What’s new in atopic eczema? An analysis of systematic reviews published in 2019. Part 1: Risk factors and prevention

Abstract

Summary This review is part of an annual evidence update on atopic eczema (AE), providing a summary of key findings from 18 systematic reviews published in 2019 on AE risk factors and prevention. Parental atopy, particularly AE, is a risk factor for offspring AE, and this risk is augmented both by the number of parental atopic diseases present and the number of affected parents. Low‐quality evidence suggests that autumn or winter birth increases childhood AE risk compared with birth in spring. There is some evidence to support filaggrin gene–environment interactions; however, this is limited by small underpowered studies. There is no evidence to suggest that polymorphisms in the –1082, –592 and –819 loci of the interleukin‐10 gene increase susceptibility to AE. There is no robust evidence to support a relationship between childhood AE development and either yoghurt consumption in the first year of life, gut microbiota variants, prenatal or infantile paracetamol exposure, maternal antibiotic exposure or air pollution. Three systematic reviews investigated the effect of probiotics given during pregnancy or infancy; although low‐quality evidence suggests benefits of combined probiotics, these studies were limited by significant heterogeneity. No relationship between the age at which complementary food and beverages are introduced and the risk of developing AE in infancy was identified. Consistent evidence showed no relationship between human milk feeding and infant AE development, aside from limited evidence suggesting a protective role in those with atopic heredity. This summary of recent evidence related to AE risk factors and prevention highlights the complex aetiology of AE.

Prenatal and early‐life antibiotic exposure and the risk of atopic dermatitis in children: A nationwide population‐based cohort study

“…In line with our results, they found the risk of AD was greater in children exposed to prenatal antibiotics than in those who were not exposed (aHR 1.10, 95% CI 1.09–1.12), whereas no such increased risk was found in the sibling‐control analysis, suggesting some familial confounders 25 . Based on the covariates they adjusted for, we further adjusted the maternal comorbidities, maternal AD, maternal allergic rhinitis, gestational infections, and maternal acetaminophen use during pregnancy, which may be potential risk factors according to previous studies 12,26,27 . In addition, their study revealed an apparent dose–response relationship and the category of infection did not modify the association of maternal antibiotic use and child AD, which was consistent with our results.…”

“…25 Based on the covariates they adjusted for, we further adjusted the maternal comorbidities, maternal AD, maternal allergic rhinitis, gestational infections, and maternal acetaminophen use during pregnancy, which may be potential risk factors according to previous studies. 12,26,27 In addition, their study revealed an apparent doseresponse relationship and the category of infection did not modify the association of maternal antibiotic use and child AD, which was consistent with our results. In terms of the trimester-specific association between antibiotic exposure during pregnancy and childhood AD, their results were comparable with our results in that the risk increased in all trimesters; however, our data showed a slightly higher risk in the first and second trimesters compared with the third trimester, which might be explained by antibioticsrelated dysbiosis or immunomodulatory effects, phenomena that are known to have a greater impact during early pregnancy.…”

Prenatal antibiotic exposure and the risk of atopic dermatitis in children: a nationwide population-based cohort study.

“…24 Based on the covariates they adjusted for, we further adjusted the maternal comorbidities, maternal AD, maternal allergic rhinitis, gestational infections, and maternal acetaminophen use during pregnancy, which may be potential risk factors according to previous studies. 12,25,26 In addition, their study revealed an apparent doseresponse relationship, and the category of infection did not modify the association of maternal antibiotic use and child AD, which was consistent with our results. In terms of the trimester-specific association between antibiotic exposure during pregnancy and childhood AD, their results were comparable with our results in that the risk increased in all trimesters; however, our data showed a slightly higher risk in the first and second trimesters compared with the third trimester, which might be explained by antibiotics-related dysbiosis or immunomodulatory effects, phenomena that are known to have a greater impact during early pregnancy.…”