Seborrheic Dermatitis Associated with an Increased Risk of Scarring Alopecia:A Multi-Center Retrospective Cohort Analysis
Recommended Citation
Ahmad N, Felix A, Hollins C. Seborrheic Dermatitis Associated with an Increased Risk of Scarring Alopecia:A Multi-Center Retrospective Cohort Analysis. J Am Acad Dermatol 2026; 95(1):AB400.
Document Type
Conference Proceeding
Publication Date
7-1-2026
Publication Title
J Am Acad Dermatol
Keywords
Dermatology
Abstract
Seborrheic dermatitis (SD) is a chronic inflammatory skin condition commonly affecting the scalp, face, and intertriginous areas. It has been reported as a frequent comorbidity among patients with scarring alopecia (SA), a group of disorders characterized by permanent hair loss due to follicular destruction and fibrous replacement. Using the TriNetX US Collaborative Network, which includes approximately 65 million deidentified patients, we evaluated the association between SD and subsequent SA. Patients with SD were identified using ICD-10 code L21 and compared with a control cohort without SD. SA was identified using ICD-10 code L66, which includes pseudopelade, lichen planopilaris, folliculitis decalvans, perifolliculitis capitis abscedens, folliculitis ulerythematosa reticulata, and other nonspecified cicatricial alopecias. A 1:1 greedy nearest-neighbor propensity score matching algorithm controlled for baseline demographics including age, sex, and race/ethnicity. Statistical analyses included chi-square tests and odds ratios (OR) with 95% confidence intervals (CI). After matching, 878,678 patients with SD were compared to 881,049 controls. The mean age was 34.0 years, with most patients female (51%), White (57%), and non-Hispanic/Latino (70%). Patients with SD had significantly greater odds of developing SA (OR 2.674, 95% CI 2.571–2.781, p < 0.001). Findings suggest SD may be a risk factor for SA, potentially through Malassezia-associated inflammation leading to follicular damage and fibrosis. Limitations include diagnostic coding variability, inability to assess disease severity, and lack of subtype specificity. These results highlight the importance of recognizing SD as a possible precursor to SA, warranting further mechanistic and clinical investigation.
Volume
95
Issue
1
First Page
AB400
