학술논문

What's new in atopic eczema? An analysis of systematic reviews published in 2019. Part 1: Risk factors and prevention.
Document Type
Article
Source
Clinical & Experimental Dermatology. Oct2021, Vol. 46 Issue 7, p1205-1210. 6p.
Subject
*ATOPIC dermatitis
*ATOPY
*GENOTYPE-environment interaction
*GUT microbiome
*LOCUS (Genetics)
*DISEASE risk factors
Language
ISSN
0307-6938
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. Click here for the corresponding questions to this CME article. [ABSTRACT FROM AUTHOR]