Abstract

Prenatal treatment with dexamethasone (DEX) has been used to avoid virilization in girls with Congenital Adrenal Hyperplasia (CAH). However, it has potential short- and long-term risks and has been associated with cognitive impairments. Here, the authors investigate whether epigenetic modification of DNA during early developmental stages may be a key mediating mechanism by which prenatal DEX treatment could result in poor outcomes in the offspring by comparing genome-wide DNA methylation, from peripheral CD4+ T-cells, between prenatal DEX-treated individuals without CAH and population controls.

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