safdieh said he thinks Step 2 will be next to go the pass/fail route. In reading between the lines of the announcement, he believes the test cosponsors didn’t make both pass/fail at once because it would have been “a nuclear bomb to the system.”
He credited the cosponsors with making what he called a “bold and momentous decision to initiate radical change in the overall transition between undergraduate and graduate medical education.”
Dr. Safdieh added that few in medicine were expecting Wednesday’s announcement.
“I think many of us were expecting them to go to quartile grading, not to go this far,” he said.
Dr. Safdieh suggested that, among those who may see downstream effects from the pass/fail move are offshore schools, such as those in the Caribbean. “Those schools rely on Step 1 to demonstrate that their students are meeting the rigor,” he said. But he hopes that this will lead to more holistic review.
“We’re hoping that this will force change in the system so that residency directors will look at more than just test-taking ability. They’ll look at publications and scholarship, community service and advocacy and performance in medical school,” Dr. Safdieh said.
Alison J. Whelan, MD, chief medical education officer of the Association of American Medical Colleges said in a statement, “The transition from medical school to residency training is a matter of great concern throughout academic medicine.
“The decision by the NBME and FSMB to change USMLE Step 1 score reporting to pass/fail was very carefully considered to balance student learning and student well-being,” she said. “The medical education community must now work together to identify and implement additional changes to improve the overall UME-GME [undergraduate and graduate medical education] transition system for all stakeholders and the AAMC is committed to helping lead this work.”
Dr. Fathy, Dr. Carmody, and Dr. Safdieh have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
News that the United States Medical Licensing Examination (USMLE) program will change its Step 1 scoring from a 3-digit number to pass/fail starting Jan. 1, 2022, has set off a flurry of shocked responses from students and physicians.
J. Bryan Carmody, MD, MPH, an assistant professor at Eastern Virginia Medical School in Norfolk, said in an interview that he was “stunned” when he heard the news on Wednesday and said the switch presents “the single biggest opportunity for medical school education reform since the Flexner Report,” which in 1910 established standards for modern medical education.
Numbers will continue for some tests
The USMLE cosponsors – the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME) – said that the Step 2 Clinical Knowledge (CK) exam and Step 3 will continue to be scored numerically. Step 2 Clinical Skills (CS) will continue its pass/fail system.
The change was made after Step 1 had been roundly criticized as playing too big a role in the process of becoming a physician and for causing students to study for the test instead of engaging fully in their medical education.
Ramie Fathy, a third-year medical student at the University of Pennsylvania, Philadelphia, currently studying for Step 1, said in an interview that it would have been nice personally to have the pass/fail choice, but he predicts both good and unintended consequences in the change.
The positive news, Mr. Fathy said, is that less emphasis will be put on the Step 1 test, which includes memorizing basic science details that may or not be relevant depending on later specialty choice.
“It’s not necessarily measuring what the test makers intended, which was whether or not a student can understand and apply basic science concepts to the practice of medicine,” he said.
“The current system encourages students to get as high a score as possible, which – after a certain point – translates to memorizing many little details that become increasingly less practically relevant,” Mr. Fathy said.
Pressure may move elsewhere?
However, Mr. Fathy worries that, without a scoring system to help decide who stands out in Step 1, residency program directors will depend more on the reputation of candidates’ medical school and the clout of the person writing a letter of recommendation – factors that are often influenced by family resources and social standing. That could wedge a further economic divide into the path to becoming a physician.
Mr. Fathy said he and fellow students are watching for information on what the passing bar will be and what happens with Step 2 Clinical Knowledge exam. USMLE has promised more information as soon as it is available.
“The question is whether that test will replace Step 1 as the standardized metric of student competency,” Mr. Fathy said, which would put more pressure on students further down the medical path.
Will Step 2 anxiety increase?
Dr. Carmody agreed that there is the danger that students now will spend their time studying for Step 2 CK at the expense of other parts of their education.
Meaningful reform will depend on the pass/fail move being coupled with other reforms, most importantly application caps, said Dr. Carmody, who teaches preclinical medical students and works with the residency program.
He has been blogging about Step 1 pass/fail for the past year.
Currently students can apply for as many residencies as they can pay for and Carmody said the number of applications per student has been rising over the past decade.
“That puts program directors under an impossible burden,” he said. “With our Step 1-based system, there’s significant inequality in the number of interviews people get. Programs end up overinviting the same group of people who look good on paper.”
People outside that group respond by sending more applications than they need to just to get a few interviews, Dr. Carmody added.
With caps, students would have an incentive to apply to only those programs in which they had a sincere interest, he said. Program directors also would then be better able to evaluate each application.
Switching Step 1 to pass/fail may have some effect on medical school burnout, Dr. Carmody said.
“It’s one thing to work hard when you’re on call and your patients depend on it,” he said. “But I would have a hard time staying up late every night studying something that I know in my heart is not going to help my patients, but I have to do it because I have to do better than the person who’s studying in the apartment next to me.”
Test has strayed from original purpose
Joseph Safdieh, MD, an assistant dean for clinical curriculum and director of the medical student neurology clerkship for the Weill Cornell Medicine, New York, sees the move as positive overall.
“We should not be using any single metric to define or describe our students’ overall profile,” he said in an interview.
“This has been a very significant anxiety point for our medical students for quite a number of years,” Dr. Safdieh said. “They were frustrated that their entire 4 years of medical school seemingly came down to one number.”
The test was created originally as one of three parts of licensure, he pointed out.
“Over the past 10 or 15 years, the exam has morphed to become a litmus test for very specific residency programs,” he said.
However, Dr. Safdieh has concerns that Step 2 will cultivate the same anxiety and may get too big a spotlight without the Step 1 metric, “although one could argue that test does more accurately reflect clinical material,” he said.
He also worries that students who have selected a specialty by the time they take Step 2 may find late in the game that they are less competitive in their field than they thought they were and may have to make a last-minute switch.
Dr. Safdieh said he thinks Step 2 will be next to go the pass/fail route. In reading between the lines of the announcement, he believes the test cosponsors didn’t make both pass/fail at once because it would have been “a nuclear bomb to the system.”
He credited the cosponsors with making what he called a “bold and momentous decision to initiate radical change in the overall transition between undergraduate and graduate medical education.”
Dr. Safdieh added that few in medicine were expecting Wednesday’s announcement.
“I think many of us were expecting them to go to quartile grading, not to go this far,” he said.
Dr. Safdieh suggested that, among those who may see downstream effects from the pass/fail move are offshore schools, such as those in the Caribbean. “Those schools rely on Step 1 to demonstrate that their students are meeting the rigor,” he said. But he hopes that this will lead to more holistic review.
“We’re hoping that this will force change in the system so that residency directors will look at more than just test-taking ability. They’ll look at publications and scholarship, community service and advocacy and performance in medical school,” Dr. Safdieh said.
Alison J. Whelan, MD, chief medical education officer of the Association of American Medical Colleges said in a statement, “The transition from medical school to residency training is a matter of great concern throughout academic medicine.
“The decision by the NBME and FSMB to change USMLE Step 1 score reporting to pass/fail was very carefully considered to balance student learning and student well-being,” she said. “The medical education community must now work together to identify and implement additional changes to improve the overall UME-GME [undergraduate and graduate medical education] transition system for all stakeholders and the AAMC is committed to helping lead this work.”
Dr. Fathy, Dr. Carmody, and Dr. Safdieh have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
News that the United States Medical Licensing Examination (USMLE) program will change its Step 1 scoring from a 3-digit number to pass/fail starting Jan. 1, 2022, has set off a flurry of shocked responses from students and physicians.
J. Bryan Carmody, MD, MPH, an assistant professor at Eastern Virginia Medical School in Norfolk, said in an interview that he was “stunned” when he heard the news on Wednesday and said the switch presents “the single biggest opportunity for medical school education reform since the Flexner Report,” which in 1910 established standards for modern medical education.
Numbers will continue for some tests
The USMLE cosponsors – the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME) – said that the Step 2 Clinical Knowledge (CK) exam and Step 3 will continue to be scored numerically. Step 2 Clinical Skills (CS) will continue its pass/fail system.
The change was made after Step 1 had been roundly criticized as playing too big a role in the process of becoming a physician and for causing students to study for the test instead of engaging fully in their medical education.
Ramie Fathy, a third-year medical student at the University of Pennsylvania, Philadelphia, currently studying for Step 1, said in an interview that it would have been nice personally to have the pass/fail choice, but he predicts both good and unintended consequences in the change.
The positive news, Mr. Fathy said, is that less emphasis will be put on the Step 1 test, which includes memorizing basic science details that may or not be relevant depending on later specialty choice.
“It’s not necessarily measuring what the test makers intended, which was whether or not a student can understand and apply basic science concepts to the practice of medicine,” he said.
“The current system encourages students to get as high a score as possible, which – after a certain point – translates to memorizing many little details that become increasingly less practically relevant,” Mr. Fathy said.
Pressure may move elsewhere?
However, Mr. Fathy worries that, without a scoring system to help decide who stands out in Step 1, residency program directors will depend more on the reputation of candidates’ medical school and the clout of the person writing a letter of recommendation – factors that are often influenced by family resources and social standing. That could wedge a further economic divide into the path to becoming a physician.
Mr. Fathy said he and fellow students are watching for information on what the passing bar will be and what happens with Step 2 Clinical Knowledge exam. USMLE has promised more information as soon as it is available.
“The question is whether that test will replace Step 1 as the standardized metric of student competency,” Mr. Fathy said, which would put more pressure on students further down the medical path.
Will Step 2 anxiety increase?
Dr. Carmody agreed that there is the danger that students now will spend their time studying for Step 2 CK at the expense of other parts of their education.
Meaningful reform will depend on the pass/fail move being coupled with other reforms, most importantly application caps, said Dr. Carmody, who teaches preclinical medical students and works with the residency program.
He has been blogging about Step 1 pass/fail for the past year.
Currently students can apply for as many residencies as they can pay for and Carmody said the number of applications per student has been rising over the past decade.
“That puts program directors under an impossible burden,” he said. “With our Step 1-based system, there’s significant inequality in the number of interviews people get. Programs end up overinviting the same group of people who look good on paper.”
People outside that group respond by sending more applications than they need to just to get a few interviews, Dr. Carmody added.
With caps, students would have an incentive to apply to only those programs in which they had a sincere interest, he said. Program directors also would then be better able to evaluate each application.
Switching Step 1 to pass/fail may have some effect on medical school burnout, Dr. Carmody said.
“It’s one thing to work hard when you’re on call and your patients depend on it,” he said. “But I would have a hard time staying up late every night studying something that I know in my heart is not going to help my patients, but I have to do it because I have to do better than the person who’s studying in the apartment next to me.”
Test has strayed from original purpose
Joseph Safdieh, MD, an assistant dean for clinical curriculum and director of the medical student neurology clerkship for the Weill Cornell Medicine, New York, sees the move as positive overall.
“We should not be using any single metric to define or describe our students’ overall profile,” he said in an interview.
“This has been a very significant anxiety point for our medical students for quite a number of years,” Dr. Safdieh said. “They were frustrated that their entire 4 years of medical school seemingly came down to one number.”
The test was created originally as one of three parts of licensure, he pointed out.
“Over the past 10 or 15 years, the exam has morphed to become a litmus test for very specific residency programs,” he said.
However, Dr. Safdieh has concerns that Step 2 will cultivate the same anxiety and may get too big a spotlight without the Step 1 metric, “although one could argue that test does more accurately reflect clinical material,” he said.
He also worries that students who have selected a specialty by the time they take Step 2 may find late in the game that they are less competitive in their field than they thought they were and may have to make a last-minute switch.
Dr. Safdieh said he thinks Step 2 will be next to go the pass/fail route. In reading between the lines of the announcement, he believes the test cosponsors didn’t make both pass/fail at once because it would have been “a nuclear bomb to the system.”
He credited the cosponsors with making what he called a “bold and momentous decision to initiate radical change in the overall transition between undergraduate and graduate medical education.”
Dr. Safdieh added that few in medicine were expecting Wednesday’s announcement.
“I think many of us were expecting them to go to quartile grading, not to go this far,” he said.
Dr. Safdieh suggested that, among those who may see downstream effects from the pass/fail move are offshore schools, such as those in the Caribbean. “Those schools rely on Step 1 to demonstrate that their students are meeting the rigor,” he said. But he hopes that this will lead to more holistic review.
“We’re hoping that this will force change in the system so that residency directors will look at more than just test-taking ability. They’ll look at publications and scholarship, community service and advocacy and performance in medical school,” Dr. Safdieh said.
Alison J. Whelan, MD, chief medical education officer of the Association of American Medical Colleges said in a statement, “The transition from medical school to residency training is a matter of great concern throughout academic medicine.
“The decision by the NBME and FSMB to change USMLE Step 1 score reporting to pass/fail was very carefully considered to balance student learning and student well-being,” she said. “The medical education community must now work together to identify and implement additional changes to improve the overall UME-GME [undergraduate and graduate medical education] transition system for all stakeholders and the AAMC is committed to helping lead this work.”
Dr. Fathy, Dr. Carmody, and Dr. Safdieh have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
Critical care admissions up for pediatric opioid poisonings
ORLANDO – The proportion of children and adolescents admitted to critical care for serious poisonings has increased in recent years, according to authors of a study of more than 750,000 reported opioid exposures.
Critical care units were involved in 10% of pediatric opioid poisoning cases registered in 2015-2018, up from 7% in 2005-2009, reported Megan E. Land, MD, of Emory University, Atlanta, and coinvestigators.
Attempted suicide has represented an increasingly large proportion of pediatric opioid poisonings from 2005 to 2018, according to the researchers, based on retrospective analysis of cases reported to U.S. poison centers.
Mortality related to these pediatric poisonings increased over time, and among children and adolescents admitted to a pediatric ICU, CPR and naloxone use also increased over time, Dr. Land and associates noted.
These said Dr. Land, who presented the findings at the Critical Care Congress sponsored by the Society of Critical Care Medicine.
“I think that this really requires a two-pronged approach,” she explained. “One is that we need to increase mental health resources for kids to address adolescent suicidality, and secondly, we need to decrease access to opioids in the hands of pediatric patients by decreasing prescribing and then also getting those that are unused out of the homes.”
Jeffrey Zimmerman, MD, past president of SCCM, said these findings on pediatric opioid poisonings represent the “iceberg tip” of a much larger societal issue that has impacts well beyond critical care.
“I think acutely, we’re well equipped to deal with the situation in terms of interventions,” Dr. Zimmerman said in an interview. “The bigger issue is dealing with what happens afterward, when the patient leaves the ICU in the hospital.”
When the issue is chronic opioid use among adolescents or children, critical care specialists can help by initiating opioid tapering in the hospital setting, rather than allowing the complete weaning process to play out at home, he said.
All clinicians can help prevent future injury by asking questions of the child and family to ensure that any opiates and other prescription medications at home are locked up, he added.
“These aren’t very glamorous things, but they’re common sense, and there’s more need for this common sense now than there ever has been,” Dr. Zimmerman concluded.
The study by Dr. Land and colleagues included data on primary opioid ingestions registered at 55 poison control centers in the United States. They assessed trends over three time periods: 2005-2009, 2010-2014, and 2015-2018.
They found that children under 19 years of age accounted for 28% of the 753,592 opioid poisonings reported over that time period.
The overall number of reported opioid poisonings among children declined somewhat since about 2010. However, the proportion admitted to a critical care unit increased from 7% in the 2005-2009 period to 10% in the 2015-2018 period, said Dr. Land, who added that the probability of a moderate or major effect increased by 0.55% and 0.11% per year, respectively, over the 14 years studied.
Mortality – 0.21% overall – increased from 0.18% in the earliest era to 0.28% in the most recent era, according to the investigators.
Suicidal intent increased from 14% in the earliest era to 21% in the most recent era, and was linked to near tenfold odds of undergoing a pediatric ICU procedure, Dr. Land and colleagues reported.
Among those children admitted to a pediatric ICU, use of CPR increased from 1% to 3% in the earliest and latest time periods, respectively; likewise, naloxone administration increased from 42% to 51% over those two time periods. By contrast, there was no change in use of mechanical ventilation (12%) or vasopressors (3%) over time, they added.
The opioids most commonly linked to pediatric ICU procedures were fentanyl (odds ratio, 12), heroin (OR, 11), and methadone (OR, 15).
Some funding for the study came from the Georgia Poison Center. Dr. Land had no disclosures relevant to the research.
SOURCE: Land M et al. Crit Care Med. 2020 doi: 10.1097/01.ccm.0000618708.38414.ea.
ORLANDO – The proportion of children and adolescents admitted to critical care for serious poisonings has increased in recent years, according to authors of a study of more than 750,000 reported opioid exposures.
Critical care units were involved in 10% of pediatric opioid poisoning cases registered in 2015-2018, up from 7% in 2005-2009, reported Megan E. Land, MD, of Emory University, Atlanta, and coinvestigators.
Attempted suicide has represented an increasingly large proportion of pediatric opioid poisonings from 2005 to 2018, according to the researchers, based on retrospective analysis of cases reported to U.S. poison centers.
Mortality related to these pediatric poisonings increased over time, and among children and adolescents admitted to a pediatric ICU, CPR and naloxone use also increased over time, Dr. Land and associates noted.
These said Dr. Land, who presented the findings at the Critical Care Congress sponsored by the Society of Critical Care Medicine.
“I think that this really requires a two-pronged approach,” she explained. “One is that we need to increase mental health resources for kids to address adolescent suicidality, and secondly, we need to decrease access to opioids in the hands of pediatric patients by decreasing prescribing and then also getting those that are unused out of the homes.”
Jeffrey Zimmerman, MD, past president of SCCM, said these findings on pediatric opioid poisonings represent the “iceberg tip” of a much larger societal issue that has impacts well beyond critical care.
“I think acutely, we’re well equipped to deal with the situation in terms of interventions,” Dr. Zimmerman said in an interview. “The bigger issue is dealing with what happens afterward, when the patient leaves the ICU in the hospital.”
When the issue is chronic opioid use among adolescents or children, critical care specialists can help by initiating opioid tapering in the hospital setting, rather than allowing the complete weaning process to play out at home, he said.
All clinicians can help prevent future injury by asking questions of the child and family to ensure that any opiates and other prescription medications at home are locked up, he added.
“These aren’t very glamorous things, but they’re common sense, and there’s more need for this common sense now than there ever has been,” Dr. Zimmerman concluded.
The study by Dr. Land and colleagues included data on primary opioid ingestions registered at 55 poison control centers in the United States. They assessed trends over three time periods: 2005-2009, 2010-2014, and 2015-2018.
They found that children under 19 years of age accounted for 28% of the 753,592 opioid poisonings reported over that time period.
The overall number of reported opioid poisonings among children declined somewhat since about 2010. However, the proportion admitted to a critical care unit increased from 7% in the 2005-2009 period to 10% in the 2015-2018 period, said Dr. Land, who added that the probability of a moderate or major effect increased by 0.55% and 0.11% per year, respectively, over the 14 years studied.
Mortality – 0.21% overall – increased from 0.18% in the earliest era to 0.28% in the most recent era, according to the investigators.
Suicidal intent increased from 14% in the earliest era to 21% in the most recent era, and was linked to near tenfold odds of undergoing a pediatric ICU procedure, Dr. Land and colleagues reported.
Among those children admitted to a pediatric ICU, use of CPR increased from 1% to 3% in the earliest and latest time periods, respectively; likewise, naloxone administration increased from 42% to 51% over those two time periods. By contrast, there was no change in use of mechanical ventilation (12%) or vasopressors (3%) over time, they added.
The opioids most commonly linked to pediatric ICU procedures were fentanyl (odds ratio, 12), heroin (OR, 11), and methadone (OR, 15).
Some funding for the study came from the Georgia Poison Center. Dr. Land had no disclosures relevant to the research.
SOURCE: Land M et al. Crit Care Med. 2020 doi: 10.1097/01.ccm.0000618708.38414.ea.
ORLANDO – The proportion of children and adolescents admitted to critical care for serious poisonings has increased in recent years, according to authors of a study of more than 750,000 reported opioid exposures.
Critical care units were involved in 10% of pediatric opioid poisoning cases registered in 2015-2018, up from 7% in 2005-2009, reported Megan E. Land, MD, of Emory University, Atlanta, and coinvestigators.
Attempted suicide has represented an increasingly large proportion of pediatric opioid poisonings from 2005 to 2018, according to the researchers, based on retrospective analysis of cases reported to U.S. poison centers.
Mortality related to these pediatric poisonings increased over time, and among children and adolescents admitted to a pediatric ICU, CPR and naloxone use also increased over time, Dr. Land and associates noted.
These said Dr. Land, who presented the findings at the Critical Care Congress sponsored by the Society of Critical Care Medicine.
“I think that this really requires a two-pronged approach,” she explained. “One is that we need to increase mental health resources for kids to address adolescent suicidality, and secondly, we need to decrease access to opioids in the hands of pediatric patients by decreasing prescribing and then also getting those that are unused out of the homes.”
Jeffrey Zimmerman, MD, past president of SCCM, said these findings on pediatric opioid poisonings represent the “iceberg tip” of a much larger societal issue that has impacts well beyond critical care.
“I think acutely, we’re well equipped to deal with the situation in terms of interventions,” Dr. Zimmerman said in an interview. “The bigger issue is dealing with what happens afterward, when the patient leaves the ICU in the hospital.”
When the issue is chronic opioid use among adolescents or children, critical care specialists can help by initiating opioid tapering in the hospital setting, rather than allowing the complete weaning process to play out at home, he said.
All clinicians can help prevent future injury by asking questions of the child and family to ensure that any opiates and other prescription medications at home are locked up, he added.
“These aren’t very glamorous things, but they’re common sense, and there’s more need for this common sense now than there ever has been,” Dr. Zimmerman concluded.
The study by Dr. Land and colleagues included data on primary opioid ingestions registered at 55 poison control centers in the United States. They assessed trends over three time periods: 2005-2009, 2010-2014, and 2015-2018.
They found that children under 19 years of age accounted for 28% of the 753,592 opioid poisonings reported over that time period.
The overall number of reported opioid poisonings among children declined somewhat since about 2010. However, the proportion admitted to a critical care unit increased from 7% in the 2005-2009 period to 10% in the 2015-2018 period, said Dr. Land, who added that the probability of a moderate or major effect increased by 0.55% and 0.11% per year, respectively, over the 14 years studied.
Mortality – 0.21% overall – increased from 0.18% in the earliest era to 0.28% in the most recent era, according to the investigators.
Suicidal intent increased from 14% in the earliest era to 21% in the most recent era, and was linked to near tenfold odds of undergoing a pediatric ICU procedure, Dr. Land and colleagues reported.
Among those children admitted to a pediatric ICU, use of CPR increased from 1% to 3% in the earliest and latest time periods, respectively; likewise, naloxone administration increased from 42% to 51% over those two time periods. By contrast, there was no change in use of mechanical ventilation (12%) or vasopressors (3%) over time, they added.
The opioids most commonly linked to pediatric ICU procedures were fentanyl (odds ratio, 12), heroin (OR, 11), and methadone (OR, 15).
Some funding for the study came from the Georgia Poison Center. Dr. Land had no disclosures relevant to the research.
SOURCE: Land M et al. Crit Care Med. 2020 doi: 10.1097/01.ccm.0000618708.38414.ea.
REPORTING FROM CCC49
Brain imaging offers new insight into persistent antisocial behavior
Individuals who exhibit antisocial behavior over a lifetime have a thinner cortex and smaller surface area in key brain regions relative to their counterparts who do not engage in antisocial behavior, new research shows.
However, investigators found no widespread structural brain abnormalities in the group of individuals who exhibited antisocial behavior only during adolescence.
These brain differences seem to be “quite specific and unique” to individuals who exhibit persistent antisocial behavior over their life, lead researcher Christina O. Carlisi, PhD, of University College London, said during a press briefing.
“Critically, the findings don’t directly link brain structure abnormalities to antisocial behavior,” she said. Nor do they mean that anyone with a smaller brain or brain area is destined to be antisocial or to commit a crime.
“Our findings support the idea that, for the small proportion of individuals with life-course–persistent antisocial behavior, there may be differences in their brain structure that make it difficult for them to develop social skills that prevent them from engaging in antisocial behavior,” Dr. Carlisi said in a news release. “These people could benefit from more support throughout their lives.”
It was published online Feb. 17 in the Lancet Psychiatry (doi: 10.1016/S2215-0366[20]30002-X).
Support for second chances
Speaking at the press briefing, coauthor Terrie E. Moffitt, PhD, of Duke University, Durham, N.C., said it’s well known that most young criminals are between the ages of 16 and 25.
Breaking the law is not at all rare in this age group, but not all of these young offenders are alike, she noted. Only a few become persistent repeat offenders.
“They start as a young child with aggressive conduct problems and eventually sink into a long-term lifestyle of repetitive serious crime that lasts well into adulthood, but this is a small group,” Dr. Moffitt explained. “In contrast, the larger majority of offenders will have only a short-term brush with lawbreaking and then grow up to become law-abiding members of society.”
The current study suggests that what makes short-term offenders behave differently from long-term offenders might involve some vulnerability at the level of the structure of the brain, Dr. Moffitt said.
The findings stem from 672 individuals in the Dunedin Multidisciplinary Health and Development Study, a population-representative, longitudinal birth cohort that assesses health and behavior.
On the basis of reports from parents, care givers, and teachers, as well as self-reports of conduct problems in persons aged 7-26 years, 80 participants (12%) had “life-course–persistent” antisocial behavior, 151 (23%) had adolescent-only antisocial behavior, and 441 (66%) had “low” antisocial behavior (control group, whose members never had a pervasive or persistent pattern of antisocial behavior).
Brain MRI obtained at age 45 years showed that, among individuals with persistent antisocial behavior, mean surface area was smaller (95% confidence interval, –0.24 to –0.11; P less than .0001) and mean cortical thickness was lower (95% CI, –0.19 to –0.02; P = .020) than was those of their peers in the control group.
For those in the life-course–persistent group, surface area was reduced in 282 of 360 anatomically defined brain parcels, and cortex was thinner in 11 of 360 parcels encompassing frontal and temporal regions (which were associated with executive function, emotion regulation, and motivation), compared with the control group.
Widespread differences in brain surface morphometry were not found in those who exhibited antisocial behavior during adolescence only. Such behavior was likely the result of their having to navigate through socially tough years.
“These findings underscore prior research that really highlights that there are different types of young offenders. They are not all the same; they should not all be treated the same,” coauthor Essi Viding, PhD, who also is affiliated with University College London, told reporters.
The findings support current strategies aimed at giving young offenders “a second chance” as opposed to enforcing harsher policies that prioritize incarceration for all young offenders, Dr. Viding added.
Important contribution
The authors of an accompanying commentary noted that, despite “remarkable progress in the past 3 decades, the etiology of antisocial behavior remains elusive” (Lancet Psychiatry. 2020 Feb 17. doi: 10.1016/S2215-0366[20]30035-3).
This study makes “an important contribution by identifying structural brain correlates of antisocial behavior that could be used to differentiate among individuals with life-course-persistent antisocial behavior, those with adolescence-limited antisocial behavior, and non-antisocial controls,” write Inti A. Brazil, PhD, of the Donders Institute for Brain, Cognition and Behavior, Radboud University, Nijmegen, the Netherlands, and Macià Buades-Rotger, PhD, of the Institute of Psychology II, University of Lübeck, Germany.
They noted that the findings might help to move the field closer to achieving the long-standing goal of incorporating neural data into assessment protocols for antisocial behavior.
The discovery of “meaningful morphologic differences between individuals with life-course–persistent and adolescence-limited antisocial behavior offers an important advance in the use of brain metrics for differentiating among individuals with antisocial dispositions.
“Importantly, however, it remains to be determined whether and how measuring the brain can be used to bridge the different taxometric views and theories on the etiology of antisocial behavior,” Dr. Brazil and Dr. Buades-Rotger concluded.
The study was funded by the U.S. National Institute on Aging; the Health Research Council of New Zealand; the New Zealand Ministry of Business, Innovation and Employment; the U.K. Medical Research Council; the Avielle Foundation; and the Wellcome Trust. The study authors and the authors of the commentary disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Individuals who exhibit antisocial behavior over a lifetime have a thinner cortex and smaller surface area in key brain regions relative to their counterparts who do not engage in antisocial behavior, new research shows.
However, investigators found no widespread structural brain abnormalities in the group of individuals who exhibited antisocial behavior only during adolescence.
These brain differences seem to be “quite specific and unique” to individuals who exhibit persistent antisocial behavior over their life, lead researcher Christina O. Carlisi, PhD, of University College London, said during a press briefing.
“Critically, the findings don’t directly link brain structure abnormalities to antisocial behavior,” she said. Nor do they mean that anyone with a smaller brain or brain area is destined to be antisocial or to commit a crime.
“Our findings support the idea that, for the small proportion of individuals with life-course–persistent antisocial behavior, there may be differences in their brain structure that make it difficult for them to develop social skills that prevent them from engaging in antisocial behavior,” Dr. Carlisi said in a news release. “These people could benefit from more support throughout their lives.”
It was published online Feb. 17 in the Lancet Psychiatry (doi: 10.1016/S2215-0366[20]30002-X).
Support for second chances
Speaking at the press briefing, coauthor Terrie E. Moffitt, PhD, of Duke University, Durham, N.C., said it’s well known that most young criminals are between the ages of 16 and 25.
Breaking the law is not at all rare in this age group, but not all of these young offenders are alike, she noted. Only a few become persistent repeat offenders.
“They start as a young child with aggressive conduct problems and eventually sink into a long-term lifestyle of repetitive serious crime that lasts well into adulthood, but this is a small group,” Dr. Moffitt explained. “In contrast, the larger majority of offenders will have only a short-term brush with lawbreaking and then grow up to become law-abiding members of society.”
The current study suggests that what makes short-term offenders behave differently from long-term offenders might involve some vulnerability at the level of the structure of the brain, Dr. Moffitt said.
The findings stem from 672 individuals in the Dunedin Multidisciplinary Health and Development Study, a population-representative, longitudinal birth cohort that assesses health and behavior.
On the basis of reports from parents, care givers, and teachers, as well as self-reports of conduct problems in persons aged 7-26 years, 80 participants (12%) had “life-course–persistent” antisocial behavior, 151 (23%) had adolescent-only antisocial behavior, and 441 (66%) had “low” antisocial behavior (control group, whose members never had a pervasive or persistent pattern of antisocial behavior).
Brain MRI obtained at age 45 years showed that, among individuals with persistent antisocial behavior, mean surface area was smaller (95% confidence interval, –0.24 to –0.11; P less than .0001) and mean cortical thickness was lower (95% CI, –0.19 to –0.02; P = .020) than was those of their peers in the control group.
For those in the life-course–persistent group, surface area was reduced in 282 of 360 anatomically defined brain parcels, and cortex was thinner in 11 of 360 parcels encompassing frontal and temporal regions (which were associated with executive function, emotion regulation, and motivation), compared with the control group.
Widespread differences in brain surface morphometry were not found in those who exhibited antisocial behavior during adolescence only. Such behavior was likely the result of their having to navigate through socially tough years.
“These findings underscore prior research that really highlights that there are different types of young offenders. They are not all the same; they should not all be treated the same,” coauthor Essi Viding, PhD, who also is affiliated with University College London, told reporters.
The findings support current strategies aimed at giving young offenders “a second chance” as opposed to enforcing harsher policies that prioritize incarceration for all young offenders, Dr. Viding added.
Important contribution
The authors of an accompanying commentary noted that, despite “remarkable progress in the past 3 decades, the etiology of antisocial behavior remains elusive” (Lancet Psychiatry. 2020 Feb 17. doi: 10.1016/S2215-0366[20]30035-3).
This study makes “an important contribution by identifying structural brain correlates of antisocial behavior that could be used to differentiate among individuals with life-course-persistent antisocial behavior, those with adolescence-limited antisocial behavior, and non-antisocial controls,” write Inti A. Brazil, PhD, of the Donders Institute for Brain, Cognition and Behavior, Radboud University, Nijmegen, the Netherlands, and Macià Buades-Rotger, PhD, of the Institute of Psychology II, University of Lübeck, Germany.
They noted that the findings might help to move the field closer to achieving the long-standing goal of incorporating neural data into assessment protocols for antisocial behavior.
The discovery of “meaningful morphologic differences between individuals with life-course–persistent and adolescence-limited antisocial behavior offers an important advance in the use of brain metrics for differentiating among individuals with antisocial dispositions.
“Importantly, however, it remains to be determined whether and how measuring the brain can be used to bridge the different taxometric views and theories on the etiology of antisocial behavior,” Dr. Brazil and Dr. Buades-Rotger concluded.
The study was funded by the U.S. National Institute on Aging; the Health Research Council of New Zealand; the New Zealand Ministry of Business, Innovation and Employment; the U.K. Medical Research Council; the Avielle Foundation; and the Wellcome Trust. The study authors and the authors of the commentary disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Individuals who exhibit antisocial behavior over a lifetime have a thinner cortex and smaller surface area in key brain regions relative to their counterparts who do not engage in antisocial behavior, new research shows.
However, investigators found no widespread structural brain abnormalities in the group of individuals who exhibited antisocial behavior only during adolescence.
These brain differences seem to be “quite specific and unique” to individuals who exhibit persistent antisocial behavior over their life, lead researcher Christina O. Carlisi, PhD, of University College London, said during a press briefing.
“Critically, the findings don’t directly link brain structure abnormalities to antisocial behavior,” she said. Nor do they mean that anyone with a smaller brain or brain area is destined to be antisocial or to commit a crime.
“Our findings support the idea that, for the small proportion of individuals with life-course–persistent antisocial behavior, there may be differences in their brain structure that make it difficult for them to develop social skills that prevent them from engaging in antisocial behavior,” Dr. Carlisi said in a news release. “These people could benefit from more support throughout their lives.”
It was published online Feb. 17 in the Lancet Psychiatry (doi: 10.1016/S2215-0366[20]30002-X).
Support for second chances
Speaking at the press briefing, coauthor Terrie E. Moffitt, PhD, of Duke University, Durham, N.C., said it’s well known that most young criminals are between the ages of 16 and 25.
Breaking the law is not at all rare in this age group, but not all of these young offenders are alike, she noted. Only a few become persistent repeat offenders.
“They start as a young child with aggressive conduct problems and eventually sink into a long-term lifestyle of repetitive serious crime that lasts well into adulthood, but this is a small group,” Dr. Moffitt explained. “In contrast, the larger majority of offenders will have only a short-term brush with lawbreaking and then grow up to become law-abiding members of society.”
The current study suggests that what makes short-term offenders behave differently from long-term offenders might involve some vulnerability at the level of the structure of the brain, Dr. Moffitt said.
The findings stem from 672 individuals in the Dunedin Multidisciplinary Health and Development Study, a population-representative, longitudinal birth cohort that assesses health and behavior.
On the basis of reports from parents, care givers, and teachers, as well as self-reports of conduct problems in persons aged 7-26 years, 80 participants (12%) had “life-course–persistent” antisocial behavior, 151 (23%) had adolescent-only antisocial behavior, and 441 (66%) had “low” antisocial behavior (control group, whose members never had a pervasive or persistent pattern of antisocial behavior).
Brain MRI obtained at age 45 years showed that, among individuals with persistent antisocial behavior, mean surface area was smaller (95% confidence interval, –0.24 to –0.11; P less than .0001) and mean cortical thickness was lower (95% CI, –0.19 to –0.02; P = .020) than was those of their peers in the control group.
For those in the life-course–persistent group, surface area was reduced in 282 of 360 anatomically defined brain parcels, and cortex was thinner in 11 of 360 parcels encompassing frontal and temporal regions (which were associated with executive function, emotion regulation, and motivation), compared with the control group.
Widespread differences in brain surface morphometry were not found in those who exhibited antisocial behavior during adolescence only. Such behavior was likely the result of their having to navigate through socially tough years.
“These findings underscore prior research that really highlights that there are different types of young offenders. They are not all the same; they should not all be treated the same,” coauthor Essi Viding, PhD, who also is affiliated with University College London, told reporters.
The findings support current strategies aimed at giving young offenders “a second chance” as opposed to enforcing harsher policies that prioritize incarceration for all young offenders, Dr. Viding added.
Important contribution
The authors of an accompanying commentary noted that, despite “remarkable progress in the past 3 decades, the etiology of antisocial behavior remains elusive” (Lancet Psychiatry. 2020 Feb 17. doi: 10.1016/S2215-0366[20]30035-3).
This study makes “an important contribution by identifying structural brain correlates of antisocial behavior that could be used to differentiate among individuals with life-course-persistent antisocial behavior, those with adolescence-limited antisocial behavior, and non-antisocial controls,” write Inti A. Brazil, PhD, of the Donders Institute for Brain, Cognition and Behavior, Radboud University, Nijmegen, the Netherlands, and Macià Buades-Rotger, PhD, of the Institute of Psychology II, University of Lübeck, Germany.
They noted that the findings might help to move the field closer to achieving the long-standing goal of incorporating neural data into assessment protocols for antisocial behavior.
The discovery of “meaningful morphologic differences between individuals with life-course–persistent and adolescence-limited antisocial behavior offers an important advance in the use of brain metrics for differentiating among individuals with antisocial dispositions.
“Importantly, however, it remains to be determined whether and how measuring the brain can be used to bridge the different taxometric views and theories on the etiology of antisocial behavior,” Dr. Brazil and Dr. Buades-Rotger concluded.
The study was funded by the U.S. National Institute on Aging; the Health Research Council of New Zealand; the New Zealand Ministry of Business, Innovation and Employment; the U.K. Medical Research Council; the Avielle Foundation; and the Wellcome Trust. The study authors and the authors of the commentary disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
My inspiration
Kobe Bryant knew me. Not personally, of course. I never received an autograph or shook his hand. But once in a while if I was up early enough, I’d run into Kobe at the gym in Newport Beach where he and I both worked out. As he did for all his fans at the gym, he’d make eye contact with me and nod hello. He was always focused on his workout – working with a trainer, never with headphones on. In person, he appeared enormous. Unlike most retired professional athletes, he still was in great shape. No doubt he could have suited up in purple and gold, and played against the Clippers that night if needed.
Being from New England, I never was a Laker fan. But I thought, if Kobe can head to the gym after midnight and take a 1,000 shots to prepare for a game, then I could set my alarm for 4 a.m. and take a few dozen more questions from my First Aid books. Head down, “Kryptonite” cranked on my iPod, I wasn’t going to let anyone in that test room outwork me. Neither did he. I put in the time and, like Kobe in the 2002 conference finals against Sacramento, I crushed it.*
When we moved to California, I followed Kobe and the Lakers until he retired. To be clear, I didn’t aspire to be like him, firstly because I’m slightly shorter than Michael Bloomberg, but also because although accomplished, Kobe made some poor choices at times. Indeed, it seems he might have been kinder and more considerate when he was at the top. But in his retirement he looked to be toiling to make reparations, refocusing his prodigious energy and talent for the benefit of others rather than for just for scoring 81 points. His Rolls Royce was there before mine at the gym, and I was there early. He was still getting up early and now preparing to be a great venture capitalist, podcaster, author, and father to his girls.
Watching him carry kettle bells across the floor one morning, I wondered, do people like Kobe Bryant look to others for inspiration? Or are they are born with an endless supply of it? For me, I seemed to push harder and faster when watching idols pass by. Whether it was Kobe or Clayton Christensen (author of “The Innovator’s Dilemma”), Joe Jorizzo, or Barack Obama, I found I could do just a bit more if I had them in mind.
On game days, Kobe spoke of arriving at the arena early, long before anyone. He would use the silent, solo time to reflect on what he needed to do perform that night. I tried this last week, arriving at our clinic early, before any patients or staff. I turned the lights on and took a few minutes to think about what we needed to accomplish that day. I previewed patients on my schedule, searched Up to Date for the latest recommendations on a difficult case. I didn’t know Kobe, but I felt like I did.
When I received the text that Kobe Bryant had died, I was actually working on this column. So I decided to change the topic to write about people who inspire me, ironically inspired by him again. May he rest in peace.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.
*This article was updated 2/19/2020.
Kobe Bryant knew me. Not personally, of course. I never received an autograph or shook his hand. But once in a while if I was up early enough, I’d run into Kobe at the gym in Newport Beach where he and I both worked out. As he did for all his fans at the gym, he’d make eye contact with me and nod hello. He was always focused on his workout – working with a trainer, never with headphones on. In person, he appeared enormous. Unlike most retired professional athletes, he still was in great shape. No doubt he could have suited up in purple and gold, and played against the Clippers that night if needed.
Being from New England, I never was a Laker fan. But I thought, if Kobe can head to the gym after midnight and take a 1,000 shots to prepare for a game, then I could set my alarm for 4 a.m. and take a few dozen more questions from my First Aid books. Head down, “Kryptonite” cranked on my iPod, I wasn’t going to let anyone in that test room outwork me. Neither did he. I put in the time and, like Kobe in the 2002 conference finals against Sacramento, I crushed it.*
When we moved to California, I followed Kobe and the Lakers until he retired. To be clear, I didn’t aspire to be like him, firstly because I’m slightly shorter than Michael Bloomberg, but also because although accomplished, Kobe made some poor choices at times. Indeed, it seems he might have been kinder and more considerate when he was at the top. But in his retirement he looked to be toiling to make reparations, refocusing his prodigious energy and talent for the benefit of others rather than for just for scoring 81 points. His Rolls Royce was there before mine at the gym, and I was there early. He was still getting up early and now preparing to be a great venture capitalist, podcaster, author, and father to his girls.
Watching him carry kettle bells across the floor one morning, I wondered, do people like Kobe Bryant look to others for inspiration? Or are they are born with an endless supply of it? For me, I seemed to push harder and faster when watching idols pass by. Whether it was Kobe or Clayton Christensen (author of “The Innovator’s Dilemma”), Joe Jorizzo, or Barack Obama, I found I could do just a bit more if I had them in mind.
On game days, Kobe spoke of arriving at the arena early, long before anyone. He would use the silent, solo time to reflect on what he needed to do perform that night. I tried this last week, arriving at our clinic early, before any patients or staff. I turned the lights on and took a few minutes to think about what we needed to accomplish that day. I previewed patients on my schedule, searched Up to Date for the latest recommendations on a difficult case. I didn’t know Kobe, but I felt like I did.
When I received the text that Kobe Bryant had died, I was actually working on this column. So I decided to change the topic to write about people who inspire me, ironically inspired by him again. May he rest in peace.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.
*This article was updated 2/19/2020.
Kobe Bryant knew me. Not personally, of course. I never received an autograph or shook his hand. But once in a while if I was up early enough, I’d run into Kobe at the gym in Newport Beach where he and I both worked out. As he did for all his fans at the gym, he’d make eye contact with me and nod hello. He was always focused on his workout – working with a trainer, never with headphones on. In person, he appeared enormous. Unlike most retired professional athletes, he still was in great shape. No doubt he could have suited up in purple and gold, and played against the Clippers that night if needed.
Being from New England, I never was a Laker fan. But I thought, if Kobe can head to the gym after midnight and take a 1,000 shots to prepare for a game, then I could set my alarm for 4 a.m. and take a few dozen more questions from my First Aid books. Head down, “Kryptonite” cranked on my iPod, I wasn’t going to let anyone in that test room outwork me. Neither did he. I put in the time and, like Kobe in the 2002 conference finals against Sacramento, I crushed it.*
When we moved to California, I followed Kobe and the Lakers until he retired. To be clear, I didn’t aspire to be like him, firstly because I’m slightly shorter than Michael Bloomberg, but also because although accomplished, Kobe made some poor choices at times. Indeed, it seems he might have been kinder and more considerate when he was at the top. But in his retirement he looked to be toiling to make reparations, refocusing his prodigious energy and talent for the benefit of others rather than for just for scoring 81 points. His Rolls Royce was there before mine at the gym, and I was there early. He was still getting up early and now preparing to be a great venture capitalist, podcaster, author, and father to his girls.
Watching him carry kettle bells across the floor one morning, I wondered, do people like Kobe Bryant look to others for inspiration? Or are they are born with an endless supply of it? For me, I seemed to push harder and faster when watching idols pass by. Whether it was Kobe or Clayton Christensen (author of “The Innovator’s Dilemma”), Joe Jorizzo, or Barack Obama, I found I could do just a bit more if I had them in mind.
On game days, Kobe spoke of arriving at the arena early, long before anyone. He would use the silent, solo time to reflect on what he needed to do perform that night. I tried this last week, arriving at our clinic early, before any patients or staff. I turned the lights on and took a few minutes to think about what we needed to accomplish that day. I previewed patients on my schedule, searched Up to Date for the latest recommendations on a difficult case. I didn’t know Kobe, but I felt like I did.
When I received the text that Kobe Bryant had died, I was actually working on this column. So I decided to change the topic to write about people who inspire me, ironically inspired by him again. May he rest in peace.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.
*This article was updated 2/19/2020.
Infection with 2019 novel coronavirus extends to infants
between Dec. 8, 2019, and Feb. 6, 2020, based on data from the Chinese central government and local health departments.
“As of February 6, 2020, China reported 31,211 confirmed cases of COVID-19 and 637 fatalities,” wrote Min Wei, MD, of Wuhan University, China, and colleagues. However, “few infections in children have been reported.”
In a research letter published in JAMA, the investigators reviewed data from nine infants aged 28 days to 1 year who were hospitalized with a diagnosis of COVID-19 between Dec. 8, 2019, and Feb. 6, 2020. The ages of the infants ranged from 1 month to 11 months, and seven were female. The patients included two children from Beijing, two from Hainan, and one each from the areas of Guangdong, Anhui, Shanghai, Zhejiang, and Guizhou.
All infected infants had at least one infected family member, and the infants’ infections occurred after the family members’ infections; seven infants lived in Wuhan or had family members who had visited Wuhan.
One of the infants had no symptoms but tested positive for the 2019 novel coronavirus, and two others had a diagnosis but missing information on any symptoms. Fever occurred in four patients, and mild upper respiratory tract symptoms occurred in two patients.
None of the infants died, and none reported severe complications or the need for intensive care or mechanical ventilation, the investigators said. The fact that most of the infants were female might suggest that they are more susceptible to the virus than males, although overall COVID-19 viral infections have been more common in adult men, especially those with chronic comorbidities, Dr. Wei and associates noted.
The study findings were limited by the small sample size and lack of symptom data for some patients, the researchers said. However, the results confirm that the COVID-19 virus is transmissible to infants younger than 1 year, and adult caregivers should exercise protective measures including wearing masks, washing hands before contact with infants, and routinely sterilizing toys and tableware, they emphasized.
The study was supported by the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The researchers had no financial conflicts to disclose.
SOURCE: Wei M et al. JAMA. 2020 Feb 14. doi:10.1001/jama.2020.2131.
between Dec. 8, 2019, and Feb. 6, 2020, based on data from the Chinese central government and local health departments.
“As of February 6, 2020, China reported 31,211 confirmed cases of COVID-19 and 637 fatalities,” wrote Min Wei, MD, of Wuhan University, China, and colleagues. However, “few infections in children have been reported.”
In a research letter published in JAMA, the investigators reviewed data from nine infants aged 28 days to 1 year who were hospitalized with a diagnosis of COVID-19 between Dec. 8, 2019, and Feb. 6, 2020. The ages of the infants ranged from 1 month to 11 months, and seven were female. The patients included two children from Beijing, two from Hainan, and one each from the areas of Guangdong, Anhui, Shanghai, Zhejiang, and Guizhou.
All infected infants had at least one infected family member, and the infants’ infections occurred after the family members’ infections; seven infants lived in Wuhan or had family members who had visited Wuhan.
One of the infants had no symptoms but tested positive for the 2019 novel coronavirus, and two others had a diagnosis but missing information on any symptoms. Fever occurred in four patients, and mild upper respiratory tract symptoms occurred in two patients.
None of the infants died, and none reported severe complications or the need for intensive care or mechanical ventilation, the investigators said. The fact that most of the infants were female might suggest that they are more susceptible to the virus than males, although overall COVID-19 viral infections have been more common in adult men, especially those with chronic comorbidities, Dr. Wei and associates noted.
The study findings were limited by the small sample size and lack of symptom data for some patients, the researchers said. However, the results confirm that the COVID-19 virus is transmissible to infants younger than 1 year, and adult caregivers should exercise protective measures including wearing masks, washing hands before contact with infants, and routinely sterilizing toys and tableware, they emphasized.
The study was supported by the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The researchers had no financial conflicts to disclose.
SOURCE: Wei M et al. JAMA. 2020 Feb 14. doi:10.1001/jama.2020.2131.
between Dec. 8, 2019, and Feb. 6, 2020, based on data from the Chinese central government and local health departments.
“As of February 6, 2020, China reported 31,211 confirmed cases of COVID-19 and 637 fatalities,” wrote Min Wei, MD, of Wuhan University, China, and colleagues. However, “few infections in children have been reported.”
In a research letter published in JAMA, the investigators reviewed data from nine infants aged 28 days to 1 year who were hospitalized with a diagnosis of COVID-19 between Dec. 8, 2019, and Feb. 6, 2020. The ages of the infants ranged from 1 month to 11 months, and seven were female. The patients included two children from Beijing, two from Hainan, and one each from the areas of Guangdong, Anhui, Shanghai, Zhejiang, and Guizhou.
All infected infants had at least one infected family member, and the infants’ infections occurred after the family members’ infections; seven infants lived in Wuhan or had family members who had visited Wuhan.
One of the infants had no symptoms but tested positive for the 2019 novel coronavirus, and two others had a diagnosis but missing information on any symptoms. Fever occurred in four patients, and mild upper respiratory tract symptoms occurred in two patients.
None of the infants died, and none reported severe complications or the need for intensive care or mechanical ventilation, the investigators said. The fact that most of the infants were female might suggest that they are more susceptible to the virus than males, although overall COVID-19 viral infections have been more common in adult men, especially those with chronic comorbidities, Dr. Wei and associates noted.
The study findings were limited by the small sample size and lack of symptom data for some patients, the researchers said. However, the results confirm that the COVID-19 virus is transmissible to infants younger than 1 year, and adult caregivers should exercise protective measures including wearing masks, washing hands before contact with infants, and routinely sterilizing toys and tableware, they emphasized.
The study was supported by the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The researchers had no financial conflicts to disclose.
SOURCE: Wei M et al. JAMA. 2020 Feb 14. doi:10.1001/jama.2020.2131.
FROM JAMA