Obesity-associated transcriptomic remodelling in hidradenitis suppurativa and treatment response
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Localization, Identification, and Excision of Murine Adipose Depots
Published on: December 4, 2014
Sahil Kapur1,2, Xzaviar K Solone1,2, Randy Mi1,2
1Center for Cutaneous Biology and Immunology, Department of Dermatology, Henry Ford Health, Detroit, Michigan, USA.
Abstract:
Obesity is characterized by chronic low-grade inflammation and metabolic dysfunction. It is a major risk factor for hidradenitis suppurativa (HS), where it is associated with increased disease severity and metabolic comorbidity. Obesity promotes a pro-inflammatory, immunometabolic state marked by adipokine imbalance and alters the local skin environment through mechanical stress, occlusion and microbiome disruption. Mechanistic transcriptomic analyses further suggest that obesity induces tissue-specific changes in HS skin, including metabolic signalling in lesions and early barrier dysfunction in perilesional skin. In practice, obesity is associated with more severe and treatment-refractory disease but remains a modifiable risk factor. Weight loss, bariatric surgery and metabolism-directed therapies show potential to reduce disease burden, although controlled studies are limited. Overall, obesity acts as both a systemic and local modifier of HS, supporting its classification as an immunometabolic disorder.