ArticleArchives of gynecology and obstetrics2026
Maternal diabetes subtypes and offspring cutaneous health: developmental programming of sebaceous gland function in over 330,000 live births.
Article in Archives of gynecology and obstetrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveMaternal diabetes is a known driver of fetal metabolic programming, yet its impact on offspring cutaneous health remains poorly characterized. We investigated the impact of intrauterine exposure to various maternal diabetes subtypes on the risk of offspring seborrheic dermatitis (SD), and to explore whether this risk is modulated by maternal glycemic control or treatment modality.
methodsThis large-scale, population-based cohort study included 331,335 mother-child pairs. Maternal diabetes subtypes-type 1 (T1DM), type 2 (T2DM), and gestational diabetes mellitus (GDM)-were assessed, along with glycemic control (HbA1c) and pharmacological treatment. SD was identified using physician-documented diagnoses and medication records. Multivariable logistic regression models adjusted for maternal and perinatal factors were used to estimate adjusted odds ratios (aORs).
resultsThe incidence of SD was 4.5%. SD was significantly more frequent among offspring of mothers with diabetes (4.9% vs. 4.4%, p < 0.001), primarily driven by GDM. T1DM and T2DM showed similar trends but weren't statistically significant. SD risk did not differ by treatment modality or glycemic control. While overall associations for T1DM and T2DM did not reach significance in the full cohort, age-stratified analysis revealed that maternal diabetes was significantly associated with increased SD risk across all subtypes within the first year of life (T1DM: p = 0.033, T2DM: p = 0.024, GDM: p = 0.019). Multivariable analysis showed maternal diabetes was independently associated with increased SD risk (aOR 1.16, 95% CI 1.08-1.24).
conclusionMaternal diabetes is associated with a significantly increased risk of infantile SD across all diabetes subtypes, suggesting that the intrauterine diabetic environment may influence early-life cutaneous homeostasis through metabolic programming of the pilosebaceous unit.
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