Cohort Study Analyzes AD Risk Associated With Parental Atopy

A maternal or parental history of atopic dermatitis (AD) or asthma is associated with an increased risk of AD in offspring in the first 2 years of life, an analysis of a large birth cohort found.

“The prevalence of AD in children has increased dramatically in recent years, and most studies reporting the impact of parental atopic history on AD are based on older data,” wrote the study authors, led by Cathal O’Connor, MD. “Given the recent interest in early intervention to prevent AD and other allergic diseases, enhanced early identification of infants at risk of AD is increasingly important.”

The detailed analysis of AD risk associated with parental atopy in early life “may help to risk stratify infants to optimize early interventions for prevention or early treatment of AD,” they wrote.

For the analysis, O’Connor of the department of pediatrics and child health at University College Cork (Ireland) and colleagues conducted a secondary analysis of the Cork Babies After Scope: Evaluating the Longitudinal Impact Using Neurological and Nutritional Endpoints (BASELINE) Birth Cohort Study.

The study recruited 2,183 healthy first-born babies between August 2009 and October 2011 to examine the effects of environmental factors during pregnancy and infancy on childhood health and development. Skin barrier assessments were performed at birth, 2 months, 6 months, 12 months, and 24 months using a validated open chamber system to measure transepidermal water loss.

Parental atopy was self-reported at 2 months. Parents were asked at 2 months if the infant had an “itchy rash on the face or in the folds of the arms or legs,” as a screening question for AD. Experienced health care personnel used UK Working Party criteria to diagnose AD at 6, 12, and 24 months.

Complete data on AD status was available for 1,505 children in the cohort. O’Connor and colleagues calculated an overall AD prevalence of 18.6% at 6 months, 15.2% at 12 months, and 16.5% at 24 months.

Overall prevalence of AD was highest at 6 months. The study showed a similar or slightly higher impact of paternal atopy on offspring AD development, compared to maternal atopy.

Multivariable logistic regression analysis revealed that the odds of AD were 1.57 at 6 months and 1.66 at 12 months for maternal AD; 1.90 at 6 months and 1.85 at 24 months for paternal AD; 1.76 at 6 months and 1.75 at 12 months for maternal asthma; and 1.70 at 6 months, 1.86 at 12 months, and 1.99 at 24 months for paternal asthma.

“Parental allergic rhinitis was not associated with AD in offspring in the first 2 years, except for maternal rhinitis at 24 months [an adjusted odds ratio of 1.79],” the authors wrote. “The genetic predisposition to allergic rhinitis, given the key role of aeroallergen sensitization in its pathogenesis, may not be associated with early onset AD, but may have a greater impact in later onset or persistent AD.”

The authors acknowledged certain limitations of the study, including the fact that it was a secondary data analysis, and that parental AD, asthma, and rhinitis were self-reported, “which may reduce reliability and may contribute to the differences seen between the impact of maternal and paternal reported atopy on offspring,” they wrote. “Data on siblings were not captured, as participants in the study were first-born children. Filaggrin mutational analysis was not performed, which would have provided richer detail.”

Kelly M. Cordoro, MD, professor of dermatology and pediatrics at the University of California, San Francisco, who was asked to comment on the work, said that the study confirms the well-known association between parental atopy and the risk of atopy in offspring, which has been shown in several studies dating back decades.

“The authors try to parse risk based on maternal or paternal or biparental history of AD and/or asthma and/or rhinitis, but this type of nuanced analysis when diagnosis is based solely on parental report may be an over-reach,” she said.

“Given that this data supports the association between parental atopy and risk of AD in infants at various time points, the clinically relevant immediate next question is how can we leverage this knowledge to prevent onset of AD in infants at risk?” she said. “To date, interventions such as early introduction of emollients have been evaluated with mixed results.”

A recent Cochrane analysis concluded that, based on available data, skin care interventions such as emollient use during the first year of life in otherwise healthy infants is probably not effective for preventing eczema and may increase risk of skin infection.

“Effects of skin care interventions on risk of asthma are also uncertain,” said Cordoro, who is also chief of the division of pediatric dermatology at UCSF.

“In sum, this study offers additional data in support of the link between atopy in parents and offspring,” she said. “Understanding how to mitigate risk and prevent atopy requires unraveling of the complex interplay between genetic, environmental, immunologic, microbial and other factors. For now, dermatologists are unable to make broad evidence-based recommendations for otherwise healthy (i.e., with normal skin) but at-risk infants in terms of approaches to skin care that might prevent eczema and asthma.”

This article originally appeared on, part of the Medscape Professional Network.

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