Atopy is characterized by immediate hypersensitivity, driven by Th2 immune response and high IgE levels. The dysfunctional epidermal barrier and altered immune pathways in atopic dermatitis (AD) may contribute to increased susceptibility to fungal infections and hypersensitivity reactions,¹ due to dermatophytes and Malassezia species, respectively.² In addition, immediate hypersensitivity triggered by dermatophyte antigen stimulation causes IgE classs-witching and eosinophilic recruitment, which may exacerbate atopic disease.³ Furthermore, patients with AD and dermatophytosis have had resolution of AD following systemic antifungal treatment.³ Therefore, we evaluated for potential associations between AD and dermatophytosis in a retrospective database cohort study to inform screening and intervention strategies.

TriNetX, a research network with patient data from 30 countries, was searched on June 30, 2025, for patients with vs without AD, 2005-2025. Cohorts were propensity score matched by age, sex, race, ethnicity, HIV infection status, organ transplant status, long-term corticosteroid use, immunodeficiency, diabetes mellitus, and obesity (Supplementary Appendix, available via Mendeley at https://data.mendeley.com/datasets/nk6zmcdnyx/1). Odds ratios and 95% CIs of dermatophytosis occurrence ≥1-day following AD diagnosis were calculated. Bonferroni correction for multiple hypothesis testing (8 independent queries) was applied.

Overall, 1,062,994 patients with AD (mean followup 4.32 years) and 1,062,994 matched controls (mean follow-up 3.98 years) were included. After matching, demographics were similar between cohorts, with all standardized mean differences <0.06 (Table I). Patients with vs without AD had increased odds of dermatophytosis (odds ratio [95% CI] = 1.95 [1.911.99], P < .001), with the highest odds for tinea manuum (5.32 [4.12-6.87], P <.001), followed by tinea imbricata (2.98 [2.72-3.26], P < .001), tinea pedis (2.37 [2.28-2.47], P < .001), tinea corporis (2.27 [2.18-2.37], P <.001), tinea cruris (2.14 [2.01-2.28], P <.001), tinea barbae/capitis (2.09 [1.95-2.23], P < .001), and tinea unguium (1.62 [1.56-1.68], P < .001) (Table II).

We found that patients with AD were more likely to develop dermatophytosis, including all analyzed subtypes, compared to controls. Similarly, in a crosssectional study of 180 randomly selected patients, with 19% (35/180) having chronic dermatophytosis, chronic dermatophytosis was ~3-fold more common in patients with vs without atopic disease (41% vs 14%, P value not reported), and 79% (11/14) of chronically infected, atopic patients had immediate hypersensitivity to dermatophyte antigen.⁴ In addition, in a retrospective study of 198,102,435 emergency department visits, including 3,070,678 (primary) and 1,848,130 (secondary) AD diagnoses, AD was associated with increased odds of any skin infection (1.93 [1.89-1.97]), including dermatophytosis (6.32 [6.08-6.56]).⁵

Limitations include potential miscoding, a single International Classification of Diseases code for tinea barbae/capitis, and lack of information on diagnostic method, if any. While tinea manuum/imbricata are uncommon, small cohorts for these subtypes limit the strength of conclusions. Large, prospective studies involving dermatologist evaluations and mycologic confirmation might help corroborate our findings. We could not assess dermatophytosis chronicity, AD disease severity, and all possible potential confounders.

In conclusion, AD diagnosis was associated with increased odds of subsequent dermatophyte infection. Our findings suggest a need for heightened physician awareness and patient education regarding dermatophytosis in patients with AD to ensure prompt testing and treatment. Prospective studies with mycologic confirmation are needed to corroborate these results. Further research is needed to better understand the immunological mechanism of the atopy-dermatophytosis relationship and assess the response of atopic disease to dermatophytosis treatment.