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Clues to rosacea in patients of skin of color
NEW YORK – A middle-aged patient with Fitzpatrick type V skin comes to the office with a 10-year history of “breakouts” on her face. When asked about topical treatments, she reports that “everything burns or stings,” and says she just has very sensitive skin. What could this be?
Rosacea may often be missed in skin of color, said Dr. Alexis, speaking at the summer meeting of the American Academy of Dermatology. “It’s reportedly rare in darker skin types, especially in blacks,” and as a result, dermatologists and patients alike have a low index of suspicion for the diagnosis, he noted.
Also, rosacea looks different on darker skin than it does on lighter skin, which is featured in much of the dermatology teaching material. “In richly pigmented [Fitzpatrick] type VI skin, the erythema of rosacea can be masked,” said Dr. Alexis, chairman of the department of dermatology at Mount Sinai St. Luke’s and at Mount Sinai West, both in New York.
Dermatologists, in this case, may have to do some detective work: looking at the distribution of the lesions, thinking about trigger factors from the patient history, and noting the lack of comedones – although the patient has “pimples.” Patient complaints that they are sensitive to almost all topical products and experience stinging with “everything” is another very good clue that the patient may have rosacea.
Keep rosacea on the differential for this picture, advised Dr. Alexis. In skin of color, “rosacea may not be as rare as previously thought – less common, maybe – but not rare.”
Dr. Alexis reported financial relationships with multiple pharmaceutical companies.
[email protected]
On Twitter @karioakes
NEW YORK – A middle-aged patient with Fitzpatrick type V skin comes to the office with a 10-year history of “breakouts” on her face. When asked about topical treatments, she reports that “everything burns or stings,” and says she just has very sensitive skin. What could this be?
Rosacea may often be missed in skin of color, said Dr. Alexis, speaking at the summer meeting of the American Academy of Dermatology. “It’s reportedly rare in darker skin types, especially in blacks,” and as a result, dermatologists and patients alike have a low index of suspicion for the diagnosis, he noted.
Also, rosacea looks different on darker skin than it does on lighter skin, which is featured in much of the dermatology teaching material. “In richly pigmented [Fitzpatrick] type VI skin, the erythema of rosacea can be masked,” said Dr. Alexis, chairman of the department of dermatology at Mount Sinai St. Luke’s and at Mount Sinai West, both in New York.
Dermatologists, in this case, may have to do some detective work: looking at the distribution of the lesions, thinking about trigger factors from the patient history, and noting the lack of comedones – although the patient has “pimples.” Patient complaints that they are sensitive to almost all topical products and experience stinging with “everything” is another very good clue that the patient may have rosacea.
Keep rosacea on the differential for this picture, advised Dr. Alexis. In skin of color, “rosacea may not be as rare as previously thought – less common, maybe – but not rare.”
Dr. Alexis reported financial relationships with multiple pharmaceutical companies.
[email protected]
On Twitter @karioakes
NEW YORK – A middle-aged patient with Fitzpatrick type V skin comes to the office with a 10-year history of “breakouts” on her face. When asked about topical treatments, she reports that “everything burns or stings,” and says she just has very sensitive skin. What could this be?
Rosacea may often be missed in skin of color, said Dr. Alexis, speaking at the summer meeting of the American Academy of Dermatology. “It’s reportedly rare in darker skin types, especially in blacks,” and as a result, dermatologists and patients alike have a low index of suspicion for the diagnosis, he noted.
Also, rosacea looks different on darker skin than it does on lighter skin, which is featured in much of the dermatology teaching material. “In richly pigmented [Fitzpatrick] type VI skin, the erythema of rosacea can be masked,” said Dr. Alexis, chairman of the department of dermatology at Mount Sinai St. Luke’s and at Mount Sinai West, both in New York.
Dermatologists, in this case, may have to do some detective work: looking at the distribution of the lesions, thinking about trigger factors from the patient history, and noting the lack of comedones – although the patient has “pimples.” Patient complaints that they are sensitive to almost all topical products and experience stinging with “everything” is another very good clue that the patient may have rosacea.
Keep rosacea on the differential for this picture, advised Dr. Alexis. In skin of color, “rosacea may not be as rare as previously thought – less common, maybe – but not rare.”
Dr. Alexis reported financial relationships with multiple pharmaceutical companies.
[email protected]
On Twitter @karioakes
EXPERT ANALYSIS FROM THE 2017 AAD SUMMER MEETING
HPV vaccination rose after ACA implementation
Human papillomavirus vaccination in girls and women has increased significantly since the implementation of the Affordable Care Act (ACA), according an analysis of federal survey data.
Overall, girls and women were 3.3 times more likely to receive the vaccine (95% confidence interval, 2.0, 5.5; P less than .0001) in the post–ACA implementation period, compared with the pre-ACA period. They were 5.8 times more likely to receive all three doses of the vaccine (95% CI, 2.5-13.6; P = .0001) post ACA, compared with one dose during that period, according to Rosemary Corriero of the University of Georgia, Athens, who is also a fellow at the Centers for Disease Control and Prevention, and her coauthors (J Pediatr Adolesc Gynecol. 2017 Jul 26. doi: 10.1016/j.jpag.2017.07.002).
The cross-sectional analysis included four waves of data from 2007-2008, 2009-2010, 2011-2012, and 2013-2014 – two waves before the ACA and two waves after. The data comes from the National Health and Nutrition Examination Survey (NHANES) questionnaire. In the pre-ACA surveys, 2,452 teenage girls and women were included, compared with 2,147 in the post-ACA years. The majority of participants were white, and analysis was limited to those aged 9-33 years.
The increase in vaccination could be due to the ACA’s provision requiring coverage of preventive health services without patient cost sharing in most health plans, but the investigators couldn’t say for sure.
Vaccination uptake was significantly higher for those with insurance coverage in both pre- and post-ACA groups (P = .0007 and P = .01, respectively).
Despite these increases, vaccination rates are still low. There has been progress, but “physicians and public health professionals could assist in the acceleration of HPV vaccination uptake by increasing communication of HPV vaccination importance and by utilizing campaigns and materials that are readily available,” the investigators wrote.
The study was limited by a lack of data for teenage boys and men before implementation of the ACA and by the overlap in pre- and post-ACA data in the 2009-2010 wave because of the timing of the provision. Additionally, the data was self-reported.
The investigators reported having no relevant financial disclosures.
Human papillomavirus vaccination in girls and women has increased significantly since the implementation of the Affordable Care Act (ACA), according an analysis of federal survey data.
Overall, girls and women were 3.3 times more likely to receive the vaccine (95% confidence interval, 2.0, 5.5; P less than .0001) in the post–ACA implementation period, compared with the pre-ACA period. They were 5.8 times more likely to receive all three doses of the vaccine (95% CI, 2.5-13.6; P = .0001) post ACA, compared with one dose during that period, according to Rosemary Corriero of the University of Georgia, Athens, who is also a fellow at the Centers for Disease Control and Prevention, and her coauthors (J Pediatr Adolesc Gynecol. 2017 Jul 26. doi: 10.1016/j.jpag.2017.07.002).
The cross-sectional analysis included four waves of data from 2007-2008, 2009-2010, 2011-2012, and 2013-2014 – two waves before the ACA and two waves after. The data comes from the National Health and Nutrition Examination Survey (NHANES) questionnaire. In the pre-ACA surveys, 2,452 teenage girls and women were included, compared with 2,147 in the post-ACA years. The majority of participants were white, and analysis was limited to those aged 9-33 years.
The increase in vaccination could be due to the ACA’s provision requiring coverage of preventive health services without patient cost sharing in most health plans, but the investigators couldn’t say for sure.
Vaccination uptake was significantly higher for those with insurance coverage in both pre- and post-ACA groups (P = .0007 and P = .01, respectively).
Despite these increases, vaccination rates are still low. There has been progress, but “physicians and public health professionals could assist in the acceleration of HPV vaccination uptake by increasing communication of HPV vaccination importance and by utilizing campaigns and materials that are readily available,” the investigators wrote.
The study was limited by a lack of data for teenage boys and men before implementation of the ACA and by the overlap in pre- and post-ACA data in the 2009-2010 wave because of the timing of the provision. Additionally, the data was self-reported.
The investigators reported having no relevant financial disclosures.
Human papillomavirus vaccination in girls and women has increased significantly since the implementation of the Affordable Care Act (ACA), according an analysis of federal survey data.
Overall, girls and women were 3.3 times more likely to receive the vaccine (95% confidence interval, 2.0, 5.5; P less than .0001) in the post–ACA implementation period, compared with the pre-ACA period. They were 5.8 times more likely to receive all three doses of the vaccine (95% CI, 2.5-13.6; P = .0001) post ACA, compared with one dose during that period, according to Rosemary Corriero of the University of Georgia, Athens, who is also a fellow at the Centers for Disease Control and Prevention, and her coauthors (J Pediatr Adolesc Gynecol. 2017 Jul 26. doi: 10.1016/j.jpag.2017.07.002).
The cross-sectional analysis included four waves of data from 2007-2008, 2009-2010, 2011-2012, and 2013-2014 – two waves before the ACA and two waves after. The data comes from the National Health and Nutrition Examination Survey (NHANES) questionnaire. In the pre-ACA surveys, 2,452 teenage girls and women were included, compared with 2,147 in the post-ACA years. The majority of participants were white, and analysis was limited to those aged 9-33 years.
The increase in vaccination could be due to the ACA’s provision requiring coverage of preventive health services without patient cost sharing in most health plans, but the investigators couldn’t say for sure.
Vaccination uptake was significantly higher for those with insurance coverage in both pre- and post-ACA groups (P = .0007 and P = .01, respectively).
Despite these increases, vaccination rates are still low. There has been progress, but “physicians and public health professionals could assist in the acceleration of HPV vaccination uptake by increasing communication of HPV vaccination importance and by utilizing campaigns and materials that are readily available,” the investigators wrote.
The study was limited by a lack of data for teenage boys and men before implementation of the ACA and by the overlap in pre- and post-ACA data in the 2009-2010 wave because of the timing of the provision. Additionally, the data was self-reported.
The investigators reported having no relevant financial disclosures.
FROM THE JOURNAL OF PEDIATRIC & ADOLESCENT GYNECOLOGY
Key clinical point:
Major finding: Girls and women were 3.3 times more likely to receive the HPV vaccine in the period after the ACA was implemented (95% confidence interval, 2.0-5.5; P less than .0001).
Data source: A cross-sectional analysis of the NHANES questionnaire that included responses from more than 4,500 girls and women aged 9-33 years.
Disclosures: The investigators reported having no relevant financial disclosures.
Prenatal ART regimen with lowest risk is TDF-FTC-EFV
The antiretroviral therapy (ART) regimen associated with the least risk of adverse birth outcomes among pregnant women with HIV, relative to other regimens, is tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and efavirenz (EFV), according to a new study.
“Our results provide reassurance for the more than 90% of HIV-infected women who live in countries that follow WHO recommendations to use TDF-FTC-EFV,” wrote Rebecca Zash, MD, of Beth Israel Deaconess Medical Center in Boston and her associates in JAMA Pediatrics.
Using data collected from August 2014 through August 2016, the researchers compared outcomes among 47,027 births by women from Botswana, average age 26 years, who reached at least 24 weeks’ gestation. The study’s data came from eight government hospitals throughout Botswana, where approximately 45% of births had occurred nationwide.
The 11,932 infants exposed to HIV, representing about a quarter of all infants in the study, had a higher risk of adverse birth outcomes: 39.6% of HIV-exposed infants had adverse outcomes, compared with 28.9% of unexposed infants.
Nearly half (48.4%) of the HIV-exposed infants had also been exposed to ART from conception. Among these 5,780 infants, those exposed to the ART regimen comprising tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and efavirenz (EFV) had the lowest rate of adverse birth outcomes. The following percentages of infants exposed to different ART regimens had adverse outcomes:
- 36.4% of infants exposed to TDF-FTC-EFV.
- 41.7% of infants exposed to TDF-FTC and nevirapine (NVP).
- 44.9% of infants exposed to zidovudine (ZDV), lamivudine (3TC), and lopinavir-ritonavir (LPV-R).
- 47.4% of infants exposed to ZDV-3TC-NVP.
- 48.5% of infants exposed to TDF-FTC-LPV-R.
The risk of adverse birth outcomes, compared with exposure to TDF-FTC-EFV, was 15% higher for TDF-FTC-NVP, 21% higher for ZDV-3TC-LPV-R, 30% higher for ZDV-3TC-NVP, and 31% higher for TDF-FTC-LPV-R after researchers adjusted for age and potential sociodemographic confounders.
The risk of severe adverse outcomes for ART exposure from conception was as follows:
- 12.3% for exposure to TDF-FTC-EFV.
- 17.9% for exposure to TDF-FTC-NVP.
- 19.5% for TDF-FTC–LPV-R.
- 20.7% for ZDV-3TC-NVP.
- 23.4% for ZDV-3TC–LPV-R.
The risk for giving birth to an infant small for gestational age was lowest for TDF-FTC-EFV, compared with the other regimens.
“Differences between TDF-FTC-EFV and other ART regimens were greater for small for gestational age than for preterm birth,” suggesting a “drug-specific mechanism at the placental level because the health of the placenta is directly related to fetal growth,” the researchers wrote. “An ART effect at the level of the placenta may also explain why women receiving ART before conception have more adverse outcomes than [do] those who start ART after conception because endothelial dysfunction during placentation would be expected to have a more detrimental effect on the pregnancy,” they added.
The ZDV-3TC-NVP regimen was linked to greater risk for stillbirth, very preterm birth, and neonatal death; the ZDV-3TC-LPV-R regimen was linked to a greater risk of preterm and very preterm birth, as well as neonatal death.
“Our study findings may be difficult to integrate into settings with ART regimen choices beyond those available in Botswana,” the authors wrote. “Whether the magnitude of the differences we found in Botswana will be similar in higher-resource settings is unclear.”
The research was funded by the National Institutes of Health. The authors reported no conflicts of interest.
The antiretroviral therapy (ART) regimen associated with the least risk of adverse birth outcomes among pregnant women with HIV, relative to other regimens, is tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and efavirenz (EFV), according to a new study.
“Our results provide reassurance for the more than 90% of HIV-infected women who live in countries that follow WHO recommendations to use TDF-FTC-EFV,” wrote Rebecca Zash, MD, of Beth Israel Deaconess Medical Center in Boston and her associates in JAMA Pediatrics.
Using data collected from August 2014 through August 2016, the researchers compared outcomes among 47,027 births by women from Botswana, average age 26 years, who reached at least 24 weeks’ gestation. The study’s data came from eight government hospitals throughout Botswana, where approximately 45% of births had occurred nationwide.
The 11,932 infants exposed to HIV, representing about a quarter of all infants in the study, had a higher risk of adverse birth outcomes: 39.6% of HIV-exposed infants had adverse outcomes, compared with 28.9% of unexposed infants.
Nearly half (48.4%) of the HIV-exposed infants had also been exposed to ART from conception. Among these 5,780 infants, those exposed to the ART regimen comprising tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and efavirenz (EFV) had the lowest rate of adverse birth outcomes. The following percentages of infants exposed to different ART regimens had adverse outcomes:
- 36.4% of infants exposed to TDF-FTC-EFV.
- 41.7% of infants exposed to TDF-FTC and nevirapine (NVP).
- 44.9% of infants exposed to zidovudine (ZDV), lamivudine (3TC), and lopinavir-ritonavir (LPV-R).
- 47.4% of infants exposed to ZDV-3TC-NVP.
- 48.5% of infants exposed to TDF-FTC-LPV-R.
The risk of adverse birth outcomes, compared with exposure to TDF-FTC-EFV, was 15% higher for TDF-FTC-NVP, 21% higher for ZDV-3TC-LPV-R, 30% higher for ZDV-3TC-NVP, and 31% higher for TDF-FTC-LPV-R after researchers adjusted for age and potential sociodemographic confounders.
The risk of severe adverse outcomes for ART exposure from conception was as follows:
- 12.3% for exposure to TDF-FTC-EFV.
- 17.9% for exposure to TDF-FTC-NVP.
- 19.5% for TDF-FTC–LPV-R.
- 20.7% for ZDV-3TC-NVP.
- 23.4% for ZDV-3TC–LPV-R.
The risk for giving birth to an infant small for gestational age was lowest for TDF-FTC-EFV, compared with the other regimens.
“Differences between TDF-FTC-EFV and other ART regimens were greater for small for gestational age than for preterm birth,” suggesting a “drug-specific mechanism at the placental level because the health of the placenta is directly related to fetal growth,” the researchers wrote. “An ART effect at the level of the placenta may also explain why women receiving ART before conception have more adverse outcomes than [do] those who start ART after conception because endothelial dysfunction during placentation would be expected to have a more detrimental effect on the pregnancy,” they added.
The ZDV-3TC-NVP regimen was linked to greater risk for stillbirth, very preterm birth, and neonatal death; the ZDV-3TC-LPV-R regimen was linked to a greater risk of preterm and very preterm birth, as well as neonatal death.
“Our study findings may be difficult to integrate into settings with ART regimen choices beyond those available in Botswana,” the authors wrote. “Whether the magnitude of the differences we found in Botswana will be similar in higher-resource settings is unclear.”
The research was funded by the National Institutes of Health. The authors reported no conflicts of interest.
The antiretroviral therapy (ART) regimen associated with the least risk of adverse birth outcomes among pregnant women with HIV, relative to other regimens, is tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and efavirenz (EFV), according to a new study.
“Our results provide reassurance for the more than 90% of HIV-infected women who live in countries that follow WHO recommendations to use TDF-FTC-EFV,” wrote Rebecca Zash, MD, of Beth Israel Deaconess Medical Center in Boston and her associates in JAMA Pediatrics.
Using data collected from August 2014 through August 2016, the researchers compared outcomes among 47,027 births by women from Botswana, average age 26 years, who reached at least 24 weeks’ gestation. The study’s data came from eight government hospitals throughout Botswana, where approximately 45% of births had occurred nationwide.
The 11,932 infants exposed to HIV, representing about a quarter of all infants in the study, had a higher risk of adverse birth outcomes: 39.6% of HIV-exposed infants had adverse outcomes, compared with 28.9% of unexposed infants.
Nearly half (48.4%) of the HIV-exposed infants had also been exposed to ART from conception. Among these 5,780 infants, those exposed to the ART regimen comprising tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and efavirenz (EFV) had the lowest rate of adverse birth outcomes. The following percentages of infants exposed to different ART regimens had adverse outcomes:
- 36.4% of infants exposed to TDF-FTC-EFV.
- 41.7% of infants exposed to TDF-FTC and nevirapine (NVP).
- 44.9% of infants exposed to zidovudine (ZDV), lamivudine (3TC), and lopinavir-ritonavir (LPV-R).
- 47.4% of infants exposed to ZDV-3TC-NVP.
- 48.5% of infants exposed to TDF-FTC-LPV-R.
The risk of adverse birth outcomes, compared with exposure to TDF-FTC-EFV, was 15% higher for TDF-FTC-NVP, 21% higher for ZDV-3TC-LPV-R, 30% higher for ZDV-3TC-NVP, and 31% higher for TDF-FTC-LPV-R after researchers adjusted for age and potential sociodemographic confounders.
The risk of severe adverse outcomes for ART exposure from conception was as follows:
- 12.3% for exposure to TDF-FTC-EFV.
- 17.9% for exposure to TDF-FTC-NVP.
- 19.5% for TDF-FTC–LPV-R.
- 20.7% for ZDV-3TC-NVP.
- 23.4% for ZDV-3TC–LPV-R.
The risk for giving birth to an infant small for gestational age was lowest for TDF-FTC-EFV, compared with the other regimens.
“Differences between TDF-FTC-EFV and other ART regimens were greater for small for gestational age than for preterm birth,” suggesting a “drug-specific mechanism at the placental level because the health of the placenta is directly related to fetal growth,” the researchers wrote. “An ART effect at the level of the placenta may also explain why women receiving ART before conception have more adverse outcomes than [do] those who start ART after conception because endothelial dysfunction during placentation would be expected to have a more detrimental effect on the pregnancy,” they added.
The ZDV-3TC-NVP regimen was linked to greater risk for stillbirth, very preterm birth, and neonatal death; the ZDV-3TC-LPV-R regimen was linked to a greater risk of preterm and very preterm birth, as well as neonatal death.
“Our study findings may be difficult to integrate into settings with ART regimen choices beyond those available in Botswana,” the authors wrote. “Whether the magnitude of the differences we found in Botswana will be similar in higher-resource settings is unclear.”
The research was funded by the National Institutes of Health. The authors reported no conflicts of interest.
FROM JAMA PEDIATRICS
Key clinical point: Different antiretroviral regimens pose different adverse birth outcome risks for pregnant women with HIV.
Major finding: The ART regimen with the lowest level of risk was tenofovir, emtricitabine, and efavirenz, with a 36.5% risk for adverse outcomes and 12.3% risk for serious adverse outcomes.
Data source: The findings are based on an observational study of 47,027 births to women at eight government hospitals in Botswana from 2014 to 2016.
Disclosures: The research was funded by the National Institutes of Health. The authors reported no conflicts of interest.
Improving children’s sleep may reduce internalizing problems long term
SAN FRANCISCO –
, new research showed.“Interventions addressing externalizing difficulties may lead to improvements in sleep, but addressing internalizing difficulties are unlikely to lead to benefits for children’s sleep,” concluded Jon Quach, PhD, of the University of Melbourne and Murdoch Children’s Research Institute, Victoria, Australia, and his colleagues.
Although they also conclude that “addressing sleep problems at earlier time points may reduce both internalizing and externalizing difficulties,” the researchers said the data are inconsistent, only weakly suggesting that sleep influences later externalizing problems at only two different age points, Dr. Quach said when presenting the findings at the Pediatric Academic Societies meeting.
Data collection every 2 years included parent-reported sleep problems and child behavior. Behavior assessment came from the parent-reported Strengths and Difficulties Questionnaire for externalizing and internalizing difficulties. Parents reported severity of sleep difficulties and presence of specific problems at least 4 nights a week: difficulty falling asleep, night waking, sleep restlessness, and not wanting to sleep alone.
The researchers investigated the direction of influence – potential but unproven causation – between sleep problems and internalizing and externalizing problems. The analysis also assessed the extent of the associations. The first pair of analyses examined the relationship between sleeping and either externalizing or internalizing problems, independently assessed.
The findings revealed that sleeping problems were primarily associated with later internalizing difficulties, strongly suggesting that sleeping issues may cause or contribute to internalizing issues 2 years later.
With externalizing problems, however, the effect of poor sleep was inconsistent: Only at one point did it appear that sleeping difficulties contributed to externalizing difficulties. Instead, externalizing problems appeared to contribute to sleeping difficulties at three out of four time points. (The exception was that externalizing problems at ages 8-9 years did not appear to affect sleep at ages 10-11 years.) Though inconsistent, the results suggest that externalizing problems likely affect difficulty sleeping much more so than the other way around.
Then the researchers assessed the interacting associations between all three factors together. At all ages, poor sleep appeared to lead to internalizing difficulties 2 years later. Only once – at ages 6-7 years – did internalizing problems appear to influence sleep 2 years later.
The relationship between sleeping problems and externalizing problems was more complex and less consistent. Externalizing problems often, but not always, were positively associated with sleeping problems 2 years later. And only at ages 4-5 years did difficulty sleeping appear to lead to externalizing problems at ages 6-7 years.
In addition, independent of any interaction with sleeping problems, externalizing difficulties appeared to lead to internalizing problems at all time points.
Although this type of analysis can strongly suggest a direction of causality, Dr. Quach noted, the associations remain subject to the limitations of any observational data, where clearly determining causation or its direction is not possible.
The Australian Research Council and the National Health Medical Research Council in Australia funded the research. The authors did not report any conflicts of interest.
SAN FRANCISCO –
, new research showed.“Interventions addressing externalizing difficulties may lead to improvements in sleep, but addressing internalizing difficulties are unlikely to lead to benefits for children’s sleep,” concluded Jon Quach, PhD, of the University of Melbourne and Murdoch Children’s Research Institute, Victoria, Australia, and his colleagues.
Although they also conclude that “addressing sleep problems at earlier time points may reduce both internalizing and externalizing difficulties,” the researchers said the data are inconsistent, only weakly suggesting that sleep influences later externalizing problems at only two different age points, Dr. Quach said when presenting the findings at the Pediatric Academic Societies meeting.
Data collection every 2 years included parent-reported sleep problems and child behavior. Behavior assessment came from the parent-reported Strengths and Difficulties Questionnaire for externalizing and internalizing difficulties. Parents reported severity of sleep difficulties and presence of specific problems at least 4 nights a week: difficulty falling asleep, night waking, sleep restlessness, and not wanting to sleep alone.
The researchers investigated the direction of influence – potential but unproven causation – between sleep problems and internalizing and externalizing problems. The analysis also assessed the extent of the associations. The first pair of analyses examined the relationship between sleeping and either externalizing or internalizing problems, independently assessed.
The findings revealed that sleeping problems were primarily associated with later internalizing difficulties, strongly suggesting that sleeping issues may cause or contribute to internalizing issues 2 years later.
With externalizing problems, however, the effect of poor sleep was inconsistent: Only at one point did it appear that sleeping difficulties contributed to externalizing difficulties. Instead, externalizing problems appeared to contribute to sleeping difficulties at three out of four time points. (The exception was that externalizing problems at ages 8-9 years did not appear to affect sleep at ages 10-11 years.) Though inconsistent, the results suggest that externalizing problems likely affect difficulty sleeping much more so than the other way around.
Then the researchers assessed the interacting associations between all three factors together. At all ages, poor sleep appeared to lead to internalizing difficulties 2 years later. Only once – at ages 6-7 years – did internalizing problems appear to influence sleep 2 years later.
The relationship between sleeping problems and externalizing problems was more complex and less consistent. Externalizing problems often, but not always, were positively associated with sleeping problems 2 years later. And only at ages 4-5 years did difficulty sleeping appear to lead to externalizing problems at ages 6-7 years.
In addition, independent of any interaction with sleeping problems, externalizing difficulties appeared to lead to internalizing problems at all time points.
Although this type of analysis can strongly suggest a direction of causality, Dr. Quach noted, the associations remain subject to the limitations of any observational data, where clearly determining causation or its direction is not possible.
The Australian Research Council and the National Health Medical Research Council in Australia funded the research. The authors did not report any conflicts of interest.
SAN FRANCISCO –
, new research showed.“Interventions addressing externalizing difficulties may lead to improvements in sleep, but addressing internalizing difficulties are unlikely to lead to benefits for children’s sleep,” concluded Jon Quach, PhD, of the University of Melbourne and Murdoch Children’s Research Institute, Victoria, Australia, and his colleagues.
Although they also conclude that “addressing sleep problems at earlier time points may reduce both internalizing and externalizing difficulties,” the researchers said the data are inconsistent, only weakly suggesting that sleep influences later externalizing problems at only two different age points, Dr. Quach said when presenting the findings at the Pediatric Academic Societies meeting.
Data collection every 2 years included parent-reported sleep problems and child behavior. Behavior assessment came from the parent-reported Strengths and Difficulties Questionnaire for externalizing and internalizing difficulties. Parents reported severity of sleep difficulties and presence of specific problems at least 4 nights a week: difficulty falling asleep, night waking, sleep restlessness, and not wanting to sleep alone.
The researchers investigated the direction of influence – potential but unproven causation – between sleep problems and internalizing and externalizing problems. The analysis also assessed the extent of the associations. The first pair of analyses examined the relationship between sleeping and either externalizing or internalizing problems, independently assessed.
The findings revealed that sleeping problems were primarily associated with later internalizing difficulties, strongly suggesting that sleeping issues may cause or contribute to internalizing issues 2 years later.
With externalizing problems, however, the effect of poor sleep was inconsistent: Only at one point did it appear that sleeping difficulties contributed to externalizing difficulties. Instead, externalizing problems appeared to contribute to sleeping difficulties at three out of four time points. (The exception was that externalizing problems at ages 8-9 years did not appear to affect sleep at ages 10-11 years.) Though inconsistent, the results suggest that externalizing problems likely affect difficulty sleeping much more so than the other way around.
Then the researchers assessed the interacting associations between all three factors together. At all ages, poor sleep appeared to lead to internalizing difficulties 2 years later. Only once – at ages 6-7 years – did internalizing problems appear to influence sleep 2 years later.
The relationship between sleeping problems and externalizing problems was more complex and less consistent. Externalizing problems often, but not always, were positively associated with sleeping problems 2 years later. And only at ages 4-5 years did difficulty sleeping appear to lead to externalizing problems at ages 6-7 years.
In addition, independent of any interaction with sleeping problems, externalizing difficulties appeared to lead to internalizing problems at all time points.
Although this type of analysis can strongly suggest a direction of causality, Dr. Quach noted, the associations remain subject to the limitations of any observational data, where clearly determining causation or its direction is not possible.
The Australian Research Council and the National Health Medical Research Council in Australia funded the research. The authors did not report any conflicts of interest.
AT PAS 17
Key clinical point: Improving children’s sleep may reduce internalizing problems 2 years later.
Major finding: Externalizing problems were associated with sleep problems later on, and sleeping difficulties were linked to later internalizing problems.
Data source: The findings are based on analysis of four longitudinal, biennial questionnaires from parents of 4,983 Australian children aged 4-5 years, starting in 2004.
Disclosures: The Australian Research Council and the National Health Medical Research Council in Australia funded the research. The authors did not report any conflicts of interest.
Stevens-Johnson Syndrome Secondary to Isolated Albuterol Use
To the Editor:
A 22-year-old obese man with untreated mild asthma diagnosed in childhood presented to the emergency department with cheilitis (Figure 1); conjunctivitis; and painful desquamation of the oral mucosa, penis (Figure 2), and perirectal area (Figure 3). Physical examination was notable for palpebral conjunctiva; mucosal involvement with stomatitis (Figure 1B); and isolated 0.5- to 2-cm erosions and ulcerations with positive Nikolsky sign of the scrotum (Figure 2), trunk, back, and arms and legs. Some areas had evidence of hemorrhagic crust, flaccid bullae, and denudation. Few scant targetoid lesions and dusky red macules on the trunk, face, palms, and soles also were present.
One week prior to presentation he had an episode of diarrhea and dyspnea with symptoms of mild heat stroke after working outdoors, and he self-treated with ibuprofen, which he had taken intermittently for years. He was subsequently seen at an outpatient clinic and was prescribed an albuterol inhaler for previously untreated childhood asthma. The patient stated that he inhaled 2 puffs every 6 hours for a total of 3 treatments. Shortly after the last dose, he noticed a tingling sensation of the oral mucosa that developed into a painful 2-cm bullous ulcer. Over the next 3 days, he developed several more oral ulcers and erosions. Three days before admission he developed dysuria and tense bullae at the glans penis. After admission, he developed cheilitis, conjunctivitis, dysuria, odynophagia, and dysphagia to solids. One day after admission, the patient had the onset of systemic symptoms, including cough with worsening dyspnea, fever, chills, hemoptysis, epistaxis, nausea, diarrhea, loss of appetite, joint pain, and myalgia. Review of systems was otherwise negative. A radiograph was performed at admission and was notable for mild atelectasis but was otherwise normal. The chest radiograph was negative for signs of perihilar lymphadenopathy, pleural effusion, pneumothorax, or lobar infiltrates suggestive of bacterial pneumonia. It also did not show signs of patchy opacities or air bronchograms suggestive of an interstitial pneumonia. On admission, he was started on acyclovir, fluconazole, methylprednisolone, nystatin, pantoprazole, acetaminophen, topical bacitracin, oxycodone, and topical silver nitrate.
At the time of admission our patient was afebrile with a normal heart rate, blood pressure, and respiratory rate. However, he was hypoxic, with a pulse oximetry of 86% on room air and 94% on 40% fraction of inspired oxygen. Complete blood cell count, electrolytes, and liver function tests were all within reference range. Urinalysis revealed evidence of scant red blood cells without pyuria, and the erythrocyte sedimentation rate and creatine kinase level were both elevated. Two blood cultures; sputum cultures; and polymerase chain reaction for Mycoplasma pneumoniae, herpes simplex virus, varicella-zoster virus, cytomegalovirus, and Epstein-Barr virus were negative. Human immunodeficiency virus panel, antinuclear antibody screen, and hepatitis B and C panels were all negative. Four punch biopsies were obtained showing full-thickness epidermal necrosis with neutrophils, few dyskeratotic cells, and sparse inflammatory infiltrate compatible with Stevens-Johnson syndrome (SJS).
After hospital admission, the patient’s mucosal desquamation progressively improved. By day 3, he required minimal supplemental oxygen with resolution of bowel symptoms and improved mucosal and skin findings. He was discharged on day 4 with supplemental oxygen and a 7-day course of prednisone, fluconazole, liquid oxycodone, pantoprazole, and acetaminophen. He showed continued improvement at a follow-up outpatient visit 2 days following discharge.
Stevens-Johnson syndrome is a rare severe drug reaction characterized by high fevers, mucosal erosions, tenderness, and skin detachment approximately 1 to 3 weeks after an inciting event.1,2 Although SJS has been linked to infections and less commonly to immunizations, in more than 80% of cases, SJS is strongly associated with a recent medication change.3 The classes of drugs that have been implicated in SJS most commonly include antibiotics, anticonvulsants, and nonsteroidal anti-inflammatory drugs.4 Stevens-Johnson syndrome from drug reactions is not uncommon; however, SJS secondary to isolated albuterol use is rare.
Although it is presumed that albuterol was the key inciting factor in our patient’s case of SJS, it also is recognized that mucosal SJS can be associated with M pneumoniae infection. For this reason, we performed polymerase chain reaction for M pneumoniae as well as a chest radiograph to rule out this possibility. In addition, our patient had denied prolonged respiratory symptoms suggestive of a mycoplasma pneumonia infection, such as a prodrome of cough, myalgia, headache, sore throat, or fever. A report of 8 patients with documented SJS and M pneumoniae as well as a review of the literature also demonstrated a mean of 10 days of prodromal symptoms prior to the onset of mucosal lesions and/or a rash.5 However, mucosal SJS associated with mycoplasma pneumonia is an important clinical entity that should not be forgotten during the workup of a young patient with mucosal lesions or rash suggestive of SJS.
The exact etiology and mechanism of drug-induced SJS is not well understood at this time; however, evidence suggests that SJS is strongly linked to the host’s inability to detoxify drug metabolites.6,7 It has been postulated that SJS occurs secondary to a cell-mediated immune response, which activates cytotoxic T lymphocytes and subsequently results in keratinocyte apoptosis. Keratinocyte apoptosis occurs via the CD95-CD95 death receptor and soluble or membrane-bound ligand interaction.3,8,9 Stevens-Johnson syndrome is thought to occur from an interaction involving an HLA antigen–restricted presentation of drug metabolites to cytotoxic T cells, which can be further supported by evidence of strong genetic associations with HLA antigen alleles B15.02 and B58.01 in the cases of carbamazepine- and allopurinol-induced SJS, respectively.6,7 However, the genetic associations of specific HLA antigen alleles and polymorphisms with SJS and other cutaneous reactions is thought to be drug specific and HLA antigen subtype specific.7 Therefore, it is difficult to determine or correlate the clinical outcomes and manifestations of drug reactions in individualized patients. The precise mechanism of antigenicity of albuterol in initiating this cascade has not yet been determined. However, these investigations provide strong evidence for a correlation between specific HLA antigen haplotypes and occurrence of drug antigenicity resulting in SJS and other cutaneous reactions in susceptible patient populations.
Although the specific molecular pathway and etiology of SJS is not well delineated, pathology in combination with clinical correlation allows for diagnosis. Early-stage biopsies in SJS typically show apoptotic keratinocytes throughout the epidermis. Late-stage biopsies exhibit subepidermal blisters and full-thickness epidermal necrosis.1 Histopathology was performed on 4-mm punch biopsies of the chest and back and demonstrated full-thickness epidermal necrosis with neutrophils and a few dyskeratotic cells, likely representing a late stage of epidermal involvement. Given the predominance of neutrophils, other diagnostic considerations based solely on the biopsy results included contact dermatitis or phototoxic dermatitis. The remaining inflammatory infiltrate was sparse. Immunofluorescence was pan-negative.
This report illustrates a rare case of SJS from isolated albuterol use. This adverse drug reaction has not been well reported in the literature and may be an important consideration in the management of a patient with asthma.
- Stern RS. Clinical practice. exanthematous drug eruptions. N Engl J Med. 2012;366:2492-2501.
- Tartarone A, Lerose R. Stevens-Johnson syndrome and toxic epidermal necrolysis: what do we know? Ther Drug Monit. 2010;32:669-672.
- Ferrandiz-Pulido C, Garcia-Patos V. A review of causes of Stevens-Johnson syndrome and toxic epidermal necrolysis in children. Arch Dis Child. 2013;98:998-1003.
- Mockenhaupt M, Viboud C, Dunant A, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: assessment of medication risks with emphasis on recently marketed drugs. the EuroSCAR-study. J Invest Dermatol. 2008;128:35-44.
- Levy M, Shear NH. Mycoplasma pneumoniae infections and Stevens-Johnson syndrome. report of eight cases and review of the literature. Clin Pediatr (Phila). 1991;30:42-49.
- Chung WH, Hung SI. Genetic markers and danger signals in Stevens-Johnson syndrome and toxic epidermal necrolysis [published online October 25, 2010]. Allergol Int. 2010;59:325-332.
- Chung WH, Hung SI. Recent advances in the genetics and immunology of Stevens-Johnson syndrome and toxic epidermal necrosis. J Dermatol Sci. 2012;66:190-196.
- Bharadwaj M, Illing P, Theodossis A, et al. Drug hypersensitivity and human leukocyte antigens of the major histocompatibility complex. Annu Rev Pharmacol Toxicol. 2012;52:401-431.
- Chessman D, Kostenko L, Lethborg T, et al. Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity. Immunity. 2008;28:822-832.
To the Editor:
A 22-year-old obese man with untreated mild asthma diagnosed in childhood presented to the emergency department with cheilitis (Figure 1); conjunctivitis; and painful desquamation of the oral mucosa, penis (Figure 2), and perirectal area (Figure 3). Physical examination was notable for palpebral conjunctiva; mucosal involvement with stomatitis (Figure 1B); and isolated 0.5- to 2-cm erosions and ulcerations with positive Nikolsky sign of the scrotum (Figure 2), trunk, back, and arms and legs. Some areas had evidence of hemorrhagic crust, flaccid bullae, and denudation. Few scant targetoid lesions and dusky red macules on the trunk, face, palms, and soles also were present.
One week prior to presentation he had an episode of diarrhea and dyspnea with symptoms of mild heat stroke after working outdoors, and he self-treated with ibuprofen, which he had taken intermittently for years. He was subsequently seen at an outpatient clinic and was prescribed an albuterol inhaler for previously untreated childhood asthma. The patient stated that he inhaled 2 puffs every 6 hours for a total of 3 treatments. Shortly after the last dose, he noticed a tingling sensation of the oral mucosa that developed into a painful 2-cm bullous ulcer. Over the next 3 days, he developed several more oral ulcers and erosions. Three days before admission he developed dysuria and tense bullae at the glans penis. After admission, he developed cheilitis, conjunctivitis, dysuria, odynophagia, and dysphagia to solids. One day after admission, the patient had the onset of systemic symptoms, including cough with worsening dyspnea, fever, chills, hemoptysis, epistaxis, nausea, diarrhea, loss of appetite, joint pain, and myalgia. Review of systems was otherwise negative. A radiograph was performed at admission and was notable for mild atelectasis but was otherwise normal. The chest radiograph was negative for signs of perihilar lymphadenopathy, pleural effusion, pneumothorax, or lobar infiltrates suggestive of bacterial pneumonia. It also did not show signs of patchy opacities or air bronchograms suggestive of an interstitial pneumonia. On admission, he was started on acyclovir, fluconazole, methylprednisolone, nystatin, pantoprazole, acetaminophen, topical bacitracin, oxycodone, and topical silver nitrate.
At the time of admission our patient was afebrile with a normal heart rate, blood pressure, and respiratory rate. However, he was hypoxic, with a pulse oximetry of 86% on room air and 94% on 40% fraction of inspired oxygen. Complete blood cell count, electrolytes, and liver function tests were all within reference range. Urinalysis revealed evidence of scant red blood cells without pyuria, and the erythrocyte sedimentation rate and creatine kinase level were both elevated. Two blood cultures; sputum cultures; and polymerase chain reaction for Mycoplasma pneumoniae, herpes simplex virus, varicella-zoster virus, cytomegalovirus, and Epstein-Barr virus were negative. Human immunodeficiency virus panel, antinuclear antibody screen, and hepatitis B and C panels were all negative. Four punch biopsies were obtained showing full-thickness epidermal necrosis with neutrophils, few dyskeratotic cells, and sparse inflammatory infiltrate compatible with Stevens-Johnson syndrome (SJS).
After hospital admission, the patient’s mucosal desquamation progressively improved. By day 3, he required minimal supplemental oxygen with resolution of bowel symptoms and improved mucosal and skin findings. He was discharged on day 4 with supplemental oxygen and a 7-day course of prednisone, fluconazole, liquid oxycodone, pantoprazole, and acetaminophen. He showed continued improvement at a follow-up outpatient visit 2 days following discharge.
Stevens-Johnson syndrome is a rare severe drug reaction characterized by high fevers, mucosal erosions, tenderness, and skin detachment approximately 1 to 3 weeks after an inciting event.1,2 Although SJS has been linked to infections and less commonly to immunizations, in more than 80% of cases, SJS is strongly associated with a recent medication change.3 The classes of drugs that have been implicated in SJS most commonly include antibiotics, anticonvulsants, and nonsteroidal anti-inflammatory drugs.4 Stevens-Johnson syndrome from drug reactions is not uncommon; however, SJS secondary to isolated albuterol use is rare.
Although it is presumed that albuterol was the key inciting factor in our patient’s case of SJS, it also is recognized that mucosal SJS can be associated with M pneumoniae infection. For this reason, we performed polymerase chain reaction for M pneumoniae as well as a chest radiograph to rule out this possibility. In addition, our patient had denied prolonged respiratory symptoms suggestive of a mycoplasma pneumonia infection, such as a prodrome of cough, myalgia, headache, sore throat, or fever. A report of 8 patients with documented SJS and M pneumoniae as well as a review of the literature also demonstrated a mean of 10 days of prodromal symptoms prior to the onset of mucosal lesions and/or a rash.5 However, mucosal SJS associated with mycoplasma pneumonia is an important clinical entity that should not be forgotten during the workup of a young patient with mucosal lesions or rash suggestive of SJS.
The exact etiology and mechanism of drug-induced SJS is not well understood at this time; however, evidence suggests that SJS is strongly linked to the host’s inability to detoxify drug metabolites.6,7 It has been postulated that SJS occurs secondary to a cell-mediated immune response, which activates cytotoxic T lymphocytes and subsequently results in keratinocyte apoptosis. Keratinocyte apoptosis occurs via the CD95-CD95 death receptor and soluble or membrane-bound ligand interaction.3,8,9 Stevens-Johnson syndrome is thought to occur from an interaction involving an HLA antigen–restricted presentation of drug metabolites to cytotoxic T cells, which can be further supported by evidence of strong genetic associations with HLA antigen alleles B15.02 and B58.01 in the cases of carbamazepine- and allopurinol-induced SJS, respectively.6,7 However, the genetic associations of specific HLA antigen alleles and polymorphisms with SJS and other cutaneous reactions is thought to be drug specific and HLA antigen subtype specific.7 Therefore, it is difficult to determine or correlate the clinical outcomes and manifestations of drug reactions in individualized patients. The precise mechanism of antigenicity of albuterol in initiating this cascade has not yet been determined. However, these investigations provide strong evidence for a correlation between specific HLA antigen haplotypes and occurrence of drug antigenicity resulting in SJS and other cutaneous reactions in susceptible patient populations.
Although the specific molecular pathway and etiology of SJS is not well delineated, pathology in combination with clinical correlation allows for diagnosis. Early-stage biopsies in SJS typically show apoptotic keratinocytes throughout the epidermis. Late-stage biopsies exhibit subepidermal blisters and full-thickness epidermal necrosis.1 Histopathology was performed on 4-mm punch biopsies of the chest and back and demonstrated full-thickness epidermal necrosis with neutrophils and a few dyskeratotic cells, likely representing a late stage of epidermal involvement. Given the predominance of neutrophils, other diagnostic considerations based solely on the biopsy results included contact dermatitis or phototoxic dermatitis. The remaining inflammatory infiltrate was sparse. Immunofluorescence was pan-negative.
This report illustrates a rare case of SJS from isolated albuterol use. This adverse drug reaction has not been well reported in the literature and may be an important consideration in the management of a patient with asthma.
To the Editor:
A 22-year-old obese man with untreated mild asthma diagnosed in childhood presented to the emergency department with cheilitis (Figure 1); conjunctivitis; and painful desquamation of the oral mucosa, penis (Figure 2), and perirectal area (Figure 3). Physical examination was notable for palpebral conjunctiva; mucosal involvement with stomatitis (Figure 1B); and isolated 0.5- to 2-cm erosions and ulcerations with positive Nikolsky sign of the scrotum (Figure 2), trunk, back, and arms and legs. Some areas had evidence of hemorrhagic crust, flaccid bullae, and denudation. Few scant targetoid lesions and dusky red macules on the trunk, face, palms, and soles also were present.
One week prior to presentation he had an episode of diarrhea and dyspnea with symptoms of mild heat stroke after working outdoors, and he self-treated with ibuprofen, which he had taken intermittently for years. He was subsequently seen at an outpatient clinic and was prescribed an albuterol inhaler for previously untreated childhood asthma. The patient stated that he inhaled 2 puffs every 6 hours for a total of 3 treatments. Shortly after the last dose, he noticed a tingling sensation of the oral mucosa that developed into a painful 2-cm bullous ulcer. Over the next 3 days, he developed several more oral ulcers and erosions. Three days before admission he developed dysuria and tense bullae at the glans penis. After admission, he developed cheilitis, conjunctivitis, dysuria, odynophagia, and dysphagia to solids. One day after admission, the patient had the onset of systemic symptoms, including cough with worsening dyspnea, fever, chills, hemoptysis, epistaxis, nausea, diarrhea, loss of appetite, joint pain, and myalgia. Review of systems was otherwise negative. A radiograph was performed at admission and was notable for mild atelectasis but was otherwise normal. The chest radiograph was negative for signs of perihilar lymphadenopathy, pleural effusion, pneumothorax, or lobar infiltrates suggestive of bacterial pneumonia. It also did not show signs of patchy opacities or air bronchograms suggestive of an interstitial pneumonia. On admission, he was started on acyclovir, fluconazole, methylprednisolone, nystatin, pantoprazole, acetaminophen, topical bacitracin, oxycodone, and topical silver nitrate.
At the time of admission our patient was afebrile with a normal heart rate, blood pressure, and respiratory rate. However, he was hypoxic, with a pulse oximetry of 86% on room air and 94% on 40% fraction of inspired oxygen. Complete blood cell count, electrolytes, and liver function tests were all within reference range. Urinalysis revealed evidence of scant red blood cells without pyuria, and the erythrocyte sedimentation rate and creatine kinase level were both elevated. Two blood cultures; sputum cultures; and polymerase chain reaction for Mycoplasma pneumoniae, herpes simplex virus, varicella-zoster virus, cytomegalovirus, and Epstein-Barr virus were negative. Human immunodeficiency virus panel, antinuclear antibody screen, and hepatitis B and C panels were all negative. Four punch biopsies were obtained showing full-thickness epidermal necrosis with neutrophils, few dyskeratotic cells, and sparse inflammatory infiltrate compatible with Stevens-Johnson syndrome (SJS).
After hospital admission, the patient’s mucosal desquamation progressively improved. By day 3, he required minimal supplemental oxygen with resolution of bowel symptoms and improved mucosal and skin findings. He was discharged on day 4 with supplemental oxygen and a 7-day course of prednisone, fluconazole, liquid oxycodone, pantoprazole, and acetaminophen. He showed continued improvement at a follow-up outpatient visit 2 days following discharge.
Stevens-Johnson syndrome is a rare severe drug reaction characterized by high fevers, mucosal erosions, tenderness, and skin detachment approximately 1 to 3 weeks after an inciting event.1,2 Although SJS has been linked to infections and less commonly to immunizations, in more than 80% of cases, SJS is strongly associated with a recent medication change.3 The classes of drugs that have been implicated in SJS most commonly include antibiotics, anticonvulsants, and nonsteroidal anti-inflammatory drugs.4 Stevens-Johnson syndrome from drug reactions is not uncommon; however, SJS secondary to isolated albuterol use is rare.
Although it is presumed that albuterol was the key inciting factor in our patient’s case of SJS, it also is recognized that mucosal SJS can be associated with M pneumoniae infection. For this reason, we performed polymerase chain reaction for M pneumoniae as well as a chest radiograph to rule out this possibility. In addition, our patient had denied prolonged respiratory symptoms suggestive of a mycoplasma pneumonia infection, such as a prodrome of cough, myalgia, headache, sore throat, or fever. A report of 8 patients with documented SJS and M pneumoniae as well as a review of the literature also demonstrated a mean of 10 days of prodromal symptoms prior to the onset of mucosal lesions and/or a rash.5 However, mucosal SJS associated with mycoplasma pneumonia is an important clinical entity that should not be forgotten during the workup of a young patient with mucosal lesions or rash suggestive of SJS.
The exact etiology and mechanism of drug-induced SJS is not well understood at this time; however, evidence suggests that SJS is strongly linked to the host’s inability to detoxify drug metabolites.6,7 It has been postulated that SJS occurs secondary to a cell-mediated immune response, which activates cytotoxic T lymphocytes and subsequently results in keratinocyte apoptosis. Keratinocyte apoptosis occurs via the CD95-CD95 death receptor and soluble or membrane-bound ligand interaction.3,8,9 Stevens-Johnson syndrome is thought to occur from an interaction involving an HLA antigen–restricted presentation of drug metabolites to cytotoxic T cells, which can be further supported by evidence of strong genetic associations with HLA antigen alleles B15.02 and B58.01 in the cases of carbamazepine- and allopurinol-induced SJS, respectively.6,7 However, the genetic associations of specific HLA antigen alleles and polymorphisms with SJS and other cutaneous reactions is thought to be drug specific and HLA antigen subtype specific.7 Therefore, it is difficult to determine or correlate the clinical outcomes and manifestations of drug reactions in individualized patients. The precise mechanism of antigenicity of albuterol in initiating this cascade has not yet been determined. However, these investigations provide strong evidence for a correlation between specific HLA antigen haplotypes and occurrence of drug antigenicity resulting in SJS and other cutaneous reactions in susceptible patient populations.
Although the specific molecular pathway and etiology of SJS is not well delineated, pathology in combination with clinical correlation allows for diagnosis. Early-stage biopsies in SJS typically show apoptotic keratinocytes throughout the epidermis. Late-stage biopsies exhibit subepidermal blisters and full-thickness epidermal necrosis.1 Histopathology was performed on 4-mm punch biopsies of the chest and back and demonstrated full-thickness epidermal necrosis with neutrophils and a few dyskeratotic cells, likely representing a late stage of epidermal involvement. Given the predominance of neutrophils, other diagnostic considerations based solely on the biopsy results included contact dermatitis or phototoxic dermatitis. The remaining inflammatory infiltrate was sparse. Immunofluorescence was pan-negative.
This report illustrates a rare case of SJS from isolated albuterol use. This adverse drug reaction has not been well reported in the literature and may be an important consideration in the management of a patient with asthma.
- Stern RS. Clinical practice. exanthematous drug eruptions. N Engl J Med. 2012;366:2492-2501.
- Tartarone A, Lerose R. Stevens-Johnson syndrome and toxic epidermal necrolysis: what do we know? Ther Drug Monit. 2010;32:669-672.
- Ferrandiz-Pulido C, Garcia-Patos V. A review of causes of Stevens-Johnson syndrome and toxic epidermal necrolysis in children. Arch Dis Child. 2013;98:998-1003.
- Mockenhaupt M, Viboud C, Dunant A, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: assessment of medication risks with emphasis on recently marketed drugs. the EuroSCAR-study. J Invest Dermatol. 2008;128:35-44.
- Levy M, Shear NH. Mycoplasma pneumoniae infections and Stevens-Johnson syndrome. report of eight cases and review of the literature. Clin Pediatr (Phila). 1991;30:42-49.
- Chung WH, Hung SI. Genetic markers and danger signals in Stevens-Johnson syndrome and toxic epidermal necrolysis [published online October 25, 2010]. Allergol Int. 2010;59:325-332.
- Chung WH, Hung SI. Recent advances in the genetics and immunology of Stevens-Johnson syndrome and toxic epidermal necrosis. J Dermatol Sci. 2012;66:190-196.
- Bharadwaj M, Illing P, Theodossis A, et al. Drug hypersensitivity and human leukocyte antigens of the major histocompatibility complex. Annu Rev Pharmacol Toxicol. 2012;52:401-431.
- Chessman D, Kostenko L, Lethborg T, et al. Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity. Immunity. 2008;28:822-832.
- Stern RS. Clinical practice. exanthematous drug eruptions. N Engl J Med. 2012;366:2492-2501.
- Tartarone A, Lerose R. Stevens-Johnson syndrome and toxic epidermal necrolysis: what do we know? Ther Drug Monit. 2010;32:669-672.
- Ferrandiz-Pulido C, Garcia-Patos V. A review of causes of Stevens-Johnson syndrome and toxic epidermal necrolysis in children. Arch Dis Child. 2013;98:998-1003.
- Mockenhaupt M, Viboud C, Dunant A, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: assessment of medication risks with emphasis on recently marketed drugs. the EuroSCAR-study. J Invest Dermatol. 2008;128:35-44.
- Levy M, Shear NH. Mycoplasma pneumoniae infections and Stevens-Johnson syndrome. report of eight cases and review of the literature. Clin Pediatr (Phila). 1991;30:42-49.
- Chung WH, Hung SI. Genetic markers and danger signals in Stevens-Johnson syndrome and toxic epidermal necrolysis [published online October 25, 2010]. Allergol Int. 2010;59:325-332.
- Chung WH, Hung SI. Recent advances in the genetics and immunology of Stevens-Johnson syndrome and toxic epidermal necrosis. J Dermatol Sci. 2012;66:190-196.
- Bharadwaj M, Illing P, Theodossis A, et al. Drug hypersensitivity and human leukocyte antigens of the major histocompatibility complex. Annu Rev Pharmacol Toxicol. 2012;52:401-431.
- Chessman D, Kostenko L, Lethborg T, et al. Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity. Immunity. 2008;28:822-832.
Practice Points
- Think of Stevens-Johnson syndrome when new skin lesions are seen after any new medication is started.
- Perform a full-body examination to assess the extent of skin eruptions.
- When a medication is atypical for skin eruption, it becomes necessary to assess for other systemic causes and confirm pathologic results on skin biopsy.
Award for best hospital goes to … the Mayo Clinic
For the second consecutive year, the Mayo Clinic was named the top hospital in the country by U.S. News & World Report.
Also for the second consecutive year, the Cleveland Clinic is ranked second, while Johns Hopkins Hospital in Baltimore and Massachusetts General Hospital in Boston finished third and fourth – switching their places from last year’s ranking – and UCSF Medical Center in San Francisco is fifth after ranking seventh last year, according to the 2017-2018 Best Hospitals ranking.
The Mayo Clinic is nationally ranked in 15 of the 16 specialties included in the overall process, which started with 4,658 community inpatient hospitals and finished with 152 ranking nationally in at least one specialty and 20 earning Honor Roll status with high rankings in multiple specialties. The specialties used in the ranking process include 12 that are data driven – cancer; cardiology and heart surgery; diabetes and endocrinology; otolaryngology; gastroenterology and gastrointestinal surgery; geriatrics; gynecology; nephrology; neurology and neurosurgery; orthopedics; pulmonology; and urology – and four rated by reputation only – ophthalmology; psychiatry; rehabilitation; and rheumatology.
The research organization RTI International conducted the physician survey and produced the Best Hospitals methodology and national rankings under contract with U.S. News. The launch of this year’s edition of Best Hospitals is sponsored by Fidelity Investments.
For the second consecutive year, the Mayo Clinic was named the top hospital in the country by U.S. News & World Report.
Also for the second consecutive year, the Cleveland Clinic is ranked second, while Johns Hopkins Hospital in Baltimore and Massachusetts General Hospital in Boston finished third and fourth – switching their places from last year’s ranking – and UCSF Medical Center in San Francisco is fifth after ranking seventh last year, according to the 2017-2018 Best Hospitals ranking.
The Mayo Clinic is nationally ranked in 15 of the 16 specialties included in the overall process, which started with 4,658 community inpatient hospitals and finished with 152 ranking nationally in at least one specialty and 20 earning Honor Roll status with high rankings in multiple specialties. The specialties used in the ranking process include 12 that are data driven – cancer; cardiology and heart surgery; diabetes and endocrinology; otolaryngology; gastroenterology and gastrointestinal surgery; geriatrics; gynecology; nephrology; neurology and neurosurgery; orthopedics; pulmonology; and urology – and four rated by reputation only – ophthalmology; psychiatry; rehabilitation; and rheumatology.
The research organization RTI International conducted the physician survey and produced the Best Hospitals methodology and national rankings under contract with U.S. News. The launch of this year’s edition of Best Hospitals is sponsored by Fidelity Investments.
For the second consecutive year, the Mayo Clinic was named the top hospital in the country by U.S. News & World Report.
Also for the second consecutive year, the Cleveland Clinic is ranked second, while Johns Hopkins Hospital in Baltimore and Massachusetts General Hospital in Boston finished third and fourth – switching their places from last year’s ranking – and UCSF Medical Center in San Francisco is fifth after ranking seventh last year, according to the 2017-2018 Best Hospitals ranking.
The Mayo Clinic is nationally ranked in 15 of the 16 specialties included in the overall process, which started with 4,658 community inpatient hospitals and finished with 152 ranking nationally in at least one specialty and 20 earning Honor Roll status with high rankings in multiple specialties. The specialties used in the ranking process include 12 that are data driven – cancer; cardiology and heart surgery; diabetes and endocrinology; otolaryngology; gastroenterology and gastrointestinal surgery; geriatrics; gynecology; nephrology; neurology and neurosurgery; orthopedics; pulmonology; and urology – and four rated by reputation only – ophthalmology; psychiatry; rehabilitation; and rheumatology.
The research organization RTI International conducted the physician survey and produced the Best Hospitals methodology and national rankings under contract with U.S. News. The launch of this year’s edition of Best Hospitals is sponsored by Fidelity Investments.
Space Heater–Induced Bullous Erythema Ab Igne
To the Editor:
Erythema ab igne (EAI) is a reticular erythematous hyperpigmentation of skin repeatedly exposed to moderate heat.1 It usually is asymptomatic, though some patients report itching or burning at the site.2 Historically caused by exposure to coal stoves or open fires, EAI has become increasingly common among individuals using space heaters, heating pads, or laptop computers near bare skin.2,3 Although EAI itself is benign and usually resolves with the removal of the exposure, it remains of clinical importance because of its association with underlying chronic disease, as chronic pain often is managed with frequent heating pad or hot water bottle use.2 Additionally, accurate diagnosis is important given the future risk for malignancy, as chronic changes of EAI have been reported to lead to squamous cell carcinoma or rarely Merkel cell carcinoma.2 Erythema ab igne is not traditionally associated with the formation of bullae; however, we present a case of bullous EAI that we believe highlights the importance of including this condition in the differential diagnosis of bullous disorders.
A 55-year-old man was admitted for presumed cellulitis of the bilateral legs. The patient had developed hyperpigmented discoloration of the medial surface of both legs with subsequent formation of tense bullae over the last 2 months. The dermatology department was consulted, as there was concern for bullous pemphigoid. The patient’s medical history was notable for hypertension, hyperlipidemia, diet-controlled type 2 diabetes mellitus, and hepatitis C virus with cirrhosis. The patient denied pruritus, pain, or known exposure of the legs to potential irritants prior to developing the lesions; however, with additional questioning he did report frequently sitting in front of a space heater with bare legs. Physical examination revealed multiple areas of reticulated erythematous hyperpigmentation with several overlying bullae (Figure 1). Many of the bullae were unroofed with full-thickness ulceration. Biopsies were taken for hematoxylin and eosin staining (Figure 2) and direct immunofluorescence.
Basic hematologic and metabolic laboratory test results as well as blood cultures were negative. Wound culture was positive for methicillin-resistant Staphylococcus aureus. Histologic examination showed interface dermatitis with subepidermal vesicle (Figure 2). Scattered necrotic keratinocytes were present in the adjacent epidermis, and focal subtle vacuolar alteration of the dermoepidermal junction was seen (Figure 3). Sparse perivascular mononuclear cells and scattered melanophages were present in the dermis. Direct immunofluorescence showed no diagnostic immunopathologic abnormality. Focal weak nonspecific vascular positivity for IgG and C3 was seen, but IgA and IgM were negative. Although not specific, these changes were compatible with EAI in the clinical context provided. The diagnosis of bullous EAI with superimposed staphylococcal infection was made.
Although rare, there have been reports of a bullous variant of EAI. Flanagan et al4 described 3 cases of bullous EAI with histopathology similar to our case. All 3 biopsies showed subepidermal separation with a mild perivascular dermal lymphocytic infiltrate. Direct immunofluorescence was negative in 2 cases but showed nonspecific weak patchy deposition of IgM along the dermoepidermal junction.4 Although our case was negative for IgM, there was a similar weak nonspecific distribution of IgG. Kokturk et al5 described a case of bullous EAI in a man with repeated exposure to a space heater. The lesions showed subepidermal separation of the epidermis; increased elastic fibers; dilated dermal capillaries; melanophages in the upper dermis; and a mild, superficial, perivascular-lymphocytic infiltrate. Direct immunofluorescence showed no immune deposits.5 Several earlier cases of bullae associated with EAI have been reported in the literature but were thought to be bullous lichen planus superimposed on EAI.6 Our case, which exhibited similar historical, physical, and histopathologic findings, strengthens the argument for a defined bullous variant of EAI.
- Baruchin AM. Erythema ab igne—a neglected entity? Burns. 1994;20:460-462.
- Arnold AW, Itin PH. Laptop computer−induced erythema ab igne in a child and review of the literature [published online October 4, 2010]. Pediatrics. 2010;126:E1227-E1230.
- Tan S, Bertucci V. Erythema ab igne: an old condition new again. CMAJ. 2000;162:77-78.
- Flanagan N, Watson R, Sweeney E, et al. Bullous erythema ab igne. Br J Dermatol. 1996;134:1159-1160.
- Kokturk A, Kaya TI, Baz K, et al. Bullous erythema ab igne. Dermatol Online J. 2003;9:18.
- Horio T, Imamura S. Bullous lichen planus developed on erythema ab igne. J Dermatol. 1986;13:203-207.
To the Editor:
Erythema ab igne (EAI) is a reticular erythematous hyperpigmentation of skin repeatedly exposed to moderate heat.1 It usually is asymptomatic, though some patients report itching or burning at the site.2 Historically caused by exposure to coal stoves or open fires, EAI has become increasingly common among individuals using space heaters, heating pads, or laptop computers near bare skin.2,3 Although EAI itself is benign and usually resolves with the removal of the exposure, it remains of clinical importance because of its association with underlying chronic disease, as chronic pain often is managed with frequent heating pad or hot water bottle use.2 Additionally, accurate diagnosis is important given the future risk for malignancy, as chronic changes of EAI have been reported to lead to squamous cell carcinoma or rarely Merkel cell carcinoma.2 Erythema ab igne is not traditionally associated with the formation of bullae; however, we present a case of bullous EAI that we believe highlights the importance of including this condition in the differential diagnosis of bullous disorders.
A 55-year-old man was admitted for presumed cellulitis of the bilateral legs. The patient had developed hyperpigmented discoloration of the medial surface of both legs with subsequent formation of tense bullae over the last 2 months. The dermatology department was consulted, as there was concern for bullous pemphigoid. The patient’s medical history was notable for hypertension, hyperlipidemia, diet-controlled type 2 diabetes mellitus, and hepatitis C virus with cirrhosis. The patient denied pruritus, pain, or known exposure of the legs to potential irritants prior to developing the lesions; however, with additional questioning he did report frequently sitting in front of a space heater with bare legs. Physical examination revealed multiple areas of reticulated erythematous hyperpigmentation with several overlying bullae (Figure 1). Many of the bullae were unroofed with full-thickness ulceration. Biopsies were taken for hematoxylin and eosin staining (Figure 2) and direct immunofluorescence.
Basic hematologic and metabolic laboratory test results as well as blood cultures were negative. Wound culture was positive for methicillin-resistant Staphylococcus aureus. Histologic examination showed interface dermatitis with subepidermal vesicle (Figure 2). Scattered necrotic keratinocytes were present in the adjacent epidermis, and focal subtle vacuolar alteration of the dermoepidermal junction was seen (Figure 3). Sparse perivascular mononuclear cells and scattered melanophages were present in the dermis. Direct immunofluorescence showed no diagnostic immunopathologic abnormality. Focal weak nonspecific vascular positivity for IgG and C3 was seen, but IgA and IgM were negative. Although not specific, these changes were compatible with EAI in the clinical context provided. The diagnosis of bullous EAI with superimposed staphylococcal infection was made.
Although rare, there have been reports of a bullous variant of EAI. Flanagan et al4 described 3 cases of bullous EAI with histopathology similar to our case. All 3 biopsies showed subepidermal separation with a mild perivascular dermal lymphocytic infiltrate. Direct immunofluorescence was negative in 2 cases but showed nonspecific weak patchy deposition of IgM along the dermoepidermal junction.4 Although our case was negative for IgM, there was a similar weak nonspecific distribution of IgG. Kokturk et al5 described a case of bullous EAI in a man with repeated exposure to a space heater. The lesions showed subepidermal separation of the epidermis; increased elastic fibers; dilated dermal capillaries; melanophages in the upper dermis; and a mild, superficial, perivascular-lymphocytic infiltrate. Direct immunofluorescence showed no immune deposits.5 Several earlier cases of bullae associated with EAI have been reported in the literature but were thought to be bullous lichen planus superimposed on EAI.6 Our case, which exhibited similar historical, physical, and histopathologic findings, strengthens the argument for a defined bullous variant of EAI.
To the Editor:
Erythema ab igne (EAI) is a reticular erythematous hyperpigmentation of skin repeatedly exposed to moderate heat.1 It usually is asymptomatic, though some patients report itching or burning at the site.2 Historically caused by exposure to coal stoves or open fires, EAI has become increasingly common among individuals using space heaters, heating pads, or laptop computers near bare skin.2,3 Although EAI itself is benign and usually resolves with the removal of the exposure, it remains of clinical importance because of its association with underlying chronic disease, as chronic pain often is managed with frequent heating pad or hot water bottle use.2 Additionally, accurate diagnosis is important given the future risk for malignancy, as chronic changes of EAI have been reported to lead to squamous cell carcinoma or rarely Merkel cell carcinoma.2 Erythema ab igne is not traditionally associated with the formation of bullae; however, we present a case of bullous EAI that we believe highlights the importance of including this condition in the differential diagnosis of bullous disorders.
A 55-year-old man was admitted for presumed cellulitis of the bilateral legs. The patient had developed hyperpigmented discoloration of the medial surface of both legs with subsequent formation of tense bullae over the last 2 months. The dermatology department was consulted, as there was concern for bullous pemphigoid. The patient’s medical history was notable for hypertension, hyperlipidemia, diet-controlled type 2 diabetes mellitus, and hepatitis C virus with cirrhosis. The patient denied pruritus, pain, or known exposure of the legs to potential irritants prior to developing the lesions; however, with additional questioning he did report frequently sitting in front of a space heater with bare legs. Physical examination revealed multiple areas of reticulated erythematous hyperpigmentation with several overlying bullae (Figure 1). Many of the bullae were unroofed with full-thickness ulceration. Biopsies were taken for hematoxylin and eosin staining (Figure 2) and direct immunofluorescence.
Basic hematologic and metabolic laboratory test results as well as blood cultures were negative. Wound culture was positive for methicillin-resistant Staphylococcus aureus. Histologic examination showed interface dermatitis with subepidermal vesicle (Figure 2). Scattered necrotic keratinocytes were present in the adjacent epidermis, and focal subtle vacuolar alteration of the dermoepidermal junction was seen (Figure 3). Sparse perivascular mononuclear cells and scattered melanophages were present in the dermis. Direct immunofluorescence showed no diagnostic immunopathologic abnormality. Focal weak nonspecific vascular positivity for IgG and C3 was seen, but IgA and IgM were negative. Although not specific, these changes were compatible with EAI in the clinical context provided. The diagnosis of bullous EAI with superimposed staphylococcal infection was made.
Although rare, there have been reports of a bullous variant of EAI. Flanagan et al4 described 3 cases of bullous EAI with histopathology similar to our case. All 3 biopsies showed subepidermal separation with a mild perivascular dermal lymphocytic infiltrate. Direct immunofluorescence was negative in 2 cases but showed nonspecific weak patchy deposition of IgM along the dermoepidermal junction.4 Although our case was negative for IgM, there was a similar weak nonspecific distribution of IgG. Kokturk et al5 described a case of bullous EAI in a man with repeated exposure to a space heater. The lesions showed subepidermal separation of the epidermis; increased elastic fibers; dilated dermal capillaries; melanophages in the upper dermis; and a mild, superficial, perivascular-lymphocytic infiltrate. Direct immunofluorescence showed no immune deposits.5 Several earlier cases of bullae associated with EAI have been reported in the literature but were thought to be bullous lichen planus superimposed on EAI.6 Our case, which exhibited similar historical, physical, and histopathologic findings, strengthens the argument for a defined bullous variant of EAI.
- Baruchin AM. Erythema ab igne—a neglected entity? Burns. 1994;20:460-462.
- Arnold AW, Itin PH. Laptop computer−induced erythema ab igne in a child and review of the literature [published online October 4, 2010]. Pediatrics. 2010;126:E1227-E1230.
- Tan S, Bertucci V. Erythema ab igne: an old condition new again. CMAJ. 2000;162:77-78.
- Flanagan N, Watson R, Sweeney E, et al. Bullous erythema ab igne. Br J Dermatol. 1996;134:1159-1160.
- Kokturk A, Kaya TI, Baz K, et al. Bullous erythema ab igne. Dermatol Online J. 2003;9:18.
- Horio T, Imamura S. Bullous lichen planus developed on erythema ab igne. J Dermatol. 1986;13:203-207.
- Baruchin AM. Erythema ab igne—a neglected entity? Burns. 1994;20:460-462.
- Arnold AW, Itin PH. Laptop computer−induced erythema ab igne in a child and review of the literature [published online October 4, 2010]. Pediatrics. 2010;126:E1227-E1230.
- Tan S, Bertucci V. Erythema ab igne: an old condition new again. CMAJ. 2000;162:77-78.
- Flanagan N, Watson R, Sweeney E, et al. Bullous erythema ab igne. Br J Dermatol. 1996;134:1159-1160.
- Kokturk A, Kaya TI, Baz K, et al. Bullous erythema ab igne. Dermatol Online J. 2003;9:18.
- Horio T, Imamura S. Bullous lichen planus developed on erythema ab igne. J Dermatol. 1986;13:203-207.
Practice Points
- Consider erythema ab igne (EAI) as a potential differential diagnosis in bullous eruptions.
- Space heaters, heating pads, and even laptop computers should be considered as potential causes of EAI.
Acne-associated hyperpigmentation an important consideration in patients with skin of color
NEW YORK – When treating patients with skin of color for acne, treatment goals may vary from those of patients with lighter skin, according to Andrew F. Alexis, MD.
For example, in patients with Fitzpatrick skin types V and VI, the desired treatment outcome is not only resolution of acne, but also resolution of hyperpigmentation, said Dr. Alexis, chairman of the department of dermatology at Mount Sinai St. Luke’s and Mount Sinai West, New York, N.Y.
“Postinflammatory hyperpigmentation is often the driving force for the dermatology consult” in individuals with skin of color, Dr. Alexis said at the summer meeting of the American Academy of Dermatology. “They may be just as concerned about their dark spots as underlying acne,” he noted, citing a study that he coauthored (J Clin Aesthet Dermatol. 2014 Jul;7[7]:19-31).
In the study – a survey of patients with acne to determine which treatment outcomes were most important – 41.6% of the nonwhite female patients reported that clearance of postinflammatory hyperpigmentation was the most important goal, compared with 8.4% of white female respondents (P less than .0001).
It’s important to avoid undertreating patients, especially darker-skinned patients, where ongoing subclinical inflammation may contribute to hyperpigmentation. Even in lesions that appear grossly noninflamed, biopsies may find histological evidence of inflammation, with increased T-cell infiltration of the pilosebaceous units, Dr. Alexis said.
However, there’s always a balancing act in determining how aggressively to treat patients, he added. Dermatologists have to be aware of the risk of hypertrophic scar formation in darker-skinned individuals, especially in truncal areas.
When addressing the acne, step one is to aggressively reduce acne-associated inflammation to reduce potential sequelae. This can be done with any of a number of agents, such as retinoids, benzoyl peroxide, dapsone, azelaic acid, and even intralesional corticosteroid injections, he said.
“All agents have been considered in darker skin types,” he said, noting that “retinoids are particularly important because they can also treat postinflammatory hyperpigmentation.” Tretinoin 0.1% cream and tazarotene 0.1% cream are both good choices, he added.
Adapalene in a fixed combination with benzoyl peroxide has been studied in darker-skinned patients, with no difference in tolerability or higher incidence of pigmentary sequelae than in lighter-skinned patients, he pointed out.
Dapsone 5% and 7.5% have also been studied in patients with darker skin, and both concentrations showed comparable results for safety and efficacy.
The thinking about second-line agents can shift a bit when treating acne in darker skin. For example, azelaic acid as a 20% cream or 15% gel can be a good choice, and can be helpful in treating postinflammatory hyperpigmentation, but azelaic acid is “not as good an antiacne agent as retinoids,” Dr. Alexis said.
Patients should understand that any of these choices are primarily acne-directed treatments, to be deployed over the first 3-6 months of treatment. Then, beginning at about the 3-month mark and continuing for up to a year, hyperpigmentation can be addressed. “Really emphasize the duration of treatment,” when treating hyperpigmentation, Dr. Alexis advised.
Once the acne is under control and hyperpigmentation can be assessed on its own, dermatologists can consider whether bleaching agents are appropriate. “Should they be used? If so, how?” he asked.
Bleaching agents can be effective, said Dr. Alexis, who recommends lesion-directed rather than broad-field therapy, unless there are many larger hyperpigmented macules. “The more common scenario is smaller, more distributed lesions,” he said. “Superficial chemical peels, if used with caution, can be a good adjunct,” to bleaching agents, he added.
Coming down the road are topical nitric oxide preparations, which he said are looking good for darker skin in clinical trials.
“The key to great outcomes is to initiate a combination regimen that targets inflammation and reduces hyperpigmentation,” said Dr. Alexis. Then, he advised, minimize irritation but don’t undertreat, consider adjunctive chemical peels, and above all, “set realistic timeline expectations.”
Dr. Alexis reported financial relationships with multiple pharmaceutical companies.
[email protected]
On Twitter @karioakes
NEW YORK – When treating patients with skin of color for acne, treatment goals may vary from those of patients with lighter skin, according to Andrew F. Alexis, MD.
For example, in patients with Fitzpatrick skin types V and VI, the desired treatment outcome is not only resolution of acne, but also resolution of hyperpigmentation, said Dr. Alexis, chairman of the department of dermatology at Mount Sinai St. Luke’s and Mount Sinai West, New York, N.Y.
“Postinflammatory hyperpigmentation is often the driving force for the dermatology consult” in individuals with skin of color, Dr. Alexis said at the summer meeting of the American Academy of Dermatology. “They may be just as concerned about their dark spots as underlying acne,” he noted, citing a study that he coauthored (J Clin Aesthet Dermatol. 2014 Jul;7[7]:19-31).
In the study – a survey of patients with acne to determine which treatment outcomes were most important – 41.6% of the nonwhite female patients reported that clearance of postinflammatory hyperpigmentation was the most important goal, compared with 8.4% of white female respondents (P less than .0001).
It’s important to avoid undertreating patients, especially darker-skinned patients, where ongoing subclinical inflammation may contribute to hyperpigmentation. Even in lesions that appear grossly noninflamed, biopsies may find histological evidence of inflammation, with increased T-cell infiltration of the pilosebaceous units, Dr. Alexis said.
However, there’s always a balancing act in determining how aggressively to treat patients, he added. Dermatologists have to be aware of the risk of hypertrophic scar formation in darker-skinned individuals, especially in truncal areas.
When addressing the acne, step one is to aggressively reduce acne-associated inflammation to reduce potential sequelae. This can be done with any of a number of agents, such as retinoids, benzoyl peroxide, dapsone, azelaic acid, and even intralesional corticosteroid injections, he said.
“All agents have been considered in darker skin types,” he said, noting that “retinoids are particularly important because they can also treat postinflammatory hyperpigmentation.” Tretinoin 0.1% cream and tazarotene 0.1% cream are both good choices, he added.
Adapalene in a fixed combination with benzoyl peroxide has been studied in darker-skinned patients, with no difference in tolerability or higher incidence of pigmentary sequelae than in lighter-skinned patients, he pointed out.
Dapsone 5% and 7.5% have also been studied in patients with darker skin, and both concentrations showed comparable results for safety and efficacy.
The thinking about second-line agents can shift a bit when treating acne in darker skin. For example, azelaic acid as a 20% cream or 15% gel can be a good choice, and can be helpful in treating postinflammatory hyperpigmentation, but azelaic acid is “not as good an antiacne agent as retinoids,” Dr. Alexis said.
Patients should understand that any of these choices are primarily acne-directed treatments, to be deployed over the first 3-6 months of treatment. Then, beginning at about the 3-month mark and continuing for up to a year, hyperpigmentation can be addressed. “Really emphasize the duration of treatment,” when treating hyperpigmentation, Dr. Alexis advised.
Once the acne is under control and hyperpigmentation can be assessed on its own, dermatologists can consider whether bleaching agents are appropriate. “Should they be used? If so, how?” he asked.
Bleaching agents can be effective, said Dr. Alexis, who recommends lesion-directed rather than broad-field therapy, unless there are many larger hyperpigmented macules. “The more common scenario is smaller, more distributed lesions,” he said. “Superficial chemical peels, if used with caution, can be a good adjunct,” to bleaching agents, he added.
Coming down the road are topical nitric oxide preparations, which he said are looking good for darker skin in clinical trials.
“The key to great outcomes is to initiate a combination regimen that targets inflammation and reduces hyperpigmentation,” said Dr. Alexis. Then, he advised, minimize irritation but don’t undertreat, consider adjunctive chemical peels, and above all, “set realistic timeline expectations.”
Dr. Alexis reported financial relationships with multiple pharmaceutical companies.
[email protected]
On Twitter @karioakes
NEW YORK – When treating patients with skin of color for acne, treatment goals may vary from those of patients with lighter skin, according to Andrew F. Alexis, MD.
For example, in patients with Fitzpatrick skin types V and VI, the desired treatment outcome is not only resolution of acne, but also resolution of hyperpigmentation, said Dr. Alexis, chairman of the department of dermatology at Mount Sinai St. Luke’s and Mount Sinai West, New York, N.Y.
“Postinflammatory hyperpigmentation is often the driving force for the dermatology consult” in individuals with skin of color, Dr. Alexis said at the summer meeting of the American Academy of Dermatology. “They may be just as concerned about their dark spots as underlying acne,” he noted, citing a study that he coauthored (J Clin Aesthet Dermatol. 2014 Jul;7[7]:19-31).
In the study – a survey of patients with acne to determine which treatment outcomes were most important – 41.6% of the nonwhite female patients reported that clearance of postinflammatory hyperpigmentation was the most important goal, compared with 8.4% of white female respondents (P less than .0001).
It’s important to avoid undertreating patients, especially darker-skinned patients, where ongoing subclinical inflammation may contribute to hyperpigmentation. Even in lesions that appear grossly noninflamed, biopsies may find histological evidence of inflammation, with increased T-cell infiltration of the pilosebaceous units, Dr. Alexis said.
However, there’s always a balancing act in determining how aggressively to treat patients, he added. Dermatologists have to be aware of the risk of hypertrophic scar formation in darker-skinned individuals, especially in truncal areas.
When addressing the acne, step one is to aggressively reduce acne-associated inflammation to reduce potential sequelae. This can be done with any of a number of agents, such as retinoids, benzoyl peroxide, dapsone, azelaic acid, and even intralesional corticosteroid injections, he said.
“All agents have been considered in darker skin types,” he said, noting that “retinoids are particularly important because they can also treat postinflammatory hyperpigmentation.” Tretinoin 0.1% cream and tazarotene 0.1% cream are both good choices, he added.
Adapalene in a fixed combination with benzoyl peroxide has been studied in darker-skinned patients, with no difference in tolerability or higher incidence of pigmentary sequelae than in lighter-skinned patients, he pointed out.
Dapsone 5% and 7.5% have also been studied in patients with darker skin, and both concentrations showed comparable results for safety and efficacy.
The thinking about second-line agents can shift a bit when treating acne in darker skin. For example, azelaic acid as a 20% cream or 15% gel can be a good choice, and can be helpful in treating postinflammatory hyperpigmentation, but azelaic acid is “not as good an antiacne agent as retinoids,” Dr. Alexis said.
Patients should understand that any of these choices are primarily acne-directed treatments, to be deployed over the first 3-6 months of treatment. Then, beginning at about the 3-month mark and continuing for up to a year, hyperpigmentation can be addressed. “Really emphasize the duration of treatment,” when treating hyperpigmentation, Dr. Alexis advised.
Once the acne is under control and hyperpigmentation can be assessed on its own, dermatologists can consider whether bleaching agents are appropriate. “Should they be used? If so, how?” he asked.
Bleaching agents can be effective, said Dr. Alexis, who recommends lesion-directed rather than broad-field therapy, unless there are many larger hyperpigmented macules. “The more common scenario is smaller, more distributed lesions,” he said. “Superficial chemical peels, if used with caution, can be a good adjunct,” to bleaching agents, he added.
Coming down the road are topical nitric oxide preparations, which he said are looking good for darker skin in clinical trials.
“The key to great outcomes is to initiate a combination regimen that targets inflammation and reduces hyperpigmentation,” said Dr. Alexis. Then, he advised, minimize irritation but don’t undertreat, consider adjunctive chemical peels, and above all, “set realistic timeline expectations.”
Dr. Alexis reported financial relationships with multiple pharmaceutical companies.
[email protected]
On Twitter @karioakes
EXPERT ANALYSIS FROM THE 2017 SUMMER AAD MEETING
Cardiovascular risk factors more common in girls
Girls were more likely than boys to have cardiovascular disease risk factors such as poor aerobic capacity and a high percentage of body fat in a study involving almost 1,800 elementary school students.
Using the FITNESSGRAM Healthy Fitness Zone (HFZ) standards in 1,775 fourth- and fifth-grade students (879 boys, 896 girls) from an urban, predominantly black population, investigators found that significantly more girls than boys did not meet the HFZ for aerobic capacity (71% vs. 42%), percent body fat (53% vs. 30%), and body mass index (44% vs. 34%). Those who did not meet the HFZ for each measure were classified as “needs improvement” or “needs improvement – health risk.”
Overall, more than 66% of the study sample “had metabolic syndrome risk factors based on FITNESSGRAM assessments,” said Susan B. Racette, PhD, of Washington University, St. Louis, and her associates (Prev Med. 2017. doi: 10.1016/j.ypmed.2017.07.032).
More than half of the girls (51%) didn’t meet the HFZ for aerobic capacity and one of the body composition measures, compared with 32% of the boys, and 38% of the girls failed to meet the HFZ for all three measures, compared with 21% of the boys. The reverse side of that coin – those who did meet the HFZ for all three – favored the boys, 46% to 21%, the investigators reported.
“The presence of these cardiovascular disease risk factors in girls, in particular, highlights an important need for creative strategies to mitigate the long-term health and societal consequences of these modifiable risk factors,” Dr. Racette and her associates wrote.
This work was supported by the U.S. Department of Education and the Washington University division of biostatistics. The investigators said that they had no conflicts of interest.
Girls were more likely than boys to have cardiovascular disease risk factors such as poor aerobic capacity and a high percentage of body fat in a study involving almost 1,800 elementary school students.
Using the FITNESSGRAM Healthy Fitness Zone (HFZ) standards in 1,775 fourth- and fifth-grade students (879 boys, 896 girls) from an urban, predominantly black population, investigators found that significantly more girls than boys did not meet the HFZ for aerobic capacity (71% vs. 42%), percent body fat (53% vs. 30%), and body mass index (44% vs. 34%). Those who did not meet the HFZ for each measure were classified as “needs improvement” or “needs improvement – health risk.”
Overall, more than 66% of the study sample “had metabolic syndrome risk factors based on FITNESSGRAM assessments,” said Susan B. Racette, PhD, of Washington University, St. Louis, and her associates (Prev Med. 2017. doi: 10.1016/j.ypmed.2017.07.032).
More than half of the girls (51%) didn’t meet the HFZ for aerobic capacity and one of the body composition measures, compared with 32% of the boys, and 38% of the girls failed to meet the HFZ for all three measures, compared with 21% of the boys. The reverse side of that coin – those who did meet the HFZ for all three – favored the boys, 46% to 21%, the investigators reported.
“The presence of these cardiovascular disease risk factors in girls, in particular, highlights an important need for creative strategies to mitigate the long-term health and societal consequences of these modifiable risk factors,” Dr. Racette and her associates wrote.
This work was supported by the U.S. Department of Education and the Washington University division of biostatistics. The investigators said that they had no conflicts of interest.
Girls were more likely than boys to have cardiovascular disease risk factors such as poor aerobic capacity and a high percentage of body fat in a study involving almost 1,800 elementary school students.
Using the FITNESSGRAM Healthy Fitness Zone (HFZ) standards in 1,775 fourth- and fifth-grade students (879 boys, 896 girls) from an urban, predominantly black population, investigators found that significantly more girls than boys did not meet the HFZ for aerobic capacity (71% vs. 42%), percent body fat (53% vs. 30%), and body mass index (44% vs. 34%). Those who did not meet the HFZ for each measure were classified as “needs improvement” or “needs improvement – health risk.”
Overall, more than 66% of the study sample “had metabolic syndrome risk factors based on FITNESSGRAM assessments,” said Susan B. Racette, PhD, of Washington University, St. Louis, and her associates (Prev Med. 2017. doi: 10.1016/j.ypmed.2017.07.032).
More than half of the girls (51%) didn’t meet the HFZ for aerobic capacity and one of the body composition measures, compared with 32% of the boys, and 38% of the girls failed to meet the HFZ for all three measures, compared with 21% of the boys. The reverse side of that coin – those who did meet the HFZ for all three – favored the boys, 46% to 21%, the investigators reported.
“The presence of these cardiovascular disease risk factors in girls, in particular, highlights an important need for creative strategies to mitigate the long-term health and societal consequences of these modifiable risk factors,” Dr. Racette and her associates wrote.
This work was supported by the U.S. Department of Education and the Washington University division of biostatistics. The investigators said that they had no conflicts of interest.
FROM PREVENTIVE MEDICINE
Alcohol use, high-risk drinking increases in U.S. to ‘crisis’ levels
Nearly one in eight adults in the United States had been diagnosed with alcohol use disorder in 2012-2013, a nearly 50% increase from a decade earlier, according to a study published Aug. 9. Other substantial increases occurring across virtually all demographic groups included overall 12-month alcohol consumption and high-risk drinking, particularly among adults aged 65 and older, racial/ethnic minorities, women, and those with lower education and incomes.
“The marked increases in high-risk drinking and DSM-IV [alcohol use disorder] between 2001-2002 and 2012-2013 also mirror recent sharp increases in morbidity and mortality from diseases and injuries in which alcohol use has a substantial role or deceleration of previously seen declines,” wrote Bridget F. Grant, PhD, of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in Rockville, Md., and her associates. High-risk drinking was defined as five drinks (14 g of ethanol each) per occasion for men and four drinks per occasion for women at least weekly.
“Mortality among alcohol-affected drivers who were simultaneously distracted also increased between 2005 and 2009 by 63%,” they wrote (JAMA Psychiatry. 2017 Aug 9. doi: 10.1001/jamapsychiatry.2017.2161).
The researchers analyzed data from 43,093 respondents to the National Epidemiologic Survey on Alcohol and Related Conditions (April 2001-June 2002) and from 36,309 respondents to the National Epidemiologic Survey on Alcohol and Related Conditions III (April 2012-June 2013). Both surveys involved face-to-face interviews with a nationally representative sample of U.S. adults.
The findings showed that 12-month alcohol use had increased 11.2% between 2001-2002 and 2012-2013, from 65.4% to 72.7%. A substantial increase also occurred in high-risk drinking and alcohol use disorder as defined in the DSM-IV. High-risk drinking increased 29.9% during that time, from 9.7% to 12.6%, representing an increase of approximately 9.4 million Americans engaging in high-risk drinking.
Alcohol use disorder (AUD) increased 49.4%, from 8.5% to 12.7% – a percentage that accounts for an additional 12.3 million Americans with the diagnosis. That increase dwarfs the 14.8% increase in alcohol use disorder that was seen between 1991-1992 and 2001-2002, the authors pointed out. The prevalence of 12-month AUD rose significantly among adults aged 65 and older (106.7%), African American individuals (92.8%), and women (83.7%). Interestingly, all subgroups reported significant increases in AUD except for Native Americans and people living in rural areas. By comparison, the 12-month prevalence of AUD among men increased by a third (34.7%), and their high-risk drinking increased 15.5%.
“Drinking norms and values have become more permissive among women, along with increases in educational and occupational opportunities and rising numbers of women in the workforce, all of which may have contributed to increased high-risk drinking and AUD in women during the past decade,” the authors wrote. “Stress associated with pursuing a career and raising a family may lead to increases in high-risk drinking and AUD among women.”
These increases indicate potential future increases among women in alcohol-related conditions, such as breast cancer and liver cirrhosis. Increases may also occur in fetal alcohol spectrum disorder and exposure to violence, the authors wrote.
The increases in alcohol use, high-risk drinking, and AUD found among minorities may be related to increased stress and demoralization as wealth inequality widened between minorities and whites in the wake of the 2008 recession. Other inequalities, such as income and educational disparities, unemployment, residential segregation, discrimination, and less health care access may also play a role in those increases, the authors wrote.
One limitation of the study is that certain populations were not surveyed, such as homeless individuals and people who are incarcerated. This means that the prevalence of alcohol use, high-risk drinking, and AUD could be underestimated, Dr. Grant and her colleagues said. However, they said, the large sample sizes of the surveys might balance out that limitation and others.
Nevertheless, the increases found in alcohol use, high-risk drinking, and AUD “constitute a public health crisis that may be overshadowed by increases in much less prevalent substance use (marijuana, opiates, and heroin) during the same period,” Dr. Grant and her colleagues wrote. “The findings herein highlight the urgency of educating the public, policymakers, and health care professionals about high-risk drinking and AUD.” In addition, they called for broader effors to address the “individual, biological, environmental, and societal factors” influencing high-risk drinking and AUD.
The research was sponsored by the NIAAA, and funded by the National Institutes of Health. The authors reported having no disclosures.
“This timely article by Grant et al. ... makes a compelling case that the United States is facing a crisis with alcohol use, one that is currently costly and about to get worse,” Marc A. Schuckit, MD, wrote in an accompanying editorial (JAMA Psychiatry. 2017 Aug 9. doi: 10.1001/jamapsychiatry.2017.1981). However, he said, several studies show that lowering the risk for future alcohol-related problems in 18 year olds is possible.
He said his group delivered an intervention to 500 college freshmen using Internet-based videos aimed at helping them “recognize their vulnerability toward heavy drinking.” Six and 12 months after watching four 50-minute videos, the effects on how much the students drank remained significant, he wrote. In addition, other studies have identified programs that help lower drinking during pregnancy. “These are only a few examples of ongoing hopeful developments,” Dr. Schuckit wrote.
The number in the study that is especially concerning for him, Dr. Schuckit said, is the 106% increase in AUDs among older individuals because of the many preexisting medical disorders “that can be exacerbated by heavier drinking. These drinkers are also likely to be taking multiple medications that can interact adversely with alcohol, with resulting significant and costly health consequences,” according to Dr. Schuckit.
“There is also some disturbing news,” he wrote. “The proposed cuts to the National Institutes of Health budget being considered in Washington in 2017 are potentially disastrous for future efforts to decrease alcohol problems and are likely to result in higher costs for us all. Efforts to identify risk factors for substance-related problems and to test prevention approaches take time and money and are less likely to be funded in the current financial atmosphere. … If we ignore these problems, they will come back to us at much higher costs through emergency department visits, impaired children … and higher costs for jails and prisons that are the last resort for help for many.”
Dr. Schuckit is affiliated with the department of psychiatry at the University of California, San Diego. He reported having no disclosures.
“This timely article by Grant et al. ... makes a compelling case that the United States is facing a crisis with alcohol use, one that is currently costly and about to get worse,” Marc A. Schuckit, MD, wrote in an accompanying editorial (JAMA Psychiatry. 2017 Aug 9. doi: 10.1001/jamapsychiatry.2017.1981). However, he said, several studies show that lowering the risk for future alcohol-related problems in 18 year olds is possible.
He said his group delivered an intervention to 500 college freshmen using Internet-based videos aimed at helping them “recognize their vulnerability toward heavy drinking.” Six and 12 months after watching four 50-minute videos, the effects on how much the students drank remained significant, he wrote. In addition, other studies have identified programs that help lower drinking during pregnancy. “These are only a few examples of ongoing hopeful developments,” Dr. Schuckit wrote.
The number in the study that is especially concerning for him, Dr. Schuckit said, is the 106% increase in AUDs among older individuals because of the many preexisting medical disorders “that can be exacerbated by heavier drinking. These drinkers are also likely to be taking multiple medications that can interact adversely with alcohol, with resulting significant and costly health consequences,” according to Dr. Schuckit.
“There is also some disturbing news,” he wrote. “The proposed cuts to the National Institutes of Health budget being considered in Washington in 2017 are potentially disastrous for future efforts to decrease alcohol problems and are likely to result in higher costs for us all. Efforts to identify risk factors for substance-related problems and to test prevention approaches take time and money and are less likely to be funded in the current financial atmosphere. … If we ignore these problems, they will come back to us at much higher costs through emergency department visits, impaired children … and higher costs for jails and prisons that are the last resort for help for many.”
Dr. Schuckit is affiliated with the department of psychiatry at the University of California, San Diego. He reported having no disclosures.
“This timely article by Grant et al. ... makes a compelling case that the United States is facing a crisis with alcohol use, one that is currently costly and about to get worse,” Marc A. Schuckit, MD, wrote in an accompanying editorial (JAMA Psychiatry. 2017 Aug 9. doi: 10.1001/jamapsychiatry.2017.1981). However, he said, several studies show that lowering the risk for future alcohol-related problems in 18 year olds is possible.
He said his group delivered an intervention to 500 college freshmen using Internet-based videos aimed at helping them “recognize their vulnerability toward heavy drinking.” Six and 12 months after watching four 50-minute videos, the effects on how much the students drank remained significant, he wrote. In addition, other studies have identified programs that help lower drinking during pregnancy. “These are only a few examples of ongoing hopeful developments,” Dr. Schuckit wrote.
The number in the study that is especially concerning for him, Dr. Schuckit said, is the 106% increase in AUDs among older individuals because of the many preexisting medical disorders “that can be exacerbated by heavier drinking. These drinkers are also likely to be taking multiple medications that can interact adversely with alcohol, with resulting significant and costly health consequences,” according to Dr. Schuckit.
“There is also some disturbing news,” he wrote. “The proposed cuts to the National Institutes of Health budget being considered in Washington in 2017 are potentially disastrous for future efforts to decrease alcohol problems and are likely to result in higher costs for us all. Efforts to identify risk factors for substance-related problems and to test prevention approaches take time and money and are less likely to be funded in the current financial atmosphere. … If we ignore these problems, they will come back to us at much higher costs through emergency department visits, impaired children … and higher costs for jails and prisons that are the last resort for help for many.”
Dr. Schuckit is affiliated with the department of psychiatry at the University of California, San Diego. He reported having no disclosures.
Nearly one in eight adults in the United States had been diagnosed with alcohol use disorder in 2012-2013, a nearly 50% increase from a decade earlier, according to a study published Aug. 9. Other substantial increases occurring across virtually all demographic groups included overall 12-month alcohol consumption and high-risk drinking, particularly among adults aged 65 and older, racial/ethnic minorities, women, and those with lower education and incomes.
“The marked increases in high-risk drinking and DSM-IV [alcohol use disorder] between 2001-2002 and 2012-2013 also mirror recent sharp increases in morbidity and mortality from diseases and injuries in which alcohol use has a substantial role or deceleration of previously seen declines,” wrote Bridget F. Grant, PhD, of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in Rockville, Md., and her associates. High-risk drinking was defined as five drinks (14 g of ethanol each) per occasion for men and four drinks per occasion for women at least weekly.
“Mortality among alcohol-affected drivers who were simultaneously distracted also increased between 2005 and 2009 by 63%,” they wrote (JAMA Psychiatry. 2017 Aug 9. doi: 10.1001/jamapsychiatry.2017.2161).
The researchers analyzed data from 43,093 respondents to the National Epidemiologic Survey on Alcohol and Related Conditions (April 2001-June 2002) and from 36,309 respondents to the National Epidemiologic Survey on Alcohol and Related Conditions III (April 2012-June 2013). Both surveys involved face-to-face interviews with a nationally representative sample of U.S. adults.
The findings showed that 12-month alcohol use had increased 11.2% between 2001-2002 and 2012-2013, from 65.4% to 72.7%. A substantial increase also occurred in high-risk drinking and alcohol use disorder as defined in the DSM-IV. High-risk drinking increased 29.9% during that time, from 9.7% to 12.6%, representing an increase of approximately 9.4 million Americans engaging in high-risk drinking.
Alcohol use disorder (AUD) increased 49.4%, from 8.5% to 12.7% – a percentage that accounts for an additional 12.3 million Americans with the diagnosis. That increase dwarfs the 14.8% increase in alcohol use disorder that was seen between 1991-1992 and 2001-2002, the authors pointed out. The prevalence of 12-month AUD rose significantly among adults aged 65 and older (106.7%), African American individuals (92.8%), and women (83.7%). Interestingly, all subgroups reported significant increases in AUD except for Native Americans and people living in rural areas. By comparison, the 12-month prevalence of AUD among men increased by a third (34.7%), and their high-risk drinking increased 15.5%.
“Drinking norms and values have become more permissive among women, along with increases in educational and occupational opportunities and rising numbers of women in the workforce, all of which may have contributed to increased high-risk drinking and AUD in women during the past decade,” the authors wrote. “Stress associated with pursuing a career and raising a family may lead to increases in high-risk drinking and AUD among women.”
These increases indicate potential future increases among women in alcohol-related conditions, such as breast cancer and liver cirrhosis. Increases may also occur in fetal alcohol spectrum disorder and exposure to violence, the authors wrote.
The increases in alcohol use, high-risk drinking, and AUD found among minorities may be related to increased stress and demoralization as wealth inequality widened between minorities and whites in the wake of the 2008 recession. Other inequalities, such as income and educational disparities, unemployment, residential segregation, discrimination, and less health care access may also play a role in those increases, the authors wrote.
One limitation of the study is that certain populations were not surveyed, such as homeless individuals and people who are incarcerated. This means that the prevalence of alcohol use, high-risk drinking, and AUD could be underestimated, Dr. Grant and her colleagues said. However, they said, the large sample sizes of the surveys might balance out that limitation and others.
Nevertheless, the increases found in alcohol use, high-risk drinking, and AUD “constitute a public health crisis that may be overshadowed by increases in much less prevalent substance use (marijuana, opiates, and heroin) during the same period,” Dr. Grant and her colleagues wrote. “The findings herein highlight the urgency of educating the public, policymakers, and health care professionals about high-risk drinking and AUD.” In addition, they called for broader effors to address the “individual, biological, environmental, and societal factors” influencing high-risk drinking and AUD.
The research was sponsored by the NIAAA, and funded by the National Institutes of Health. The authors reported having no disclosures.
Nearly one in eight adults in the United States had been diagnosed with alcohol use disorder in 2012-2013, a nearly 50% increase from a decade earlier, according to a study published Aug. 9. Other substantial increases occurring across virtually all demographic groups included overall 12-month alcohol consumption and high-risk drinking, particularly among adults aged 65 and older, racial/ethnic minorities, women, and those with lower education and incomes.
“The marked increases in high-risk drinking and DSM-IV [alcohol use disorder] between 2001-2002 and 2012-2013 also mirror recent sharp increases in morbidity and mortality from diseases and injuries in which alcohol use has a substantial role or deceleration of previously seen declines,” wrote Bridget F. Grant, PhD, of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in Rockville, Md., and her associates. High-risk drinking was defined as five drinks (14 g of ethanol each) per occasion for men and four drinks per occasion for women at least weekly.
“Mortality among alcohol-affected drivers who were simultaneously distracted also increased between 2005 and 2009 by 63%,” they wrote (JAMA Psychiatry. 2017 Aug 9. doi: 10.1001/jamapsychiatry.2017.2161).
The researchers analyzed data from 43,093 respondents to the National Epidemiologic Survey on Alcohol and Related Conditions (April 2001-June 2002) and from 36,309 respondents to the National Epidemiologic Survey on Alcohol and Related Conditions III (April 2012-June 2013). Both surveys involved face-to-face interviews with a nationally representative sample of U.S. adults.
The findings showed that 12-month alcohol use had increased 11.2% between 2001-2002 and 2012-2013, from 65.4% to 72.7%. A substantial increase also occurred in high-risk drinking and alcohol use disorder as defined in the DSM-IV. High-risk drinking increased 29.9% during that time, from 9.7% to 12.6%, representing an increase of approximately 9.4 million Americans engaging in high-risk drinking.
Alcohol use disorder (AUD) increased 49.4%, from 8.5% to 12.7% – a percentage that accounts for an additional 12.3 million Americans with the diagnosis. That increase dwarfs the 14.8% increase in alcohol use disorder that was seen between 1991-1992 and 2001-2002, the authors pointed out. The prevalence of 12-month AUD rose significantly among adults aged 65 and older (106.7%), African American individuals (92.8%), and women (83.7%). Interestingly, all subgroups reported significant increases in AUD except for Native Americans and people living in rural areas. By comparison, the 12-month prevalence of AUD among men increased by a third (34.7%), and their high-risk drinking increased 15.5%.
“Drinking norms and values have become more permissive among women, along with increases in educational and occupational opportunities and rising numbers of women in the workforce, all of which may have contributed to increased high-risk drinking and AUD in women during the past decade,” the authors wrote. “Stress associated with pursuing a career and raising a family may lead to increases in high-risk drinking and AUD among women.”
These increases indicate potential future increases among women in alcohol-related conditions, such as breast cancer and liver cirrhosis. Increases may also occur in fetal alcohol spectrum disorder and exposure to violence, the authors wrote.
The increases in alcohol use, high-risk drinking, and AUD found among minorities may be related to increased stress and demoralization as wealth inequality widened between minorities and whites in the wake of the 2008 recession. Other inequalities, such as income and educational disparities, unemployment, residential segregation, discrimination, and less health care access may also play a role in those increases, the authors wrote.
One limitation of the study is that certain populations were not surveyed, such as homeless individuals and people who are incarcerated. This means that the prevalence of alcohol use, high-risk drinking, and AUD could be underestimated, Dr. Grant and her colleagues said. However, they said, the large sample sizes of the surveys might balance out that limitation and others.
Nevertheless, the increases found in alcohol use, high-risk drinking, and AUD “constitute a public health crisis that may be overshadowed by increases in much less prevalent substance use (marijuana, opiates, and heroin) during the same period,” Dr. Grant and her colleagues wrote. “The findings herein highlight the urgency of educating the public, policymakers, and health care professionals about high-risk drinking and AUD.” In addition, they called for broader effors to address the “individual, biological, environmental, and societal factors” influencing high-risk drinking and AUD.
The research was sponsored by the NIAAA, and funded by the National Institutes of Health. The authors reported having no disclosures.
FROM JAMA PSYCHIATRY
Key clinical point: Drinking and alcohol use disorder have substantially increased across virtually all demographic groups, particularly racial/ethnic minorities, adults aged 65 and older, and women.
Major finding: High-risk drinking increased 9.7%, and alcohol use disorder increased 49.4% among U.S. adults between 2001-2002 and 2012-2013.
Data source: The findings are based on data from 43,093 U.S. adults in 2001-2002 and 36,309 U.S. adults in 2012-2013.
Disclosures: The research was sponsored by the National Institute on Alcohol Abuse and Alcoholism, and funded by the National Institutes of Health. The authors reported having no disclosures.