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Prenatal Antibiotics May Increase Seborrheic Dermatitis Risk in Babies
, but this association was not as strong for childhood-onset SD.
The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.
SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”
In a previous study, she and colleagues showed that exposure to antibiotics both in utero and during the first 90 days of life increases the risk for atopic dermatitis (AD) in children, with risk being highest with exposure to penicillin even among children whose mothers did not have a history of AD.
For the current study, the researchers drew from a large electronic medical records database in the United Kingdom to perform a prospective cohort analysis of mother-child pairs that used proportional hazards models to examine the association between maternal in utero antibiotic exposure and SD in the child. The population included 1,023,140 children with linked maternal data who were followed for a mean of 10.2 years, which amounts to more than 10-million-person years of data. At baseline, the mean age of mothers was 28 years, 3% had SD, 14% had AD, and 51% of the children were male.
In unadjusted analyses, mothers with SD were more likely to receive an antibiotic during pregnancy than were those who did not have SD (odds ratio [OR], 1.42; 95% CI, 1.39-1.46). In addition, maternal in utero exposure to any antibiotic was associated with an increased risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) but less for childhood-onset SD (OR, 1.26; 95% CI, 1.20-1.32). “This effect changed little after adjustment and was still observed if mothers with SD and their babies were excluded,” the authors wrote in their poster abstract.
Any penicillin exposure during pregnancy increased the likelihood of a child having SD (OR, 1.54; 95% CI, 1.50-1.59), with the greater risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) than for childhood-onset SD (OR, 1.25; 95% CI, 1.18-1.32). “The trimester of the in utero penicillin exposure did not seem to affect the association with SD,” the authors wrote. The risk was also increased with cephalosporin exposure but was less for sulfonamides and not for childhood-onset SD.
“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”
She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.
Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.
A version of this article appeared on Medscape.com .
, but this association was not as strong for childhood-onset SD.
The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.
SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”
In a previous study, she and colleagues showed that exposure to antibiotics both in utero and during the first 90 days of life increases the risk for atopic dermatitis (AD) in children, with risk being highest with exposure to penicillin even among children whose mothers did not have a history of AD.
For the current study, the researchers drew from a large electronic medical records database in the United Kingdom to perform a prospective cohort analysis of mother-child pairs that used proportional hazards models to examine the association between maternal in utero antibiotic exposure and SD in the child. The population included 1,023,140 children with linked maternal data who were followed for a mean of 10.2 years, which amounts to more than 10-million-person years of data. At baseline, the mean age of mothers was 28 years, 3% had SD, 14% had AD, and 51% of the children were male.
In unadjusted analyses, mothers with SD were more likely to receive an antibiotic during pregnancy than were those who did not have SD (odds ratio [OR], 1.42; 95% CI, 1.39-1.46). In addition, maternal in utero exposure to any antibiotic was associated with an increased risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) but less for childhood-onset SD (OR, 1.26; 95% CI, 1.20-1.32). “This effect changed little after adjustment and was still observed if mothers with SD and their babies were excluded,” the authors wrote in their poster abstract.
Any penicillin exposure during pregnancy increased the likelihood of a child having SD (OR, 1.54; 95% CI, 1.50-1.59), with the greater risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) than for childhood-onset SD (OR, 1.25; 95% CI, 1.18-1.32). “The trimester of the in utero penicillin exposure did not seem to affect the association with SD,” the authors wrote. The risk was also increased with cephalosporin exposure but was less for sulfonamides and not for childhood-onset SD.
“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”
She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.
Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.
A version of this article appeared on Medscape.com .
, but this association was not as strong for childhood-onset SD.
The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.
SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”
In a previous study, she and colleagues showed that exposure to antibiotics both in utero and during the first 90 days of life increases the risk for atopic dermatitis (AD) in children, with risk being highest with exposure to penicillin even among children whose mothers did not have a history of AD.
For the current study, the researchers drew from a large electronic medical records database in the United Kingdom to perform a prospective cohort analysis of mother-child pairs that used proportional hazards models to examine the association between maternal in utero antibiotic exposure and SD in the child. The population included 1,023,140 children with linked maternal data who were followed for a mean of 10.2 years, which amounts to more than 10-million-person years of data. At baseline, the mean age of mothers was 28 years, 3% had SD, 14% had AD, and 51% of the children were male.
In unadjusted analyses, mothers with SD were more likely to receive an antibiotic during pregnancy than were those who did not have SD (odds ratio [OR], 1.42; 95% CI, 1.39-1.46). In addition, maternal in utero exposure to any antibiotic was associated with an increased risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) but less for childhood-onset SD (OR, 1.26; 95% CI, 1.20-1.32). “This effect changed little after adjustment and was still observed if mothers with SD and their babies were excluded,” the authors wrote in their poster abstract.
Any penicillin exposure during pregnancy increased the likelihood of a child having SD (OR, 1.54; 95% CI, 1.50-1.59), with the greater risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) than for childhood-onset SD (OR, 1.25; 95% CI, 1.18-1.32). “The trimester of the in utero penicillin exposure did not seem to affect the association with SD,” the authors wrote. The risk was also increased with cephalosporin exposure but was less for sulfonamides and not for childhood-onset SD.
“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”
She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.
Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.
A version of this article appeared on Medscape.com .
FROM SID 2024
Teen Cannabis Use Tied to Dramatic Increased Risk for Psychosis
, new research showed.
Investigators at the University of Toronto, The Centre for Addiction and Mental Health (CAMH), and the Institute for Clinical Evaluative Sciences (ICES), in Canada, linked recent population-based survey data from more than 11,000 youngsters to health service use records, including hospitalizations, emergency department (ED) visits, and outpatient visits.
“We found a very strong association between cannabis use and risk of psychotic disorder in adolescence [although] surprisingly, we didn’t find evidence of association in young adulthood,” lead author André J. McDonald, PhD, currently a postdoctoral fellow at the Peter Boris Centre for Addictions Research and the Michael G. DeGroote Centre for Medicinal Cannabis Research, McMaster University, Hamilton, Ontario, Canada, said in a news release.
“These findings are consistent with the neurodevelopmental theory that teens are especially vulnerable to the effects of cannabis,” said Dr. McDonald, who conducted the research.
The study was published online in Psychological Medicine.
Increased Potency
“Epidemiologic research suggests that cannabis use may be a significant risk factor for psychotic disorders,” the authors wrote. However, methodological limitations of previous studies make it difficult to estimate the strength of association, with the current evidence base relying largely on cannabis use during the twentieth century, when the drug was “significantly less potent.” It’s plausible that the strength of association has increased due to increased cannabis potency.
The researchers believe youth cannabis use and psychotic disorders is “a critical public health issue,” especially as more jurisdictions liberalize cannabis use and the perception of harm declines among youth.
To estimate the association between cannabis use during youth and the risk for a psychotic disorder diagnosis, using recent population-based data, they used data from the 2009-2012 cycles of the Canadian Community Health Survey (CCHS) linked to administrative health data at ICES to study noninstitutionalized Ontario residents, aged 12-24 years, who had completed the CCHS during that period.
They excluded respondents who used health services for psychotic disorders during the 6 years prior to their CCHS interview date.
Respondents (n = 11,363; 51% men; mean age [SD], 18.3 [15.2-21.3] years) were followed for 6-9 years, with days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder as the primary outcome.
The researchers estimated age-specific hazard ratios during adolescence (12-19 years) and young adulthood (20-33 years) and conducted sensitivity analyses to explore alternative model conditions, including restricting the outcome to hospitalizations and ED visits, to increase specificity.
Compared with no cannabis use, cannabis use was significantly associated with an 11-fold increased risk for psychotic disorders during adolescence, although not during young adulthood (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6-27.3 and aHR, 1.3; 95% CI, 0.6-2.6, respectively).
Perception of Harm Declining
When the researchers restricted the outcome to hospitalizations and ED visits only, the strength of association “increased markedly” during adolescence, with a 26-fold higher association in cannabis users than in nonusers (aHR, 26.7; 95% CI, 7.7-92.8). However, there was no meaningful change during young adulthood (aHR, 1.8; 95% CI, 0.6-5.4).
“Many have hypothesized that adolescence is a more sensitive risk period than adulthood for the effect of cannabis use on psychotic disorder development, yet prior to this study, little epidemiologic evidence existed to support this view,” the authors wrote.
The data also suggest that cannabis use is “more strongly associated with more severe psychotic outcomes, as the strength of association during adolescence increased markedly when we restricted the outcome to hospitalizations and ED visits (the most severe types of health service use),” the investigators noted.
The authors noted several limitations. For instance, it’s unclear to what extent unmeasured confounders including genetic predisposition, family history of psychotic disorders, and trauma might have biased the results. In addition, they could not assess the potential confounding impact of genetic predisposition to psychotic disorders. The possibility of reverse causality also cannot be ruled out. It’s possible, they noted, that individuals with “psychotic dispositions” may self-medicate or show greater disposition to cannabis use.
Moreover, the dataset neither captured important factors regarding the cannabis itself, including delta-9-tetrahydrocannabinol potency, mode of use, product type, or cannabis dependence, nor captured institutionalized and homeless youth.
Nevertheless, they pointed to the findings as supporting a “precautionary principle” — as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, the findings suggest that evidence-based cannabis prevention strategies for adolescents are warranted.
This study was supported by CAMH, the University of Toronto, and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. The authors declared no relevant financial relationships.
A version of this article appeared on Medscape.com.
, new research showed.
Investigators at the University of Toronto, The Centre for Addiction and Mental Health (CAMH), and the Institute for Clinical Evaluative Sciences (ICES), in Canada, linked recent population-based survey data from more than 11,000 youngsters to health service use records, including hospitalizations, emergency department (ED) visits, and outpatient visits.
“We found a very strong association between cannabis use and risk of psychotic disorder in adolescence [although] surprisingly, we didn’t find evidence of association in young adulthood,” lead author André J. McDonald, PhD, currently a postdoctoral fellow at the Peter Boris Centre for Addictions Research and the Michael G. DeGroote Centre for Medicinal Cannabis Research, McMaster University, Hamilton, Ontario, Canada, said in a news release.
“These findings are consistent with the neurodevelopmental theory that teens are especially vulnerable to the effects of cannabis,” said Dr. McDonald, who conducted the research.
The study was published online in Psychological Medicine.
Increased Potency
“Epidemiologic research suggests that cannabis use may be a significant risk factor for psychotic disorders,” the authors wrote. However, methodological limitations of previous studies make it difficult to estimate the strength of association, with the current evidence base relying largely on cannabis use during the twentieth century, when the drug was “significantly less potent.” It’s plausible that the strength of association has increased due to increased cannabis potency.
The researchers believe youth cannabis use and psychotic disorders is “a critical public health issue,” especially as more jurisdictions liberalize cannabis use and the perception of harm declines among youth.
To estimate the association between cannabis use during youth and the risk for a psychotic disorder diagnosis, using recent population-based data, they used data from the 2009-2012 cycles of the Canadian Community Health Survey (CCHS) linked to administrative health data at ICES to study noninstitutionalized Ontario residents, aged 12-24 years, who had completed the CCHS during that period.
They excluded respondents who used health services for psychotic disorders during the 6 years prior to their CCHS interview date.
Respondents (n = 11,363; 51% men; mean age [SD], 18.3 [15.2-21.3] years) were followed for 6-9 years, with days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder as the primary outcome.
The researchers estimated age-specific hazard ratios during adolescence (12-19 years) and young adulthood (20-33 years) and conducted sensitivity analyses to explore alternative model conditions, including restricting the outcome to hospitalizations and ED visits, to increase specificity.
Compared with no cannabis use, cannabis use was significantly associated with an 11-fold increased risk for psychotic disorders during adolescence, although not during young adulthood (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6-27.3 and aHR, 1.3; 95% CI, 0.6-2.6, respectively).
Perception of Harm Declining
When the researchers restricted the outcome to hospitalizations and ED visits only, the strength of association “increased markedly” during adolescence, with a 26-fold higher association in cannabis users than in nonusers (aHR, 26.7; 95% CI, 7.7-92.8). However, there was no meaningful change during young adulthood (aHR, 1.8; 95% CI, 0.6-5.4).
“Many have hypothesized that adolescence is a more sensitive risk period than adulthood for the effect of cannabis use on psychotic disorder development, yet prior to this study, little epidemiologic evidence existed to support this view,” the authors wrote.
The data also suggest that cannabis use is “more strongly associated with more severe psychotic outcomes, as the strength of association during adolescence increased markedly when we restricted the outcome to hospitalizations and ED visits (the most severe types of health service use),” the investigators noted.
The authors noted several limitations. For instance, it’s unclear to what extent unmeasured confounders including genetic predisposition, family history of psychotic disorders, and trauma might have biased the results. In addition, they could not assess the potential confounding impact of genetic predisposition to psychotic disorders. The possibility of reverse causality also cannot be ruled out. It’s possible, they noted, that individuals with “psychotic dispositions” may self-medicate or show greater disposition to cannabis use.
Moreover, the dataset neither captured important factors regarding the cannabis itself, including delta-9-tetrahydrocannabinol potency, mode of use, product type, or cannabis dependence, nor captured institutionalized and homeless youth.
Nevertheless, they pointed to the findings as supporting a “precautionary principle” — as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, the findings suggest that evidence-based cannabis prevention strategies for adolescents are warranted.
This study was supported by CAMH, the University of Toronto, and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. The authors declared no relevant financial relationships.
A version of this article appeared on Medscape.com.
, new research showed.
Investigators at the University of Toronto, The Centre for Addiction and Mental Health (CAMH), and the Institute for Clinical Evaluative Sciences (ICES), in Canada, linked recent population-based survey data from more than 11,000 youngsters to health service use records, including hospitalizations, emergency department (ED) visits, and outpatient visits.
“We found a very strong association between cannabis use and risk of psychotic disorder in adolescence [although] surprisingly, we didn’t find evidence of association in young adulthood,” lead author André J. McDonald, PhD, currently a postdoctoral fellow at the Peter Boris Centre for Addictions Research and the Michael G. DeGroote Centre for Medicinal Cannabis Research, McMaster University, Hamilton, Ontario, Canada, said in a news release.
“These findings are consistent with the neurodevelopmental theory that teens are especially vulnerable to the effects of cannabis,” said Dr. McDonald, who conducted the research.
The study was published online in Psychological Medicine.
Increased Potency
“Epidemiologic research suggests that cannabis use may be a significant risk factor for psychotic disorders,” the authors wrote. However, methodological limitations of previous studies make it difficult to estimate the strength of association, with the current evidence base relying largely on cannabis use during the twentieth century, when the drug was “significantly less potent.” It’s plausible that the strength of association has increased due to increased cannabis potency.
The researchers believe youth cannabis use and psychotic disorders is “a critical public health issue,” especially as more jurisdictions liberalize cannabis use and the perception of harm declines among youth.
To estimate the association between cannabis use during youth and the risk for a psychotic disorder diagnosis, using recent population-based data, they used data from the 2009-2012 cycles of the Canadian Community Health Survey (CCHS) linked to administrative health data at ICES to study noninstitutionalized Ontario residents, aged 12-24 years, who had completed the CCHS during that period.
They excluded respondents who used health services for psychotic disorders during the 6 years prior to their CCHS interview date.
Respondents (n = 11,363; 51% men; mean age [SD], 18.3 [15.2-21.3] years) were followed for 6-9 years, with days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder as the primary outcome.
The researchers estimated age-specific hazard ratios during adolescence (12-19 years) and young adulthood (20-33 years) and conducted sensitivity analyses to explore alternative model conditions, including restricting the outcome to hospitalizations and ED visits, to increase specificity.
Compared with no cannabis use, cannabis use was significantly associated with an 11-fold increased risk for psychotic disorders during adolescence, although not during young adulthood (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6-27.3 and aHR, 1.3; 95% CI, 0.6-2.6, respectively).
Perception of Harm Declining
When the researchers restricted the outcome to hospitalizations and ED visits only, the strength of association “increased markedly” during adolescence, with a 26-fold higher association in cannabis users than in nonusers (aHR, 26.7; 95% CI, 7.7-92.8). However, there was no meaningful change during young adulthood (aHR, 1.8; 95% CI, 0.6-5.4).
“Many have hypothesized that adolescence is a more sensitive risk period than adulthood for the effect of cannabis use on psychotic disorder development, yet prior to this study, little epidemiologic evidence existed to support this view,” the authors wrote.
The data also suggest that cannabis use is “more strongly associated with more severe psychotic outcomes, as the strength of association during adolescence increased markedly when we restricted the outcome to hospitalizations and ED visits (the most severe types of health service use),” the investigators noted.
The authors noted several limitations. For instance, it’s unclear to what extent unmeasured confounders including genetic predisposition, family history of psychotic disorders, and trauma might have biased the results. In addition, they could not assess the potential confounding impact of genetic predisposition to psychotic disorders. The possibility of reverse causality also cannot be ruled out. It’s possible, they noted, that individuals with “psychotic dispositions” may self-medicate or show greater disposition to cannabis use.
Moreover, the dataset neither captured important factors regarding the cannabis itself, including delta-9-tetrahydrocannabinol potency, mode of use, product type, or cannabis dependence, nor captured institutionalized and homeless youth.
Nevertheless, they pointed to the findings as supporting a “precautionary principle” — as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, the findings suggest that evidence-based cannabis prevention strategies for adolescents are warranted.
This study was supported by CAMH, the University of Toronto, and ICES, which is funded by an annual grant from the Ontario Ministry of Health and the Ministry of Long-Term Care. The authors declared no relevant financial relationships.
A version of this article appeared on Medscape.com.
FDA Approves Nonstimulant Liquid Onyda XR for ADHD
, drug manufacturer Tris Pharma announced in a statement.
The drug is the first approved liquid nonstimulant ADHD medication. The once-daily extended-release oral suspension, with nighttime dosing, can be used alone or as an adjunctive therapy to FDA-approved stimulant medications in pediatric patients 6 years of age or older.
“People with ADHD require a range of therapeutic options that are designed for their individual needs, because not every medication or type of therapy works for every patient,” Ann Childress, MD, a psychiatrist and president of the Las Vegas–based Center for Psychiatry and Behavioral Medicine, said in the release.
“The approval of Onyda XR, the only liquid non-stimulant ADHD medication, with nighttime dosing that shifts the release profile, is a convenient option for patients needing better ADHD control,” she added.
The approval was based on “adequate and well-controlled studies” of the company’s extended-release tablets.
Onyda XR is contraindicated in patients with a history of a hypersensitivity reaction to clonidine.
The medication can cause dose-related decreases in blood pressure and heart rate. Vital signs should be monitored frequently in at-risk patients. In studies with the extended-release tablets, somnolence and sedation were commonly reported adverse reactions. The sympatholytic action of clonidine may worsen sinus node dysfunction and atrioventricular block, especially in patients taking other sympatholytic drugs, the company noted.
Onyda XR should be available in pharmacies in the second half of 2024.
A version of this article appeared on Medscape.com.
, drug manufacturer Tris Pharma announced in a statement.
The drug is the first approved liquid nonstimulant ADHD medication. The once-daily extended-release oral suspension, with nighttime dosing, can be used alone or as an adjunctive therapy to FDA-approved stimulant medications in pediatric patients 6 years of age or older.
“People with ADHD require a range of therapeutic options that are designed for their individual needs, because not every medication or type of therapy works for every patient,” Ann Childress, MD, a psychiatrist and president of the Las Vegas–based Center for Psychiatry and Behavioral Medicine, said in the release.
“The approval of Onyda XR, the only liquid non-stimulant ADHD medication, with nighttime dosing that shifts the release profile, is a convenient option for patients needing better ADHD control,” she added.
The approval was based on “adequate and well-controlled studies” of the company’s extended-release tablets.
Onyda XR is contraindicated in patients with a history of a hypersensitivity reaction to clonidine.
The medication can cause dose-related decreases in blood pressure and heart rate. Vital signs should be monitored frequently in at-risk patients. In studies with the extended-release tablets, somnolence and sedation were commonly reported adverse reactions. The sympatholytic action of clonidine may worsen sinus node dysfunction and atrioventricular block, especially in patients taking other sympatholytic drugs, the company noted.
Onyda XR should be available in pharmacies in the second half of 2024.
A version of this article appeared on Medscape.com.
, drug manufacturer Tris Pharma announced in a statement.
The drug is the first approved liquid nonstimulant ADHD medication. The once-daily extended-release oral suspension, with nighttime dosing, can be used alone or as an adjunctive therapy to FDA-approved stimulant medications in pediatric patients 6 years of age or older.
“People with ADHD require a range of therapeutic options that are designed for their individual needs, because not every medication or type of therapy works for every patient,” Ann Childress, MD, a psychiatrist and president of the Las Vegas–based Center for Psychiatry and Behavioral Medicine, said in the release.
“The approval of Onyda XR, the only liquid non-stimulant ADHD medication, with nighttime dosing that shifts the release profile, is a convenient option for patients needing better ADHD control,” she added.
The approval was based on “adequate and well-controlled studies” of the company’s extended-release tablets.
Onyda XR is contraindicated in patients with a history of a hypersensitivity reaction to clonidine.
The medication can cause dose-related decreases in blood pressure and heart rate. Vital signs should be monitored frequently in at-risk patients. In studies with the extended-release tablets, somnolence and sedation were commonly reported adverse reactions. The sympatholytic action of clonidine may worsen sinus node dysfunction and atrioventricular block, especially in patients taking other sympatholytic drugs, the company noted.
Onyda XR should be available in pharmacies in the second half of 2024.
A version of this article appeared on Medscape.com.
Severe early-life respiratory infections heighten pediatric OSA risk
AIRWAYS DISORDERS NETWORK
Pediatric Chest Medicine Section
Children with severe lower respiratory tract infections (LRTIs) within the first 2 years of life had a 2.06-fold increased risk of developing pediatric OSA by age 5, according to a study comparing patients hospitalized with LRTI to controls without severe LRTI.1 Prior studies linked LRTI and OSA, but the impact of LRTI severity was unknown.2,3,4 They used Kaplan-Meier survival estimates and Cox proportional hazards models to evaluate the risk of OSA.
Compared with patients with severe LRTIs, controls were more likely to have been full-term births, delivered vaginally, and breastfed. The OSA rate was significantly higher among children with severe LRTIs compared with controls (14.7% vs 6.8%). In the adjusted model controlling for relevant maternal and infant covariables, severe LRTI was significantly associated with increased OSA risk (HR, 2.06; 95% CI, 1.41-3.02; P < .001). Other factors such as prematurity (HR, 1.34; 95% CI, 1.01-1.77; P = .039) and maternal obesity (HR, 1.82; 95% CI, 1.32-2.52; P < .001) were also associated with increased OSA risk.
Maria Gutierrez, MD, of the Division of Pediatric Allergy, Immunology, and Rheumatology at Johns Hopkins University School of Medicine in Baltimore led the research. The study was published in Pediatric Pulmonology (2023 Dec 2. doi: 10.1002/ppul.26810). Study limitations included the use of electronic medical record data and potential lack of generalizability. The BBC is supported by the NIH.
– Agnes S. Montgomery, MD
Fellow-in-Training
References
1. Gayoso-Liviac MG, Nino G, Montgomery AS, Hong X, Wang X, Gutierrez MJ. Infants hospitalized with lower respiratory tract infections during the first two years of life have increased risk of pediatric obstructive sleep apnea. Pediatr Pulmonol. 2024;59:679-687.
2. Snow A, Dayyat E, Montgomery‐Downs HE, Kheirandish‐Gozal L, Gozal D. Pediatric obstructive sleep apnea: a potential late consequence of respiratory syncytial virus bronchiolitis. Pediatr Pulmonol. 2009;44(12):1186‐1191.
3. Chen VC‐H, Yang Y‐H, Kuo T‐Y, et al. Increased incidence of obstructive sleep apnea in hospitalized children after enterovirus infection: a nationwide population‐based cohort study. Pediatr Infect Dis J. 2018;37(9):872‐879.
4. Gutierrez MJ, Nino G, Landeo‐Gutierrez JS, et al. Lower respiratory tract infections in early life are associated with obstructive sleep apnea diagnosis during childhood in a large birth cohort. Sleep. 2021;44:12.
AIRWAYS DISORDERS NETWORK
Pediatric Chest Medicine Section
Children with severe lower respiratory tract infections (LRTIs) within the first 2 years of life had a 2.06-fold increased risk of developing pediatric OSA by age 5, according to a study comparing patients hospitalized with LRTI to controls without severe LRTI.1 Prior studies linked LRTI and OSA, but the impact of LRTI severity was unknown.2,3,4 They used Kaplan-Meier survival estimates and Cox proportional hazards models to evaluate the risk of OSA.
Compared with patients with severe LRTIs, controls were more likely to have been full-term births, delivered vaginally, and breastfed. The OSA rate was significantly higher among children with severe LRTIs compared with controls (14.7% vs 6.8%). In the adjusted model controlling for relevant maternal and infant covariables, severe LRTI was significantly associated with increased OSA risk (HR, 2.06; 95% CI, 1.41-3.02; P < .001). Other factors such as prematurity (HR, 1.34; 95% CI, 1.01-1.77; P = .039) and maternal obesity (HR, 1.82; 95% CI, 1.32-2.52; P < .001) were also associated with increased OSA risk.
Maria Gutierrez, MD, of the Division of Pediatric Allergy, Immunology, and Rheumatology at Johns Hopkins University School of Medicine in Baltimore led the research. The study was published in Pediatric Pulmonology (2023 Dec 2. doi: 10.1002/ppul.26810). Study limitations included the use of electronic medical record data and potential lack of generalizability. The BBC is supported by the NIH.
– Agnes S. Montgomery, MD
Fellow-in-Training
References
1. Gayoso-Liviac MG, Nino G, Montgomery AS, Hong X, Wang X, Gutierrez MJ. Infants hospitalized with lower respiratory tract infections during the first two years of life have increased risk of pediatric obstructive sleep apnea. Pediatr Pulmonol. 2024;59:679-687.
2. Snow A, Dayyat E, Montgomery‐Downs HE, Kheirandish‐Gozal L, Gozal D. Pediatric obstructive sleep apnea: a potential late consequence of respiratory syncytial virus bronchiolitis. Pediatr Pulmonol. 2009;44(12):1186‐1191.
3. Chen VC‐H, Yang Y‐H, Kuo T‐Y, et al. Increased incidence of obstructive sleep apnea in hospitalized children after enterovirus infection: a nationwide population‐based cohort study. Pediatr Infect Dis J. 2018;37(9):872‐879.
4. Gutierrez MJ, Nino G, Landeo‐Gutierrez JS, et al. Lower respiratory tract infections in early life are associated with obstructive sleep apnea diagnosis during childhood in a large birth cohort. Sleep. 2021;44:12.
AIRWAYS DISORDERS NETWORK
Pediatric Chest Medicine Section
Children with severe lower respiratory tract infections (LRTIs) within the first 2 years of life had a 2.06-fold increased risk of developing pediatric OSA by age 5, according to a study comparing patients hospitalized with LRTI to controls without severe LRTI.1 Prior studies linked LRTI and OSA, but the impact of LRTI severity was unknown.2,3,4 They used Kaplan-Meier survival estimates and Cox proportional hazards models to evaluate the risk of OSA.
Compared with patients with severe LRTIs, controls were more likely to have been full-term births, delivered vaginally, and breastfed. The OSA rate was significantly higher among children with severe LRTIs compared with controls (14.7% vs 6.8%). In the adjusted model controlling for relevant maternal and infant covariables, severe LRTI was significantly associated with increased OSA risk (HR, 2.06; 95% CI, 1.41-3.02; P < .001). Other factors such as prematurity (HR, 1.34; 95% CI, 1.01-1.77; P = .039) and maternal obesity (HR, 1.82; 95% CI, 1.32-2.52; P < .001) were also associated with increased OSA risk.
Maria Gutierrez, MD, of the Division of Pediatric Allergy, Immunology, and Rheumatology at Johns Hopkins University School of Medicine in Baltimore led the research. The study was published in Pediatric Pulmonology (2023 Dec 2. doi: 10.1002/ppul.26810). Study limitations included the use of electronic medical record data and potential lack of generalizability. The BBC is supported by the NIH.
– Agnes S. Montgomery, MD
Fellow-in-Training
References
1. Gayoso-Liviac MG, Nino G, Montgomery AS, Hong X, Wang X, Gutierrez MJ. Infants hospitalized with lower respiratory tract infections during the first two years of life have increased risk of pediatric obstructive sleep apnea. Pediatr Pulmonol. 2024;59:679-687.
2. Snow A, Dayyat E, Montgomery‐Downs HE, Kheirandish‐Gozal L, Gozal D. Pediatric obstructive sleep apnea: a potential late consequence of respiratory syncytial virus bronchiolitis. Pediatr Pulmonol. 2009;44(12):1186‐1191.
3. Chen VC‐H, Yang Y‐H, Kuo T‐Y, et al. Increased incidence of obstructive sleep apnea in hospitalized children after enterovirus infection: a nationwide population‐based cohort study. Pediatr Infect Dis J. 2018;37(9):872‐879.
4. Gutierrez MJ, Nino G, Landeo‐Gutierrez JS, et al. Lower respiratory tract infections in early life are associated with obstructive sleep apnea diagnosis during childhood in a large birth cohort. Sleep. 2021;44:12.
Obesity and Cancer: Untangling a Complex Web
According to the Centers for Disease Control and Prevention (CDC), over 684,000 Americans are diagnosed with an “obesity-associated” cancer each year.
The incidence of many of these cancers has been rising in recent years, particularly among younger people — a trend that sits in contrast with the overall decline in cancers with no established relationship to excess weight, such as lung and skin cancers.
Is obesity the new smoking? Not exactly.
While about 42% of cancers — including common ones such as colorectal and postmenopausal breast cancers — are considered obesity-related, only about 8% of incident cancers are attributed to excess body weight. People often develop those diseases regardless of weight.
Although plenty of evidence points to excess body fat as a cancer risk factor, it’s unclear at what point excess weight has an effect. Is gaining weight later in life, for instance, better or worse for cancer risk than being overweight or obese from a young age?
There’s another glaring knowledge gap: Does losing weight at some point in adulthood change the picture? In other words, how many of those 684,000 diagnoses might have been prevented if people shed excess pounds?
When it comes to weight and cancer risk, “there’s a lot we don’t know,” said Jennifer W. Bea, PhD, associate professor, health promotion sciences, University of Arizona, Tucson.
A Consistent but Complicated Relationship
Given the growing incidence of obesity — which currently affects about 42% of US adults and 20% of children and teenagers — it’s no surprise that many studies have delved into the potential effects of excess weight on cancer rates.
Although virtually all the evidence comes from large cohort studies, leaving the cause-effect question open, certain associations keep showing up.
“What we know is that, consistently, a higher body mass index [BMI] — particularly in the obese category — leads to a higher risk of multiple cancers,” said Jeffrey A. Meyerhardt, MD, MPH, codirector, Colon and Rectal Cancer Center, Dana-Farber Cancer Institute, Boston.
In a widely cited report published in The New England Journal of Medicine in 2016, the International Agency for Research on Cancer (IARC) analyzed over 1000 epidemiologic studies on body fat and cancer. The agency pointed to over a dozen cancers, including some of the most common and deadly, linked to excess body weight.
That list includes esophageal adenocarcinoma and endometrial cancer — associated with the highest risk — along with kidney, liver, stomach (gastric cardia), pancreatic, colorectal, postmenopausal breast, gallbladder, ovarian, and thyroid cancers, plus multiple myeloma and meningioma. There’s also “limited” evidence linking excess weight to additional cancer types, including aggressive prostate cancer and certain head and neck cancers.
At the same time, Dr. Meyerhardt said, many of those same cancers are also associated with issues that lead to, or coexist with, overweight and obesity, including poor diet, lack of exercise, and metabolic conditions such as diabetes.
It’s a complicated web, and it’s likely, Dr. Meyerhardt said, that high BMI both directly affects cancer risk and is part of a “causal pathway” of other factors that do.
Regarding direct effects, preclinical research has pointed to multiple ways in which excess body fat could contribute to cancer, said Karen M. Basen-Engquist, PhD, MPH, professor, Division of Cancer Prevention and Population Services, The University of Texas MD Anderson Cancer Center, Houston.
One broad mechanism to help explain the obesity-cancer link is chronic systemic inflammation because excess fat tissue can raise levels of substances in the body, such as tumor necrosis factor alpha and interleukin 6, which fuel inflammation. Excess fat also contributes to hyperinsulinemia — too much insulin in the blood — which can help promote the growth and spread of tumor cells.
But the underlying reasons also appear to vary by cancer type, Dr. Basen-Engquist said. With hormonally driven cancer types, such as breast and endometrial, excess body fat may alter hormone levels in ways that spur tumor growth. Extra fat tissue may, for example, convert androgens into estrogens, which could help feed estrogen-dependent tumors.
That, Dr. Basen-Engquist noted, could be why excess weight is associated with postmenopausal, not premenopausal, breast cancer: Before menopause, body fat is a relatively minor contributor to estrogen levels but becomes more important after menopause.
How Big Is the Effect?
While more than a dozen cancers have been consistently linked to excess weight, the strength of those associations varies considerably.
Endometrial and esophageal cancers are two that stand out. In the 2016 IARC analysis, people with severe obesity had a seven-times greater risk for endometrial cancer and 4.8-times greater risk for esophageal adenocarcinoma vs people with a normal BMI.
With other cancers, the risk increases for those with severe obesity compared with a normal BMI were far more modest: 10% for ovarian cancer, 30% for colorectal cancer, and 80% for kidney and stomach cancers, for example. For postmenopausal breast cancer, every five-unit increase in BMI was associated with a 10% relative risk increase.
A 2018 study from the American Cancer Society, which attempted to estimate the proportion of cancers in the United States attributable to modifiable risk factors — including alcohol consumption, ultraviolet rays exposure, and physical inactivity — found that smoking accounted for the highest proportion of cancer cases by a wide margin (19%), but excess weight came in second (7.8%).
Again, weight appeared to play a bigger role in certain cancers than others: An estimated 60% of endometrial cancers were linked to excess weight, as were roughly one third of esophageal, kidney, and liver cancers. At the other end of the spectrum, just over 11% of breast, 5% of colorectal, and 4% of ovarian cancers were attributable to excess weight.
Even at the lower end, those rates could make a big difference on the population level, especially for groups with higher rates of obesity.
CDC data show that obesity-related cancers are rising among women younger than 50 years, most rapidly among Hispanic women, and some less common obesity-related cancers, such as stomach, thyroid and pancreatic, are also rising among Black individuals and Hispanic Americans.
Obesity may be one reason for growing cancer disparities, said Leah Ferrucci, PhD, MPH, assistant professor, epidemiology, Yale School of Public Health, New Haven, Connecticut. But, she added, the evidence is limited because Black individuals and Hispanic Americans are understudied.
When Do Extra Pounds Matter?
When it comes to cancer risk, at what point in life does excess weight, or weight gain, matter? Is the standard weight gain in middle age, for instance, as hazardous as being overweight or obese from a young age?
Some evidence suggests there’s no “safe” time for putting on excess pounds.
A recent meta-analysis concluded that weight gain at any point after age 18 years is associated with incremental increases in the risk for postmenopausal breast cancer. A 2023 study in JAMA Network Open found a similar pattern with colorectal and other gastrointestinal cancers: People who had sustained overweight or obesity from age 20 years through middle age faced an increased risk of developing those cancers after age 55 years.
The timing of weight gain didn’t seem to matter either. The same elevated risk held among people who were normal weight in their younger years but became overweight after age 55 years.
Those studies focused on later-onset disease. But, in recent years, experts have tracked a troubling rise in early-onset cancers — those diagnosed before age 50 years — particularly gastrointestinal cancers.
An obvious question, Dr. Meyerhardt said, is whether the growing prevalence of obesity among young people is partly to blame.
There’s some data to support that, he said. An analysis from the Nurses’ Health Study II found that women with obesity had double the risk for early-onset colorectal cancer as those with a normal BMI. And every 5-kg increase in weight after age 18 years was associated with a 9% increase in colorectal cancer risk.
But while obesity trends probably partly explain the rise in early-onset cancers, there is likely more to the story, Dr. Meyerhardt said.
“I think all of us who see an increasing number of patients under 50 with colorectal cancer know there’s a fair number who do not fit that [high BMI] profile,” he said. “There’s a fair number over 50 who don’t either.”
Does Weight Loss Help?
With all the evidence pointing to high BMI as a cancer risk factor, a logical conclusion is that weight loss should reduce that excess risk. However, Dr. Bea said, there’s actually little data to support that, and what exists comes from observational studies.
Some research has focused on people who had substantial weight loss after bariatric surgery, with encouraging results. A study published in JAMA found that among 5053 people who underwent bariatric surgery, 2.9% developed an obesity-related cancer over 10 years compared with 4.9% in the nonsurgery group.
Most people, however, aim for less dramatic weight loss, with the help of diet and exercise or sometimes medication. Some evidence shows that a modest degree of weight loss may lower the risks for postmenopausal breast and endometrial cancers.
A 2020 pooled analysis found, for instance, that among women aged ≥ 50 years, those who lost as little as 2.0-4.5 kg, or 4.4-10.0 pounds, and kept it off for 10 years had a lower risk for breast cancer than women whose weight remained stable. And losing more weight — 9 kg, or about 20 pounds, or more — was even better for lowering cancer risk.
But other research suggests the opposite. A recent analysis found that people who lost weight within the past 2 years through diet and exercise had a higher risk for a range of cancers compared with those who did not lose weight. Overall, though, the increased risk was quite low.
Whatever the research does, or doesn’t, show about weight and cancer risk, Dr. Basen-Engquist said, it’s important that risk factors, obesity and otherwise, aren’t “used as blame tools.”
“With obesity, behavior certainly plays into it,” she said. “But there are so many influences on our behavior that are socially determined.”
Both Dr. Basen-Engquist and Dr. Meyerhardt said it’s important for clinicians to consider the individual in front of them and for everyone to set realistic expectations.
People with obesity should not feel they have to become thin to be healthier, and no one has to leap from being sedentary to exercising several hours a week.
“We don’t want patients to feel that if they don’t get to a stated goal in a guideline, it’s all for naught,” Dr. Meyerhardt said.
A version of this article appeared on Medscape.com.
According to the Centers for Disease Control and Prevention (CDC), over 684,000 Americans are diagnosed with an “obesity-associated” cancer each year.
The incidence of many of these cancers has been rising in recent years, particularly among younger people — a trend that sits in contrast with the overall decline in cancers with no established relationship to excess weight, such as lung and skin cancers.
Is obesity the new smoking? Not exactly.
While about 42% of cancers — including common ones such as colorectal and postmenopausal breast cancers — are considered obesity-related, only about 8% of incident cancers are attributed to excess body weight. People often develop those diseases regardless of weight.
Although plenty of evidence points to excess body fat as a cancer risk factor, it’s unclear at what point excess weight has an effect. Is gaining weight later in life, for instance, better or worse for cancer risk than being overweight or obese from a young age?
There’s another glaring knowledge gap: Does losing weight at some point in adulthood change the picture? In other words, how many of those 684,000 diagnoses might have been prevented if people shed excess pounds?
When it comes to weight and cancer risk, “there’s a lot we don’t know,” said Jennifer W. Bea, PhD, associate professor, health promotion sciences, University of Arizona, Tucson.
A Consistent but Complicated Relationship
Given the growing incidence of obesity — which currently affects about 42% of US adults and 20% of children and teenagers — it’s no surprise that many studies have delved into the potential effects of excess weight on cancer rates.
Although virtually all the evidence comes from large cohort studies, leaving the cause-effect question open, certain associations keep showing up.
“What we know is that, consistently, a higher body mass index [BMI] — particularly in the obese category — leads to a higher risk of multiple cancers,” said Jeffrey A. Meyerhardt, MD, MPH, codirector, Colon and Rectal Cancer Center, Dana-Farber Cancer Institute, Boston.
In a widely cited report published in The New England Journal of Medicine in 2016, the International Agency for Research on Cancer (IARC) analyzed over 1000 epidemiologic studies on body fat and cancer. The agency pointed to over a dozen cancers, including some of the most common and deadly, linked to excess body weight.
That list includes esophageal adenocarcinoma and endometrial cancer — associated with the highest risk — along with kidney, liver, stomach (gastric cardia), pancreatic, colorectal, postmenopausal breast, gallbladder, ovarian, and thyroid cancers, plus multiple myeloma and meningioma. There’s also “limited” evidence linking excess weight to additional cancer types, including aggressive prostate cancer and certain head and neck cancers.
At the same time, Dr. Meyerhardt said, many of those same cancers are also associated with issues that lead to, or coexist with, overweight and obesity, including poor diet, lack of exercise, and metabolic conditions such as diabetes.
It’s a complicated web, and it’s likely, Dr. Meyerhardt said, that high BMI both directly affects cancer risk and is part of a “causal pathway” of other factors that do.
Regarding direct effects, preclinical research has pointed to multiple ways in which excess body fat could contribute to cancer, said Karen M. Basen-Engquist, PhD, MPH, professor, Division of Cancer Prevention and Population Services, The University of Texas MD Anderson Cancer Center, Houston.
One broad mechanism to help explain the obesity-cancer link is chronic systemic inflammation because excess fat tissue can raise levels of substances in the body, such as tumor necrosis factor alpha and interleukin 6, which fuel inflammation. Excess fat also contributes to hyperinsulinemia — too much insulin in the blood — which can help promote the growth and spread of tumor cells.
But the underlying reasons also appear to vary by cancer type, Dr. Basen-Engquist said. With hormonally driven cancer types, such as breast and endometrial, excess body fat may alter hormone levels in ways that spur tumor growth. Extra fat tissue may, for example, convert androgens into estrogens, which could help feed estrogen-dependent tumors.
That, Dr. Basen-Engquist noted, could be why excess weight is associated with postmenopausal, not premenopausal, breast cancer: Before menopause, body fat is a relatively minor contributor to estrogen levels but becomes more important after menopause.
How Big Is the Effect?
While more than a dozen cancers have been consistently linked to excess weight, the strength of those associations varies considerably.
Endometrial and esophageal cancers are two that stand out. In the 2016 IARC analysis, people with severe obesity had a seven-times greater risk for endometrial cancer and 4.8-times greater risk for esophageal adenocarcinoma vs people with a normal BMI.
With other cancers, the risk increases for those with severe obesity compared with a normal BMI were far more modest: 10% for ovarian cancer, 30% for colorectal cancer, and 80% for kidney and stomach cancers, for example. For postmenopausal breast cancer, every five-unit increase in BMI was associated with a 10% relative risk increase.
A 2018 study from the American Cancer Society, which attempted to estimate the proportion of cancers in the United States attributable to modifiable risk factors — including alcohol consumption, ultraviolet rays exposure, and physical inactivity — found that smoking accounted for the highest proportion of cancer cases by a wide margin (19%), but excess weight came in second (7.8%).
Again, weight appeared to play a bigger role in certain cancers than others: An estimated 60% of endometrial cancers were linked to excess weight, as were roughly one third of esophageal, kidney, and liver cancers. At the other end of the spectrum, just over 11% of breast, 5% of colorectal, and 4% of ovarian cancers were attributable to excess weight.
Even at the lower end, those rates could make a big difference on the population level, especially for groups with higher rates of obesity.
CDC data show that obesity-related cancers are rising among women younger than 50 years, most rapidly among Hispanic women, and some less common obesity-related cancers, such as stomach, thyroid and pancreatic, are also rising among Black individuals and Hispanic Americans.
Obesity may be one reason for growing cancer disparities, said Leah Ferrucci, PhD, MPH, assistant professor, epidemiology, Yale School of Public Health, New Haven, Connecticut. But, she added, the evidence is limited because Black individuals and Hispanic Americans are understudied.
When Do Extra Pounds Matter?
When it comes to cancer risk, at what point in life does excess weight, or weight gain, matter? Is the standard weight gain in middle age, for instance, as hazardous as being overweight or obese from a young age?
Some evidence suggests there’s no “safe” time for putting on excess pounds.
A recent meta-analysis concluded that weight gain at any point after age 18 years is associated with incremental increases in the risk for postmenopausal breast cancer. A 2023 study in JAMA Network Open found a similar pattern with colorectal and other gastrointestinal cancers: People who had sustained overweight or obesity from age 20 years through middle age faced an increased risk of developing those cancers after age 55 years.
The timing of weight gain didn’t seem to matter either. The same elevated risk held among people who were normal weight in their younger years but became overweight after age 55 years.
Those studies focused on later-onset disease. But, in recent years, experts have tracked a troubling rise in early-onset cancers — those diagnosed before age 50 years — particularly gastrointestinal cancers.
An obvious question, Dr. Meyerhardt said, is whether the growing prevalence of obesity among young people is partly to blame.
There’s some data to support that, he said. An analysis from the Nurses’ Health Study II found that women with obesity had double the risk for early-onset colorectal cancer as those with a normal BMI. And every 5-kg increase in weight after age 18 years was associated with a 9% increase in colorectal cancer risk.
But while obesity trends probably partly explain the rise in early-onset cancers, there is likely more to the story, Dr. Meyerhardt said.
“I think all of us who see an increasing number of patients under 50 with colorectal cancer know there’s a fair number who do not fit that [high BMI] profile,” he said. “There’s a fair number over 50 who don’t either.”
Does Weight Loss Help?
With all the evidence pointing to high BMI as a cancer risk factor, a logical conclusion is that weight loss should reduce that excess risk. However, Dr. Bea said, there’s actually little data to support that, and what exists comes from observational studies.
Some research has focused on people who had substantial weight loss after bariatric surgery, with encouraging results. A study published in JAMA found that among 5053 people who underwent bariatric surgery, 2.9% developed an obesity-related cancer over 10 years compared with 4.9% in the nonsurgery group.
Most people, however, aim for less dramatic weight loss, with the help of diet and exercise or sometimes medication. Some evidence shows that a modest degree of weight loss may lower the risks for postmenopausal breast and endometrial cancers.
A 2020 pooled analysis found, for instance, that among women aged ≥ 50 years, those who lost as little as 2.0-4.5 kg, or 4.4-10.0 pounds, and kept it off for 10 years had a lower risk for breast cancer than women whose weight remained stable. And losing more weight — 9 kg, or about 20 pounds, or more — was even better for lowering cancer risk.
But other research suggests the opposite. A recent analysis found that people who lost weight within the past 2 years through diet and exercise had a higher risk for a range of cancers compared with those who did not lose weight. Overall, though, the increased risk was quite low.
Whatever the research does, or doesn’t, show about weight and cancer risk, Dr. Basen-Engquist said, it’s important that risk factors, obesity and otherwise, aren’t “used as blame tools.”
“With obesity, behavior certainly plays into it,” she said. “But there are so many influences on our behavior that are socially determined.”
Both Dr. Basen-Engquist and Dr. Meyerhardt said it’s important for clinicians to consider the individual in front of them and for everyone to set realistic expectations.
People with obesity should not feel they have to become thin to be healthier, and no one has to leap from being sedentary to exercising several hours a week.
“We don’t want patients to feel that if they don’t get to a stated goal in a guideline, it’s all for naught,” Dr. Meyerhardt said.
A version of this article appeared on Medscape.com.
According to the Centers for Disease Control and Prevention (CDC), over 684,000 Americans are diagnosed with an “obesity-associated” cancer each year.
The incidence of many of these cancers has been rising in recent years, particularly among younger people — a trend that sits in contrast with the overall decline in cancers with no established relationship to excess weight, such as lung and skin cancers.
Is obesity the new smoking? Not exactly.
While about 42% of cancers — including common ones such as colorectal and postmenopausal breast cancers — are considered obesity-related, only about 8% of incident cancers are attributed to excess body weight. People often develop those diseases regardless of weight.
Although plenty of evidence points to excess body fat as a cancer risk factor, it’s unclear at what point excess weight has an effect. Is gaining weight later in life, for instance, better or worse for cancer risk than being overweight or obese from a young age?
There’s another glaring knowledge gap: Does losing weight at some point in adulthood change the picture? In other words, how many of those 684,000 diagnoses might have been prevented if people shed excess pounds?
When it comes to weight and cancer risk, “there’s a lot we don’t know,” said Jennifer W. Bea, PhD, associate professor, health promotion sciences, University of Arizona, Tucson.
A Consistent but Complicated Relationship
Given the growing incidence of obesity — which currently affects about 42% of US adults and 20% of children and teenagers — it’s no surprise that many studies have delved into the potential effects of excess weight on cancer rates.
Although virtually all the evidence comes from large cohort studies, leaving the cause-effect question open, certain associations keep showing up.
“What we know is that, consistently, a higher body mass index [BMI] — particularly in the obese category — leads to a higher risk of multiple cancers,” said Jeffrey A. Meyerhardt, MD, MPH, codirector, Colon and Rectal Cancer Center, Dana-Farber Cancer Institute, Boston.
In a widely cited report published in The New England Journal of Medicine in 2016, the International Agency for Research on Cancer (IARC) analyzed over 1000 epidemiologic studies on body fat and cancer. The agency pointed to over a dozen cancers, including some of the most common and deadly, linked to excess body weight.
That list includes esophageal adenocarcinoma and endometrial cancer — associated with the highest risk — along with kidney, liver, stomach (gastric cardia), pancreatic, colorectal, postmenopausal breast, gallbladder, ovarian, and thyroid cancers, plus multiple myeloma and meningioma. There’s also “limited” evidence linking excess weight to additional cancer types, including aggressive prostate cancer and certain head and neck cancers.
At the same time, Dr. Meyerhardt said, many of those same cancers are also associated with issues that lead to, or coexist with, overweight and obesity, including poor diet, lack of exercise, and metabolic conditions such as diabetes.
It’s a complicated web, and it’s likely, Dr. Meyerhardt said, that high BMI both directly affects cancer risk and is part of a “causal pathway” of other factors that do.
Regarding direct effects, preclinical research has pointed to multiple ways in which excess body fat could contribute to cancer, said Karen M. Basen-Engquist, PhD, MPH, professor, Division of Cancer Prevention and Population Services, The University of Texas MD Anderson Cancer Center, Houston.
One broad mechanism to help explain the obesity-cancer link is chronic systemic inflammation because excess fat tissue can raise levels of substances in the body, such as tumor necrosis factor alpha and interleukin 6, which fuel inflammation. Excess fat also contributes to hyperinsulinemia — too much insulin in the blood — which can help promote the growth and spread of tumor cells.
But the underlying reasons also appear to vary by cancer type, Dr. Basen-Engquist said. With hormonally driven cancer types, such as breast and endometrial, excess body fat may alter hormone levels in ways that spur tumor growth. Extra fat tissue may, for example, convert androgens into estrogens, which could help feed estrogen-dependent tumors.
That, Dr. Basen-Engquist noted, could be why excess weight is associated with postmenopausal, not premenopausal, breast cancer: Before menopause, body fat is a relatively minor contributor to estrogen levels but becomes more important after menopause.
How Big Is the Effect?
While more than a dozen cancers have been consistently linked to excess weight, the strength of those associations varies considerably.
Endometrial and esophageal cancers are two that stand out. In the 2016 IARC analysis, people with severe obesity had a seven-times greater risk for endometrial cancer and 4.8-times greater risk for esophageal adenocarcinoma vs people with a normal BMI.
With other cancers, the risk increases for those with severe obesity compared with a normal BMI were far more modest: 10% for ovarian cancer, 30% for colorectal cancer, and 80% for kidney and stomach cancers, for example. For postmenopausal breast cancer, every five-unit increase in BMI was associated with a 10% relative risk increase.
A 2018 study from the American Cancer Society, which attempted to estimate the proportion of cancers in the United States attributable to modifiable risk factors — including alcohol consumption, ultraviolet rays exposure, and physical inactivity — found that smoking accounted for the highest proportion of cancer cases by a wide margin (19%), but excess weight came in second (7.8%).
Again, weight appeared to play a bigger role in certain cancers than others: An estimated 60% of endometrial cancers were linked to excess weight, as were roughly one third of esophageal, kidney, and liver cancers. At the other end of the spectrum, just over 11% of breast, 5% of colorectal, and 4% of ovarian cancers were attributable to excess weight.
Even at the lower end, those rates could make a big difference on the population level, especially for groups with higher rates of obesity.
CDC data show that obesity-related cancers are rising among women younger than 50 years, most rapidly among Hispanic women, and some less common obesity-related cancers, such as stomach, thyroid and pancreatic, are also rising among Black individuals and Hispanic Americans.
Obesity may be one reason for growing cancer disparities, said Leah Ferrucci, PhD, MPH, assistant professor, epidemiology, Yale School of Public Health, New Haven, Connecticut. But, she added, the evidence is limited because Black individuals and Hispanic Americans are understudied.
When Do Extra Pounds Matter?
When it comes to cancer risk, at what point in life does excess weight, or weight gain, matter? Is the standard weight gain in middle age, for instance, as hazardous as being overweight or obese from a young age?
Some evidence suggests there’s no “safe” time for putting on excess pounds.
A recent meta-analysis concluded that weight gain at any point after age 18 years is associated with incremental increases in the risk for postmenopausal breast cancer. A 2023 study in JAMA Network Open found a similar pattern with colorectal and other gastrointestinal cancers: People who had sustained overweight or obesity from age 20 years through middle age faced an increased risk of developing those cancers after age 55 years.
The timing of weight gain didn’t seem to matter either. The same elevated risk held among people who were normal weight in their younger years but became overweight after age 55 years.
Those studies focused on later-onset disease. But, in recent years, experts have tracked a troubling rise in early-onset cancers — those diagnosed before age 50 years — particularly gastrointestinal cancers.
An obvious question, Dr. Meyerhardt said, is whether the growing prevalence of obesity among young people is partly to blame.
There’s some data to support that, he said. An analysis from the Nurses’ Health Study II found that women with obesity had double the risk for early-onset colorectal cancer as those with a normal BMI. And every 5-kg increase in weight after age 18 years was associated with a 9% increase in colorectal cancer risk.
But while obesity trends probably partly explain the rise in early-onset cancers, there is likely more to the story, Dr. Meyerhardt said.
“I think all of us who see an increasing number of patients under 50 with colorectal cancer know there’s a fair number who do not fit that [high BMI] profile,” he said. “There’s a fair number over 50 who don’t either.”
Does Weight Loss Help?
With all the evidence pointing to high BMI as a cancer risk factor, a logical conclusion is that weight loss should reduce that excess risk. However, Dr. Bea said, there’s actually little data to support that, and what exists comes from observational studies.
Some research has focused on people who had substantial weight loss after bariatric surgery, with encouraging results. A study published in JAMA found that among 5053 people who underwent bariatric surgery, 2.9% developed an obesity-related cancer over 10 years compared with 4.9% in the nonsurgery group.
Most people, however, aim for less dramatic weight loss, with the help of diet and exercise or sometimes medication. Some evidence shows that a modest degree of weight loss may lower the risks for postmenopausal breast and endometrial cancers.
A 2020 pooled analysis found, for instance, that among women aged ≥ 50 years, those who lost as little as 2.0-4.5 kg, or 4.4-10.0 pounds, and kept it off for 10 years had a lower risk for breast cancer than women whose weight remained stable. And losing more weight — 9 kg, or about 20 pounds, or more — was even better for lowering cancer risk.
But other research suggests the opposite. A recent analysis found that people who lost weight within the past 2 years through diet and exercise had a higher risk for a range of cancers compared with those who did not lose weight. Overall, though, the increased risk was quite low.
Whatever the research does, or doesn’t, show about weight and cancer risk, Dr. Basen-Engquist said, it’s important that risk factors, obesity and otherwise, aren’t “used as blame tools.”
“With obesity, behavior certainly plays into it,” she said. “But there are so many influences on our behavior that are socially determined.”
Both Dr. Basen-Engquist and Dr. Meyerhardt said it’s important for clinicians to consider the individual in front of them and for everyone to set realistic expectations.
People with obesity should not feel they have to become thin to be healthier, and no one has to leap from being sedentary to exercising several hours a week.
“We don’t want patients to feel that if they don’t get to a stated goal in a guideline, it’s all for naught,” Dr. Meyerhardt said.
A version of this article appeared on Medscape.com.
Failed IOL Promotes Poor Maternal and Fetal Outcomes for Mothers With Diabetes
Approximately one-quarter of mothers with diabetes failed induction of labor, and this failure was associated with a range of adverse outcomes for mothers and infants, based on data from more than 2,000 individuals.
Uncontrolled diabetes remains a risk factor for cesarean delivery, Ali Alhousseini, MD, of Corewell Health East, Dearborn, Michigan, and colleagues wrote in a study presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.
“Identifying and stratifying associated risk factors for failed induction of labor [IOL] may improve counseling and intrapartum care,” the researchers wrote in their abstract.
The researchers reviewed data from 2,172 mothers with diabetes who underwent IOL at a single university medical center between January 2013 and December 2021. They examined a range of maternal characteristics including age, ethnicity, gestational age, medical comorbidities, insulin administration, parity, and health insurance.
A total of 567 mothers with diabetes (26.1%) failed IOL and underwent cesarean delivery.
Overall, failed IOL was significantly associated with nulliparity (P = .0001), as well as preexisting diabetes compared with gestational diabetes, diabetes control with insulin, maternal essential hypertension, preeclampsia, and polyhydramnios (P = .001 for all). Other factors significantly associated with failed IOL included prenatal diagnosis of fetal growth restriction (P = .008), and placental abnormalities (P = .027).
Neonatal factors of weight, large for gestational age, head circumference, and height were not significantly associated with failed IOL (P > .05 for all).
As for neonatal outcomes, failed IOL was significantly associated with admission to neonatal intensive care unit, hyperbilirubinemia, and longer hospital stay (P = .001 for all). Failed IOL was significantly associated with lower 1-minute APGAR scores, but not with lower 5-minute APGAR scores, the researchers noted (P = .033 for 1-minute score). No association was noted between failed IOL and neonatal readmission, lower umbilical cord pH value, or maternal ethnicity.
The findings were limited by the retrospective design, but data analysis is ongoing, Dr. Alhousseini said. The researchers are continuing to assess the roles not only of optimal glucose control, but other maternal factors in improving maternal and neonatal outcomes, he said.
Data Add to Awareness of Risk Factors
The current study is important because of the increasing incidence of diabetes and the need to examine associated risk factors in pregnancy, Michael Richley, MD, a maternal fetal medicine physician at the University of Washington, Seattle, said in an interview. “The average age of onset of diabetes is becoming younger and type 2 diabetes in pregnancy is an increasingly common diagnosis,” said Dr. Richley, who was not involved in the study.
The increase in both maternal and neonatal adverse outcomes is expected given the risk factors identified in the study, said Dr. Richley. “The patients with diabetes also were sicker at baseline, with hypertensive disorders, growth restriction, and pregestational diabetes,” he noted.
The study findings support data from previous research, Dr. Richley said. The message to clinicians is that patients with diabetes not only have an increased risk of needing a cesarean delivery but also have an increased risk of poor outcomes if a cesarean delivery is needed, he said.
Although a prospective study would be useful to show causality as opposed to just an association, such a study is challenging in this patient population given the limitations of conducting research on labor and delivery, he said.
The study received no outside funding. The researchers and Dr. Richley had no financial conflicts to disclose.
Approximately one-quarter of mothers with diabetes failed induction of labor, and this failure was associated with a range of adverse outcomes for mothers and infants, based on data from more than 2,000 individuals.
Uncontrolled diabetes remains a risk factor for cesarean delivery, Ali Alhousseini, MD, of Corewell Health East, Dearborn, Michigan, and colleagues wrote in a study presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.
“Identifying and stratifying associated risk factors for failed induction of labor [IOL] may improve counseling and intrapartum care,” the researchers wrote in their abstract.
The researchers reviewed data from 2,172 mothers with diabetes who underwent IOL at a single university medical center between January 2013 and December 2021. They examined a range of maternal characteristics including age, ethnicity, gestational age, medical comorbidities, insulin administration, parity, and health insurance.
A total of 567 mothers with diabetes (26.1%) failed IOL and underwent cesarean delivery.
Overall, failed IOL was significantly associated with nulliparity (P = .0001), as well as preexisting diabetes compared with gestational diabetes, diabetes control with insulin, maternal essential hypertension, preeclampsia, and polyhydramnios (P = .001 for all). Other factors significantly associated with failed IOL included prenatal diagnosis of fetal growth restriction (P = .008), and placental abnormalities (P = .027).
Neonatal factors of weight, large for gestational age, head circumference, and height were not significantly associated with failed IOL (P > .05 for all).
As for neonatal outcomes, failed IOL was significantly associated with admission to neonatal intensive care unit, hyperbilirubinemia, and longer hospital stay (P = .001 for all). Failed IOL was significantly associated with lower 1-minute APGAR scores, but not with lower 5-minute APGAR scores, the researchers noted (P = .033 for 1-minute score). No association was noted between failed IOL and neonatal readmission, lower umbilical cord pH value, or maternal ethnicity.
The findings were limited by the retrospective design, but data analysis is ongoing, Dr. Alhousseini said. The researchers are continuing to assess the roles not only of optimal glucose control, but other maternal factors in improving maternal and neonatal outcomes, he said.
Data Add to Awareness of Risk Factors
The current study is important because of the increasing incidence of diabetes and the need to examine associated risk factors in pregnancy, Michael Richley, MD, a maternal fetal medicine physician at the University of Washington, Seattle, said in an interview. “The average age of onset of diabetes is becoming younger and type 2 diabetes in pregnancy is an increasingly common diagnosis,” said Dr. Richley, who was not involved in the study.
The increase in both maternal and neonatal adverse outcomes is expected given the risk factors identified in the study, said Dr. Richley. “The patients with diabetes also were sicker at baseline, with hypertensive disorders, growth restriction, and pregestational diabetes,” he noted.
The study findings support data from previous research, Dr. Richley said. The message to clinicians is that patients with diabetes not only have an increased risk of needing a cesarean delivery but also have an increased risk of poor outcomes if a cesarean delivery is needed, he said.
Although a prospective study would be useful to show causality as opposed to just an association, such a study is challenging in this patient population given the limitations of conducting research on labor and delivery, he said.
The study received no outside funding. The researchers and Dr. Richley had no financial conflicts to disclose.
Approximately one-quarter of mothers with diabetes failed induction of labor, and this failure was associated with a range of adverse outcomes for mothers and infants, based on data from more than 2,000 individuals.
Uncontrolled diabetes remains a risk factor for cesarean delivery, Ali Alhousseini, MD, of Corewell Health East, Dearborn, Michigan, and colleagues wrote in a study presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists.
“Identifying and stratifying associated risk factors for failed induction of labor [IOL] may improve counseling and intrapartum care,” the researchers wrote in their abstract.
The researchers reviewed data from 2,172 mothers with diabetes who underwent IOL at a single university medical center between January 2013 and December 2021. They examined a range of maternal characteristics including age, ethnicity, gestational age, medical comorbidities, insulin administration, parity, and health insurance.
A total of 567 mothers with diabetes (26.1%) failed IOL and underwent cesarean delivery.
Overall, failed IOL was significantly associated with nulliparity (P = .0001), as well as preexisting diabetes compared with gestational diabetes, diabetes control with insulin, maternal essential hypertension, preeclampsia, and polyhydramnios (P = .001 for all). Other factors significantly associated with failed IOL included prenatal diagnosis of fetal growth restriction (P = .008), and placental abnormalities (P = .027).
Neonatal factors of weight, large for gestational age, head circumference, and height were not significantly associated with failed IOL (P > .05 for all).
As for neonatal outcomes, failed IOL was significantly associated with admission to neonatal intensive care unit, hyperbilirubinemia, and longer hospital stay (P = .001 for all). Failed IOL was significantly associated with lower 1-minute APGAR scores, but not with lower 5-minute APGAR scores, the researchers noted (P = .033 for 1-minute score). No association was noted between failed IOL and neonatal readmission, lower umbilical cord pH value, or maternal ethnicity.
The findings were limited by the retrospective design, but data analysis is ongoing, Dr. Alhousseini said. The researchers are continuing to assess the roles not only of optimal glucose control, but other maternal factors in improving maternal and neonatal outcomes, he said.
Data Add to Awareness of Risk Factors
The current study is important because of the increasing incidence of diabetes and the need to examine associated risk factors in pregnancy, Michael Richley, MD, a maternal fetal medicine physician at the University of Washington, Seattle, said in an interview. “The average age of onset of diabetes is becoming younger and type 2 diabetes in pregnancy is an increasingly common diagnosis,” said Dr. Richley, who was not involved in the study.
The increase in both maternal and neonatal adverse outcomes is expected given the risk factors identified in the study, said Dr. Richley. “The patients with diabetes also were sicker at baseline, with hypertensive disorders, growth restriction, and pregestational diabetes,” he noted.
The study findings support data from previous research, Dr. Richley said. The message to clinicians is that patients with diabetes not only have an increased risk of needing a cesarean delivery but also have an increased risk of poor outcomes if a cesarean delivery is needed, he said.
Although a prospective study would be useful to show causality as opposed to just an association, such a study is challenging in this patient population given the limitations of conducting research on labor and delivery, he said.
The study received no outside funding. The researchers and Dr. Richley had no financial conflicts to disclose.
FROM ACOG 2024
Parental e-Cigarette Use Linked to Atopic Dermatitis Risk in Children
TOPLINE:
METHODOLOGY:
- AD is one of the most common inflammatory conditions in children and is linked to environmental risk factors, such as exposure to secondhand smoke and prenatal exposure to tobacco.
- To address the effect of e-cigarettes use on children, researchers conducted a cross-sectional analysis of data from the 2014-2018 National Health Interview Survey, a nationally representative sample of the US population.
- The analysis included 48,637,111 individuals (mean age, 8.4 years), with 6,354,515 (13%) indicating a history of AD (mean age, 8 years).
TAKEAWAY:
- The prevalence of parental e-cigarette use was 18.0% among individuals with AD, compared with 14.4% among those without AD.
- This corresponded to a 24% higher risk for AD associated with parental e-cigarette use (adjusted odds ratio, 1.24; 95% CI, 1.08-1.42).
- The association between e-cigarette use and AD in children held regardless of parent’s sex.
IN PRACTICE:
“Our results suggest that parental e-cigarette use was associated with pediatric AD,” the authors concluded. They noted that the authors of a previous study that associated e-cigarette use with AD in adults postulated that the cause was “the inflammatory state created by” e-cigarettes.
SOURCE:
This study, led by Gun Min Youn, Department of Dermatology, Stanford University School of Medicine, Stanford, California, was published online in JAMA Dermatology.
LIMITATIONS:
The cross-sectional survey design limited the ability to draw causal inferences. Defining e-cigarette use as a single past instance could affect the strength of the findings. Only past-year e-cigarette use was considered. Furthermore, data on pediatric cigarette or e-cigarette use, a potential confounder, were unavailable.
DISCLOSURES:
The study did not disclose funding information. One author reported receiving consultation fees outside the submitted work. No other disclosures were reported.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- AD is one of the most common inflammatory conditions in children and is linked to environmental risk factors, such as exposure to secondhand smoke and prenatal exposure to tobacco.
- To address the effect of e-cigarettes use on children, researchers conducted a cross-sectional analysis of data from the 2014-2018 National Health Interview Survey, a nationally representative sample of the US population.
- The analysis included 48,637,111 individuals (mean age, 8.4 years), with 6,354,515 (13%) indicating a history of AD (mean age, 8 years).
TAKEAWAY:
- The prevalence of parental e-cigarette use was 18.0% among individuals with AD, compared with 14.4% among those without AD.
- This corresponded to a 24% higher risk for AD associated with parental e-cigarette use (adjusted odds ratio, 1.24; 95% CI, 1.08-1.42).
- The association between e-cigarette use and AD in children held regardless of parent’s sex.
IN PRACTICE:
“Our results suggest that parental e-cigarette use was associated with pediatric AD,” the authors concluded. They noted that the authors of a previous study that associated e-cigarette use with AD in adults postulated that the cause was “the inflammatory state created by” e-cigarettes.
SOURCE:
This study, led by Gun Min Youn, Department of Dermatology, Stanford University School of Medicine, Stanford, California, was published online in JAMA Dermatology.
LIMITATIONS:
The cross-sectional survey design limited the ability to draw causal inferences. Defining e-cigarette use as a single past instance could affect the strength of the findings. Only past-year e-cigarette use was considered. Furthermore, data on pediatric cigarette or e-cigarette use, a potential confounder, were unavailable.
DISCLOSURES:
The study did not disclose funding information. One author reported receiving consultation fees outside the submitted work. No other disclosures were reported.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- AD is one of the most common inflammatory conditions in children and is linked to environmental risk factors, such as exposure to secondhand smoke and prenatal exposure to tobacco.
- To address the effect of e-cigarettes use on children, researchers conducted a cross-sectional analysis of data from the 2014-2018 National Health Interview Survey, a nationally representative sample of the US population.
- The analysis included 48,637,111 individuals (mean age, 8.4 years), with 6,354,515 (13%) indicating a history of AD (mean age, 8 years).
TAKEAWAY:
- The prevalence of parental e-cigarette use was 18.0% among individuals with AD, compared with 14.4% among those without AD.
- This corresponded to a 24% higher risk for AD associated with parental e-cigarette use (adjusted odds ratio, 1.24; 95% CI, 1.08-1.42).
- The association between e-cigarette use and AD in children held regardless of parent’s sex.
IN PRACTICE:
“Our results suggest that parental e-cigarette use was associated with pediatric AD,” the authors concluded. They noted that the authors of a previous study that associated e-cigarette use with AD in adults postulated that the cause was “the inflammatory state created by” e-cigarettes.
SOURCE:
This study, led by Gun Min Youn, Department of Dermatology, Stanford University School of Medicine, Stanford, California, was published online in JAMA Dermatology.
LIMITATIONS:
The cross-sectional survey design limited the ability to draw causal inferences. Defining e-cigarette use as a single past instance could affect the strength of the findings. Only past-year e-cigarette use was considered. Furthermore, data on pediatric cigarette or e-cigarette use, a potential confounder, were unavailable.
DISCLOSURES:
The study did not disclose funding information. One author reported receiving consultation fees outside the submitted work. No other disclosures were reported.
A version of this article appeared on Medscape.com.
Cortisol Test Confirms HPA Axis Recovery from Steroid Use
TOPLINE:
An early serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) has been validated as a safe and useful screening test with 100% specificity for predicting recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients on tapering regimes from long‐term chronic glucocorticoid therapy (CGT).
METHODOLOGY:
- A retrospective review of 250-µg Synacthen test (SST) results performed in patients on tapering CGT doses from a single-center rheumatology department over 12 months.
- A total of 60 SSTs were performed in 58 patients, all in the morning (7-12 AM) after withholding CGT for 48 hours.
- Peripheral blood was sampled for cortisol at baseline, 30 minutes, and 60 minutes.
- Adrenal insufficiency (AI) was defined as a peak serum cortisol concentration.
TAKEAWAY:
- The mean duration of CGT (all prednisolone) was 63 months, prescribed primarily for giant cell arteritis/polymyalgia rheumatica (48%) and inflammatory arthritis (18%), with a mean daily dose of 3.4 mg at the time of SST.
- With the investigators’ previously reported basal serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) used to confirm an intact HPA axis, no patient with AI would have been missed, but 37 of 51 (73%) unnecessary SSTs in euadrenal patients would have been avoided.
- A basal serum cortisol concentration of > 227 nmol/L had a specificity of 100% for predicting passing the SST, while a basal serum cortisol concentration of ≤ 55 nmol/L had a 100% sensitivity for predicting failure.
- A mean daily prednisolone dosing at the time of SST in patients with AI was significantly higher than that with normal SSTs (5.7 vs 2.9 mg, respectively; P = .01).
IN PRACTICE:
“This offers a more rapid, convenient, and cost‐effective screening method for patients requiring biochemical assessment of the HPA axis with the potential for significant resource savings without any adverse impact on patient safety,” the authors wrote.
SOURCE:
The study was conducted by Ella Sharma, of the Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and colleagues and published online on May 19, 2024, as a letter in Clinical Endocrinology.
LIMITATIONS:
Not provided.
DISCLOSURES:
Not provided.
A version of this article appeared on Medscape.com.
TOPLINE:
An early serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) has been validated as a safe and useful screening test with 100% specificity for predicting recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients on tapering regimes from long‐term chronic glucocorticoid therapy (CGT).
METHODOLOGY:
- A retrospective review of 250-µg Synacthen test (SST) results performed in patients on tapering CGT doses from a single-center rheumatology department over 12 months.
- A total of 60 SSTs were performed in 58 patients, all in the morning (7-12 AM) after withholding CGT for 48 hours.
- Peripheral blood was sampled for cortisol at baseline, 30 minutes, and 60 minutes.
- Adrenal insufficiency (AI) was defined as a peak serum cortisol concentration.
TAKEAWAY:
- The mean duration of CGT (all prednisolone) was 63 months, prescribed primarily for giant cell arteritis/polymyalgia rheumatica (48%) and inflammatory arthritis (18%), with a mean daily dose of 3.4 mg at the time of SST.
- With the investigators’ previously reported basal serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) used to confirm an intact HPA axis, no patient with AI would have been missed, but 37 of 51 (73%) unnecessary SSTs in euadrenal patients would have been avoided.
- A basal serum cortisol concentration of > 227 nmol/L had a specificity of 100% for predicting passing the SST, while a basal serum cortisol concentration of ≤ 55 nmol/L had a 100% sensitivity for predicting failure.
- A mean daily prednisolone dosing at the time of SST in patients with AI was significantly higher than that with normal SSTs (5.7 vs 2.9 mg, respectively; P = .01).
IN PRACTICE:
“This offers a more rapid, convenient, and cost‐effective screening method for patients requiring biochemical assessment of the HPA axis with the potential for significant resource savings without any adverse impact on patient safety,” the authors wrote.
SOURCE:
The study was conducted by Ella Sharma, of the Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and colleagues and published online on May 19, 2024, as a letter in Clinical Endocrinology.
LIMITATIONS:
Not provided.
DISCLOSURES:
Not provided.
A version of this article appeared on Medscape.com.
TOPLINE:
An early serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) has been validated as a safe and useful screening test with 100% specificity for predicting recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients on tapering regimes from long‐term chronic glucocorticoid therapy (CGT).
METHODOLOGY:
- A retrospective review of 250-µg Synacthen test (SST) results performed in patients on tapering CGT doses from a single-center rheumatology department over 12 months.
- A total of 60 SSTs were performed in 58 patients, all in the morning (7-12 AM) after withholding CGT for 48 hours.
- Peripheral blood was sampled for cortisol at baseline, 30 minutes, and 60 minutes.
- Adrenal insufficiency (AI) was defined as a peak serum cortisol concentration.
TAKEAWAY:
- The mean duration of CGT (all prednisolone) was 63 months, prescribed primarily for giant cell arteritis/polymyalgia rheumatica (48%) and inflammatory arthritis (18%), with a mean daily dose of 3.4 mg at the time of SST.
- With the investigators’ previously reported basal serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) used to confirm an intact HPA axis, no patient with AI would have been missed, but 37 of 51 (73%) unnecessary SSTs in euadrenal patients would have been avoided.
- A basal serum cortisol concentration of > 227 nmol/L had a specificity of 100% for predicting passing the SST, while a basal serum cortisol concentration of ≤ 55 nmol/L had a 100% sensitivity for predicting failure.
- A mean daily prednisolone dosing at the time of SST in patients with AI was significantly higher than that with normal SSTs (5.7 vs 2.9 mg, respectively; P = .01).
IN PRACTICE:
“This offers a more rapid, convenient, and cost‐effective screening method for patients requiring biochemical assessment of the HPA axis with the potential for significant resource savings without any adverse impact on patient safety,” the authors wrote.
SOURCE:
The study was conducted by Ella Sharma, of the Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and colleagues and published online on May 19, 2024, as a letter in Clinical Endocrinology.
LIMITATIONS:
Not provided.
DISCLOSURES:
Not provided.
A version of this article appeared on Medscape.com.
Maternal Buprenorphine Affects Fetal Breathing
Measures of fetal breathing movement were lower in fetuses of pregnant patients who received buprenorphine, compared with controls, based on data from 177 individuals.
The findings were presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists by Caroline Bulger, MD, of East Tennessee State University, Johnson City.
Pregnant patients with opioid-use disorder in the community surrounding Johnson City receive medication-assisted therapy with buprenorphine during the prenatal period, Dr. Bulger and colleagues wrote in their abstract. The current prenatal program for substance use disorder was established in 2016 based on patient requests for assistance in lowering their buprenorphine dosages during pregnancy, said senior author Martin E. Olsen, MD, also of East Tennessee State University, in an interview.
“Buprenorphine medication–assisted treatment in pregnancy is associated with long-term effects on childhood development such as smaller neonatal brains, decreased school performance, and low birth weight;” however, data on the fetal effects of buprenorphine are limited, said Dr. Olsen.
The current study was conducted to evaluate a short-term finding of the fetal effects of buprenorphine, Dr. Olsen said.
“This study was performed after obstetric sonographers at our institution noted that biophysical profile [BPP] ultrasound assessments of the fetuses of mothers on buprenorphine took longer than for other patients,” said Dr. Olsen.
The researchers conducted a retrospective chart review of 131 patients who received buprenorphine and 46 who were followed for chronic hypertension and served as high-risk controls. Patients were seen at a single institution between July 1, 2016, and June 30, 2020.
The researchers hypothesized that BPP of fetuses in patients receiving buprenorphine might be different from controls because of the effects of buprenorphine.
Overall, patients who received buprenorphine were more likely to have a fetal breathing score of zero than those who underwent a BPP for hypertension. A significant relationship emerged between buprenorphine dosage and breathing motion assessment; patients on high-dose buprenorphine were more likely than patients on low doses to have values of zero on fetal breathing motion assessment, and a chi-squared test yielded a P value of .04269.
The takeaway for clinical practice is that clinicians performing BPP ultrasounds on buprenorphine-exposed fetuses can expect that these assessments may take longer on average than assessments of other high-risk patients, said Dr. Olsen. “Additional assessment after a low BPP score is still indicated for these fetuses just as in other high-risk pregnancies,” he said.
The study was limited primarily by the retrospective design, Dr. Olsen said.
Although current treatment guidelines do not emphasize the effects of maternal buprenorphine use on fetal development, these findings support previous research showing effects of buprenorphine on fetal brain structure, the researchers wrote in their abstract. Looking ahead, “We recommend additional study on the maternal buprenorphine medication–assisted treatment dose effects for fetal and neonatal development with attention to such factors as head circumference, birth weight, achievement of developmental milestones, and school performance,” Dr. Olsen said.
“We and others have shown that the lowest effective dose of buprenorphine can lower neonatal abstinence syndrome/neonatal opioid withdrawal syndrome rates,” but data showing an impact of lowest effective dose management on long-term complications of fetal buprenorphine exposure are lacking, he noted.
The study received no outside funding. The researchers had no financial conflicts to disclose.
Measures of fetal breathing movement were lower in fetuses of pregnant patients who received buprenorphine, compared with controls, based on data from 177 individuals.
The findings were presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists by Caroline Bulger, MD, of East Tennessee State University, Johnson City.
Pregnant patients with opioid-use disorder in the community surrounding Johnson City receive medication-assisted therapy with buprenorphine during the prenatal period, Dr. Bulger and colleagues wrote in their abstract. The current prenatal program for substance use disorder was established in 2016 based on patient requests for assistance in lowering their buprenorphine dosages during pregnancy, said senior author Martin E. Olsen, MD, also of East Tennessee State University, in an interview.
“Buprenorphine medication–assisted treatment in pregnancy is associated with long-term effects on childhood development such as smaller neonatal brains, decreased school performance, and low birth weight;” however, data on the fetal effects of buprenorphine are limited, said Dr. Olsen.
The current study was conducted to evaluate a short-term finding of the fetal effects of buprenorphine, Dr. Olsen said.
“This study was performed after obstetric sonographers at our institution noted that biophysical profile [BPP] ultrasound assessments of the fetuses of mothers on buprenorphine took longer than for other patients,” said Dr. Olsen.
The researchers conducted a retrospective chart review of 131 patients who received buprenorphine and 46 who were followed for chronic hypertension and served as high-risk controls. Patients were seen at a single institution between July 1, 2016, and June 30, 2020.
The researchers hypothesized that BPP of fetuses in patients receiving buprenorphine might be different from controls because of the effects of buprenorphine.
Overall, patients who received buprenorphine were more likely to have a fetal breathing score of zero than those who underwent a BPP for hypertension. A significant relationship emerged between buprenorphine dosage and breathing motion assessment; patients on high-dose buprenorphine were more likely than patients on low doses to have values of zero on fetal breathing motion assessment, and a chi-squared test yielded a P value of .04269.
The takeaway for clinical practice is that clinicians performing BPP ultrasounds on buprenorphine-exposed fetuses can expect that these assessments may take longer on average than assessments of other high-risk patients, said Dr. Olsen. “Additional assessment after a low BPP score is still indicated for these fetuses just as in other high-risk pregnancies,” he said.
The study was limited primarily by the retrospective design, Dr. Olsen said.
Although current treatment guidelines do not emphasize the effects of maternal buprenorphine use on fetal development, these findings support previous research showing effects of buprenorphine on fetal brain structure, the researchers wrote in their abstract. Looking ahead, “We recommend additional study on the maternal buprenorphine medication–assisted treatment dose effects for fetal and neonatal development with attention to such factors as head circumference, birth weight, achievement of developmental milestones, and school performance,” Dr. Olsen said.
“We and others have shown that the lowest effective dose of buprenorphine can lower neonatal abstinence syndrome/neonatal opioid withdrawal syndrome rates,” but data showing an impact of lowest effective dose management on long-term complications of fetal buprenorphine exposure are lacking, he noted.
The study received no outside funding. The researchers had no financial conflicts to disclose.
Measures of fetal breathing movement were lower in fetuses of pregnant patients who received buprenorphine, compared with controls, based on data from 177 individuals.
The findings were presented at the annual clinical and scientific meeting of the American College of Obstetricians and Gynecologists by Caroline Bulger, MD, of East Tennessee State University, Johnson City.
Pregnant patients with opioid-use disorder in the community surrounding Johnson City receive medication-assisted therapy with buprenorphine during the prenatal period, Dr. Bulger and colleagues wrote in their abstract. The current prenatal program for substance use disorder was established in 2016 based on patient requests for assistance in lowering their buprenorphine dosages during pregnancy, said senior author Martin E. Olsen, MD, also of East Tennessee State University, in an interview.
“Buprenorphine medication–assisted treatment in pregnancy is associated with long-term effects on childhood development such as smaller neonatal brains, decreased school performance, and low birth weight;” however, data on the fetal effects of buprenorphine are limited, said Dr. Olsen.
The current study was conducted to evaluate a short-term finding of the fetal effects of buprenorphine, Dr. Olsen said.
“This study was performed after obstetric sonographers at our institution noted that biophysical profile [BPP] ultrasound assessments of the fetuses of mothers on buprenorphine took longer than for other patients,” said Dr. Olsen.
The researchers conducted a retrospective chart review of 131 patients who received buprenorphine and 46 who were followed for chronic hypertension and served as high-risk controls. Patients were seen at a single institution between July 1, 2016, and June 30, 2020.
The researchers hypothesized that BPP of fetuses in patients receiving buprenorphine might be different from controls because of the effects of buprenorphine.
Overall, patients who received buprenorphine were more likely to have a fetal breathing score of zero than those who underwent a BPP for hypertension. A significant relationship emerged between buprenorphine dosage and breathing motion assessment; patients on high-dose buprenorphine were more likely than patients on low doses to have values of zero on fetal breathing motion assessment, and a chi-squared test yielded a P value of .04269.
The takeaway for clinical practice is that clinicians performing BPP ultrasounds on buprenorphine-exposed fetuses can expect that these assessments may take longer on average than assessments of other high-risk patients, said Dr. Olsen. “Additional assessment after a low BPP score is still indicated for these fetuses just as in other high-risk pregnancies,” he said.
The study was limited primarily by the retrospective design, Dr. Olsen said.
Although current treatment guidelines do not emphasize the effects of maternal buprenorphine use on fetal development, these findings support previous research showing effects of buprenorphine on fetal brain structure, the researchers wrote in their abstract. Looking ahead, “We recommend additional study on the maternal buprenorphine medication–assisted treatment dose effects for fetal and neonatal development with attention to such factors as head circumference, birth weight, achievement of developmental milestones, and school performance,” Dr. Olsen said.
“We and others have shown that the lowest effective dose of buprenorphine can lower neonatal abstinence syndrome/neonatal opioid withdrawal syndrome rates,” but data showing an impact of lowest effective dose management on long-term complications of fetal buprenorphine exposure are lacking, he noted.
The study received no outside funding. The researchers had no financial conflicts to disclose.
ACOG 2024
Decision-Making Help for Kids With Disabilities Entering Adulthood
About one in six children (17%) between 3 and 17 years have a disability, which may affect their ability to make decisions when they transition to adulthood.
Typically, at age 18, a young adult assumes rights such as the legal right to make medical decisions (including reproductive decisions), and mental health, financial, and education decisions.
.
Several Options in the Continuum
The AAP describes a continuum of decision-making for youth with IDD from fully autonomous decisions to decisions made by an appointed guardian.
Highlighting an array of options is one way this paper is helpful, said Matthew Siegel, MD, chief of clinical enterprise with the Department of Psychiatry & Behavioral Sciences at Boston Children’s Hospital in Massachusetts. “I suspect that for a lot of practitioners what they’re aware of is guardianship or no guardianship.” These authors highlight that the options are more nuanced, he said.
Pediatricians have widely different ideas about what their role should be in facilitating decision-making in the transition period, he said, so this paper helps clarify what advocacy and discussion are needed.
The paper, written by first author Renee M. Turchi, MD, MPH, and colleagues on behalf of the Council on Children with Disabilities’ Committee on Medical Liability and Risk Management, states that, “The goal should always be the least restrictive decision-making that balances autonomy with safety and supports.”
One Alternative Is Supported Decision-Making
Supported decision-making is one alternative to guardianship. Authors explain that under that framework, a patient can choose a trusted support person and create an agreement with that person on what kinds of decisions the person needs help with and how much assistance is needed. The individual makes the final decision, not the support person.
Authors explain the benefits of that approach: “Individuals with IDD who use supported decision-making report increased confidence in themselves and their decision-making, improved decision-making skills, increased engagement with their community, and perceived more control of their lives,” the authors wrote.
Another option for people with IDD might be, rather than formally naming a substitute decision-maker, allowing a parent or caregiver access to their electronic health record or allowing that person to have independent discussions with their physician.
With guardianship, also called conservatorship in some states, a court requires clear and convincing evidence that the youth is not competent to make his or her own decisions. The court may order evaluations by many professionals, including pediatricians.
State-Specific Legal Information Is Available
Many states have recently enacted laws surrounding supported decision-making and guardianship. The authors reference a national resource center website that details the legislation for each state and points to resources and tools for pediatricians, families, and patients.
“Historically, pediatricians have rarely discussed the legal aspects of transition to adult-oriented services with the youth with IDD and subsequently, their families,” the authors wrote.
Discussions Should Start Early
Ideally, the authors wrote, the discussions about what level of supports might be necessary in the transition to adulthood should start at age 12-14 and include the youth, teachers, parents, and the medical team.
That’s earlier than some of the previous guidance, Dr. Siegel said, and it will be important to evaluate future evidence on the best age to start planning “both from a cognitive development standpoint and from a practicality standpoint.”
The authors point out that the needs for level of support may change and “pediatricians can reevaluate the decision-making arrangement as part of the annual physical/mental examinations to align with the youth’s desires, needs, and decision-making abilities over time.”
The authors and Dr. Siegel report no relevant financial relationships.
About one in six children (17%) between 3 and 17 years have a disability, which may affect their ability to make decisions when they transition to adulthood.
Typically, at age 18, a young adult assumes rights such as the legal right to make medical decisions (including reproductive decisions), and mental health, financial, and education decisions.
.
Several Options in the Continuum
The AAP describes a continuum of decision-making for youth with IDD from fully autonomous decisions to decisions made by an appointed guardian.
Highlighting an array of options is one way this paper is helpful, said Matthew Siegel, MD, chief of clinical enterprise with the Department of Psychiatry & Behavioral Sciences at Boston Children’s Hospital in Massachusetts. “I suspect that for a lot of practitioners what they’re aware of is guardianship or no guardianship.” These authors highlight that the options are more nuanced, he said.
Pediatricians have widely different ideas about what their role should be in facilitating decision-making in the transition period, he said, so this paper helps clarify what advocacy and discussion are needed.
The paper, written by first author Renee M. Turchi, MD, MPH, and colleagues on behalf of the Council on Children with Disabilities’ Committee on Medical Liability and Risk Management, states that, “The goal should always be the least restrictive decision-making that balances autonomy with safety and supports.”
One Alternative Is Supported Decision-Making
Supported decision-making is one alternative to guardianship. Authors explain that under that framework, a patient can choose a trusted support person and create an agreement with that person on what kinds of decisions the person needs help with and how much assistance is needed. The individual makes the final decision, not the support person.
Authors explain the benefits of that approach: “Individuals with IDD who use supported decision-making report increased confidence in themselves and their decision-making, improved decision-making skills, increased engagement with their community, and perceived more control of their lives,” the authors wrote.
Another option for people with IDD might be, rather than formally naming a substitute decision-maker, allowing a parent or caregiver access to their electronic health record or allowing that person to have independent discussions with their physician.
With guardianship, also called conservatorship in some states, a court requires clear and convincing evidence that the youth is not competent to make his or her own decisions. The court may order evaluations by many professionals, including pediatricians.
State-Specific Legal Information Is Available
Many states have recently enacted laws surrounding supported decision-making and guardianship. The authors reference a national resource center website that details the legislation for each state and points to resources and tools for pediatricians, families, and patients.
“Historically, pediatricians have rarely discussed the legal aspects of transition to adult-oriented services with the youth with IDD and subsequently, their families,” the authors wrote.
Discussions Should Start Early
Ideally, the authors wrote, the discussions about what level of supports might be necessary in the transition to adulthood should start at age 12-14 and include the youth, teachers, parents, and the medical team.
That’s earlier than some of the previous guidance, Dr. Siegel said, and it will be important to evaluate future evidence on the best age to start planning “both from a cognitive development standpoint and from a practicality standpoint.”
The authors point out that the needs for level of support may change and “pediatricians can reevaluate the decision-making arrangement as part of the annual physical/mental examinations to align with the youth’s desires, needs, and decision-making abilities over time.”
The authors and Dr. Siegel report no relevant financial relationships.
About one in six children (17%) between 3 and 17 years have a disability, which may affect their ability to make decisions when they transition to adulthood.
Typically, at age 18, a young adult assumes rights such as the legal right to make medical decisions (including reproductive decisions), and mental health, financial, and education decisions.
.
Several Options in the Continuum
The AAP describes a continuum of decision-making for youth with IDD from fully autonomous decisions to decisions made by an appointed guardian.
Highlighting an array of options is one way this paper is helpful, said Matthew Siegel, MD, chief of clinical enterprise with the Department of Psychiatry & Behavioral Sciences at Boston Children’s Hospital in Massachusetts. “I suspect that for a lot of practitioners what they’re aware of is guardianship or no guardianship.” These authors highlight that the options are more nuanced, he said.
Pediatricians have widely different ideas about what their role should be in facilitating decision-making in the transition period, he said, so this paper helps clarify what advocacy and discussion are needed.
The paper, written by first author Renee M. Turchi, MD, MPH, and colleagues on behalf of the Council on Children with Disabilities’ Committee on Medical Liability and Risk Management, states that, “The goal should always be the least restrictive decision-making that balances autonomy with safety and supports.”
One Alternative Is Supported Decision-Making
Supported decision-making is one alternative to guardianship. Authors explain that under that framework, a patient can choose a trusted support person and create an agreement with that person on what kinds of decisions the person needs help with and how much assistance is needed. The individual makes the final decision, not the support person.
Authors explain the benefits of that approach: “Individuals with IDD who use supported decision-making report increased confidence in themselves and their decision-making, improved decision-making skills, increased engagement with their community, and perceived more control of their lives,” the authors wrote.
Another option for people with IDD might be, rather than formally naming a substitute decision-maker, allowing a parent or caregiver access to their electronic health record or allowing that person to have independent discussions with their physician.
With guardianship, also called conservatorship in some states, a court requires clear and convincing evidence that the youth is not competent to make his or her own decisions. The court may order evaluations by many professionals, including pediatricians.
State-Specific Legal Information Is Available
Many states have recently enacted laws surrounding supported decision-making and guardianship. The authors reference a national resource center website that details the legislation for each state and points to resources and tools for pediatricians, families, and patients.
“Historically, pediatricians have rarely discussed the legal aspects of transition to adult-oriented services with the youth with IDD and subsequently, their families,” the authors wrote.
Discussions Should Start Early
Ideally, the authors wrote, the discussions about what level of supports might be necessary in the transition to adulthood should start at age 12-14 and include the youth, teachers, parents, and the medical team.
That’s earlier than some of the previous guidance, Dr. Siegel said, and it will be important to evaluate future evidence on the best age to start planning “both from a cognitive development standpoint and from a practicality standpoint.”
The authors point out that the needs for level of support may change and “pediatricians can reevaluate the decision-making arrangement as part of the annual physical/mental examinations to align with the youth’s desires, needs, and decision-making abilities over time.”
The authors and Dr. Siegel report no relevant financial relationships.
FROM PEDIATRICS