Alopecia Areata Is Associated with Atopic Diathesis: Results from a Population-Based Study of 51,561 Patients.

BACKGROUND

Evidence of T1/IFN-γ overactivation as a major pathogenic driver somewhat conflicts with data supporting robust allergic background in patients with alopecia areata (AA). Previous investigations of immunological dysregulations show that both T1- and T2-related markers are overexpressed in AA. Clinical correlations in large populations may shed light on the immune pathways most likely to result in the clinical phenotype of AA.

OBJECTIVE

To investigate the atopic comorbidities among patients with AA in a large population-based study.

METHODS

This is a cross-sectional retrospective study of patients with AA and a matched comparison group, analyzing the associations between AA and 4 atopic comorbidities: asthma, atopic dermatitis (AD), allergic rhinitis, and allergic conjunctivitis. χ and t tests were used for univariate analysis, and logistic regression model was used for multivariate analysis. The study was performed using the computerized database of the Clalit Health Services, encompassing more than 4.4 million subjects.

RESULTS

The study population included 51,561 patients with AA and 51,410 matched control subjects. The prevalence of asthma (7.8% vs 6.5%; odds ratio [OR], 1.22; 95% CI, 1.17-1.28; P < .001), AD (3.9% vs 2.6%; OR, 1.55; 95% CI, 1.44-1.66; P < .001), allergic rhinitis (16.0% vs 12.8%; OR, 1.29; 95% CI, 1.25-1.34; P < .001), and allergic conjunctivitis (23.5% vs 19.6%; OR, 1.27; 95% CI, 1.23-1.30; P < .001) was significantly higher among patients with AA as compared with matched control subjects. Patients with AA also had a significantly higher probability of having more than 1 atopic comorbidity, with increasing OR as the number of concomitant atopic conditions increased.

CONCLUSIONS

Our analysis supports the previous literature and provides strong generalizability of significant atopy in patients with AA, suggesting T2 pathogenicity in AA, and challenging the traditional view of AA as a single-axis, T1-centered disease.