Gender differences in perceived triggers and progression factors of vitiligo: evidence from Brazil

Vitiligo is a chronic immune-mediated dermatological condition with substantial psychosocial consequences. Patients' explanatory models shape coping, treatment engagement and quality of life, but evidence on how these models vary by gender outside Western settings remains scarce. Drawing on the biopsychosocial model and the Common Sense Model of self-regulation, we mapped the perceived triggers and progression factors that Brazilian adults with vitiligo deploy when explaining their condition and tested whether men and women converge or diverge in those explanatory accounts. Cross-sectional online survey with a mixed-methods analytic strategy. The sample comprised 232 Brazilian adults with a dermatologist-confirmed diagnosis (68.5% women, M = 37.65 years, SD = 12.43). Open-ended responses to a single attribution prompt were coded inductively by two trained psychologists, with inter-rater agreement assessed by Cohen's kappa and disagreements resolved through consensus. We computed code freq uencies overall and stratified by gender and used Similarity Analysis (IRaMuTeQ) to map co-occurrences between attributional themes and gender. Psychological attributions dominated the corpus. The most frequent codes were stress, emotional factors, rumination, genetics, depression, family loss and trauma. Within their gender, women cited stress, depression, sadness and anxiety more often than men did. Men were roughly four times more likely than women to cite genetic inheritance. Progression attributions clustered around generalized psychological state and were similar across gender. Brazilian adults with vitiligo construct gendered explanatory models that mirror broader cultural scripts about masculinity, femininity and the legitimacy of emotional disclosure. Care for vitiligo is likely to be improved by gender-responsive psychological assessment, validation of patient explanatory models and integrated dermatological-mental health pathways.