Background/Objectives: Diaper dermatitis (DD) is a common dermatological condition that is often exacerbated by antibiotics. Probiotics may restore microbiota balance and influence the incidence of DD. This study aimed to evaluate whether 6 weeks of Limosilactobacillus (L.) reuteri DSM 17938 supplementation during and after antibiotic treatment affects the incidence of DD. Methods: A secondary analysis of a randomised, double-blind, placebo-controlled trial that included 89 term neonates treated with antibiotics during the first 3 weeks of life was conducted. Neonates were assigned to receive either a probiotic supplement or a placebo for a total of 6 weeks. DD incidence, onset of DD, and skin care data were collected for 87 infants. Faecal samples were collected 6 weeks after study enrolment to analyse the composition of gut microbiota. Results: Twenty-four (28%) infants developed DD, of whom six (25%) had fungal DD. There was no significant difference in the incidence of DD or fungal DD between the probiotic and placebo groups (30% vs. 25% and 7% in both groups, respectively). Probiotic supplementation had no significant effect on the gut microbiota composition or diversity. In an exploratory binary logistic regression analysis based on six fungal DD events, probiotic supplementation was not associated with fungal DD, whereas breastfeeding was associated with lower odds of fungal DD; however, the overall model was not statistically significant, and this finding should be interpreted with caution because of the small number of events. Conclusions: In this exploratory secondary analysis, supplementation with L. reuteri DSM 17938 was not associated with a reduced incidence of DD or alterations in gut microbiota composition in antibiotic-treated neonates. Breastfeeding was associated with lower odds of fungal DD; however, this finding should be confirmed in larger, adequately powered studies.

Aicardi-Goutières syndrome (AGS) is a rare genetic early-onset progressive encephalopathy with variable clinical manifestations. The IFIH1 mutation has been confirmed to be responsible for type I interferon production and activation of the Janus kinase signaling pathway. We herein stress neurological observations and neuroimaging findings in a severe case report of an infant with AGS type 7 due to an IFIH1 mutation who was diagnosed in the first month of life. We also review neurological characteristics of IFIH1 mutations through recent literature.