Mastocytosis (M) represents a systemic pathology characterized by increased accumulation and clonal proliferation of mast cells in the skin and/or different organs. Broadly, M is classified into two categories: Cutaneous mastocytosis (CM) and systemic mastocytosis (SM). In children, CM is the most frequent form. Unfortunately, pathogenesis is still unclear. It is thought that genetic factors are involved, but further studies are necessary. As for features of CM, the lesions differ in clinical forms. The most important fact is evaluating a pediatric patient with CM. It must comprise laboratory exams (with baseline dosing of total serum tryptase), a skin biopsy (with a pathological exam and, if the diagnosis is unclear, immunohistochemical tests), and a complete clinical evaluation. It is also defining to distinguish between CM and other diseases with cutaneous involvement. As for the management of CM in children, the first intervention implies eliminating trigger factors. The available cures are oral H1 and/or H2 antihistamines, oral cromolyn sodium, oral methoxypsoralen therapy with long-wave psoralen plus ultraviolet A radiation, potent dermatocorticoid, and calcineurin inhibitors. In children, the prognosis of CM is excellent, especially if the disease’s onset is in the first or second years of life.

Background: Atopic dermatitis is a chronic inflammatory skin disease in children, frequently associated with skin barrier dysfunction, immune dysregulation, and dysbiosis. Infected, treatment-resistant lesions may increase disease severity and complicate management, particularly in the presence of Staphylococcus aureus colonization. Objectives: To characterize the microbiological profile of infected, non-responsive pediatric atopic dermatitis, evaluate short-term clinical outcomes following individualized treatment, and identify predictors of disease severity. Methods: This observational analytical study included 41 children with atopic dermatitis recruited at Saint Constantin Hospital, Brașov, Romania, between September 2025 and February 2026. Eligible patients fulfilled the Hanifin and Rajka criteria and presented with infected, treatment-resistant lesions. Skin cultures were subjected to an antibiogram and antifungigram. Disease severity was assessed using the Patient-Oriented Eczema Measure (POEM) and SCORAD at baseline, 7 days, and 30 days. Repeated-measures ANOVA, mixed ANOVA, and hierarchical linear regression were used for statistical analysis. Results: Staphylococcus aureus was the predominant pathogen, followed by other bacterial species. Both POEM and SCORAD scores improved significantly over the 30-day follow-up, with marked improvement after 7 days and further reduction by day 30. Although patients with S. aureus colonization and those receiving systemic therapy tended to have higher disease severity, neither factor significantly influenced the trajectory of clinical improvement. Baseline disease severity was the strongest predictor of 30-day POEM and SCORAD outcomes, whereas demographic and perinatal characteristics did not independently predict short-term clinical outcomes. Conclusions: Individualized management was associated with significant improvements in clinician-assessed disease severity and patient-reported symptoms during the 30-day follow-up. Staphylococcus aureus, particularly methicillin-sensitive S. aureus (MSSA), was the most frequently isolated pathogen. Baseline disease severity was the strongest predictor of short-term clinical outcomes, whereas the evaluated demographic and perinatal characteristics did not provide additional predictive value in this cohort. Larger prospective controlled studies are needed to confirm these findings.