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- Inflammatory disease around abnormal and dilated hair follicles with secondary involvement of apocrine glands and surrounding structures, often with superinfection.
- Genetic predisposition possible; 40% have a family history of hidradenitis supperativa.
- Immune dysregulation in innate and adaptive immune pathways.
- Pathogenesis believed to start with occlusion and dilation of the pilosebaceous unit → rupture → extrusion of follicular contents into dermis → chemotactic inflammatory response → influx of neutrophils, lymphocytes, histiocytes → abscess formation (thus it is both an inflammatory disease related to immune dysregulation and infectious disease).
- Infection appears to be a result of inflammatory occlusion of ducts rather than the underlying process for hidradenitis suppurativa.
- Microbiology: culture may yield mixed aerobic/anaerobic bacteria with S. epidermidis and S. aureus most commonly isolated.
- Up to 50% of patients are culture negative.