101 Series: Hidradenitis Suppurativa
Understanding the causes, symptoms, and treatment options
Key Takeaways
Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder characterized by painful nodules, abscesses, and tunnels (sinus tracts) in intertriginous areas.
The exact cause is unknown, but HS is believed to result from follicular occlusion, immune dysregulation, and genetic predisposition.
HS is associated with metabolic syndrome, inflammatory bowel disease, polycystic ovary syndrome (PCOS), and other systemic conditions.
Treatment options include topical and systemic therapies, biologics (such as TNF inhibitors and IL-17 inhibitors), surgical interventions, and lifestyle modifications.
Early diagnosis and treatment are essential to prevent progression and scarring. Lifestyle modifications are an important adjunct to therapy due to associated comorbidities.
Understanding Hidradenitis Suppurativa
Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition that affects approximately 1-4% of the population. It is characterized by recurrent, painful nodules, abscesses, and sinus tract formation, primarily in intertriginous areas such as the axillae, groin, perianal region, and inframammary folds. HS is associated with a significant psychosocial burden, leading to depression, anxiety, and decreased quality of life.
HS is frequently associated with systemic inflammation and multiple comorbid conditions, including:
Metabolic syndrome
Type 2 diabetes
Non-alcoholic fatty liver disease (NAFLD)
Sexual dysfunction
Depression and anxiety
Polycystic ovary syndrome (PCOS)
Inflammatory arthritis (spondyloarthritis, rheumatoid arthritis)
Inflammatory bowel disease (Crohn’s disease, ulcerative colitis)
Increased risk of stroke and cardiovascular diseases
Impaired sexual health (up to 60% of patients)
Pathogenesis
HS is now believed to be an inflammatory condition that stems from the hair follicle. The pathogenesis of HS is complex and multifactorial, involving follicular occlusion, immune system dysfunction, and genetic predisposition.
Key mechanisms include:
Follicular occlusion & rupture: The initial trigger is the occlusion of the pilosebaceous unit, leading to follicular rupture and the release of keratin and bacteria into the dermis. This triggers an inflammatory response.
Immune system dysregulation: HS is driven by innate and adaptive immune system activation. Increased levels of pro-inflammatory cytokines, including TNF-α, IL-1β, G-CSF, IL-2, IL-12, IL-17, and IL-23, contribute to chronic inflammation.
Microbial dysbiosis: While HS is not an infectious disease, dysbiosis of the skin microbiome exacerbates inflammation. Bacteria such as Staphylococcus aureus and Cutibacterium acnes are frequently found in lesions.
Genetic factors: Approximately 30-40% of patients have a family history of HS, suggesting a genetic predisposition. Mutations in the gamma-secretase gene complex (NCSTN, PSEN1, and PSENEN) have been implicated. Other identified genetic factors include newly associated loci such as SOX9, KLF5, and INAVA.
Hormonal influences: HS commonly occurs after puberty, and its association with PCOS suggests a role for androgens in disease development. However, the majority of patients have normal androgen levels, and importantly, apocrine glands—unlike sebaceous glands—do not respond to androgens.
Environmental and lifestyle factors also contribute:
Obesity: HS prevalence is 3.4 times higher in individuals with obesity, and severity correlates with BMI.
Smoking: Up to 80% of HS patients are smokers or former smokers, with a 4.1-fold increased risk compared to non-smokers.
Clinical Features
HS presents with tender, inflammatory nodules that progress to abscesses, sinus tracts, and scarring. It typically affects areas with apocrine glands and can be classified into three Hurley stages:
Stage I: Single or multiple abscesses without sinus tracts or scarring.
Stage II: Recurrent abscesses with sinus tract formation and scarring.
Stage III: Widespread involvement with multiple interconnected sinus tracts and extensive scarring.
Commonly affected areas include the axillae, groin, perineum, inframammary folds, buttocks, and inner thighs. HS flares can be triggered by stress, hormonal fluctuations, smoking, obesity, and friction.
Management and Treatment Approaches
Treatment is based on disease severity, patient preferences, and comorbid conditions. Lifestyle modifications including smoking cessation, weight management, dietary changes, supplementation, and general skincare practices are important adjuncts for all patients.
Medical Treatments - Topical
Topical clindamycin: First-line therapy for mild HS, reducing inflammation and bacterial overgrowth.
Resorcinol 15% cream: A keratolytic agent that promotes lesion resolution and reduces pain. Best used twice daily during active flares.
Benzoyl peroxide or anti-septic soap (i.e. Hibiclens): Helpful adjunct alongside other therapies and as preventative/ maintenance regimen.
Medical Treatments - Systemic
Antibiotics (tetracyclines, clindamycin + rifampin, dapsone, trimethoprim–sulfamethoxazole): Used for moderate to severe HS to control inflammation and secondary infections. Best used for active flares and as a bridge therapy to other systemic agents.
Hormonal therapy (oral contraceptives, spironolactone, metformin, finasteride): Can be beneficial for female patients with PCOS or other signs of hyperandrogenism.
Keratolytics (isotretinoin, acitretin): Used for moderate to severe HS. Benefit by normalizing keratinization and preventing the formation of follicular plugs that contribute to inflammation and abscess formation.
Metformin: Can be helpful adjunct for patients with insulin resistance by addressing underlying metabolic and hormonal factors that contribute to the disease. Metformin also has anti-inflammatory properties, reducing pro-inflammatory cytokines like TNF-α and IL-6.
Biologic therapies:
TNF-α inhibitors (adalimumab, infliximab): FDA-approved for moderate-to-severe HS, targeting inflammatory pathways.
IL-17 inhibitors (secukinumab, bimekizumab): FDA-approved for moderate-to-severe HS, providing more targeted coverage and less immunosuppression.
JAK inhibitors: Several are currently being evaluated for hidradenitis suppurativa (HS), including upadacitinib, povorcitinib, and ruxolitinib, with ongoing trials focusing on their efficacy and safety.
A robust pipeline of immunomodulatory drugs targeting TNF-α, IL-17A, IL-17A/F, JAK1, CD40, IL-36R, CXCR1/2 ligands, IL-1α/β, and C5a is in development for HS management.
Surgical Treatments
Surgical intervention is often required for patients with severe disease or those unresponsive to medical therapy.
Incision and drainage: Provides temporary relief but does not prevent recurrence.
Intralesional triamcinolone: Similar to I&D, IL (5 mg/ml) injections into early inflammatory lesions can provide temporary relief but does not prevent recurrence.
Deroofing: A minimally invasive technique to remove sinus tracts while preserving surrounding tissue.
Wide excision: The most definitive treatment, removing affected tissue and reducing recurrence risk.
Laser therapy: Carbon dioxide (CO2) laser and Nd:YAG laser have been used to ablate affected tissue and prevent new lesion formation.
Lifestyle and Adjunctive Therapies
General measures:
Minimize friction and moisture by wearing loose-fitting undergarments, using absorbent powders, and applying topical aluminum chloride.
Gentle hair care practices are crucial, including avoiding harsh hair removal methods (such as waxing and shaving) during flares. Laser hair removal can be a good option for HS patients as it can reduce the number of hair follicles, potentially decreasing flare-ups and improving symptoms
Maintain skin barrier function with daily use of moisturizing cream on affected areas
Smoking cessation: Strongly recommended, as smoking exacerbates HS.
Weight management: Obesity is a significant risk factor, and weight loss can improve disease severity.
Dietary modifications: Some patients report symptom improvement with Mediterranean, low-glycemic, or anti-inflammatory diets, though evidence is limited.
Pain management: NSAIDs and acetaminophen can be a helpful adjunct for pain relief during active flares.
Expectations for Improvement - Clinical Pearls
HS is a chronic and often progressive disease, requiring long-term management. Treatment outcomes depend on early intervention, adherence to therapy, and addressing comorbid conditions.
There is increasing evidence supporting the use of vitamin and mineral supplementation in the treatment of HS. I wrote a previous article outlining the scientific research on this, but my general go-to regimen for patients is Zinc 50 mg with copper 2 mg BID + Vitamin C 500 mg BID.
Combination therapy—such as systemic antibiotics with biologics or surgical intervention—often yields the best results. However, due to risks of antibiotic resistance and gut dysbiosis with long-term antibiotic use, clinicians should consider alternative systemic choices when possible.
In a recent meta-analysis of phase III trials, authors concluded among the biologic agents currently approved for moderate-to-severe HS, adalimumab has shown the greatest effectiveness and safety during the initial 12–16 weeks of treatment.
Real-world experiences suggest that combining biologics with other treatments, such as surgical interventions, enhances outcomes. Adjusting dosing frequencies, such as transitioning from 4-week to 2-week intervals, has also shown promise.
Conclusion
Hidradenitis suppurativa is a debilitating inflammatory skin disease with significant physical and psychosocial impact. Advances in understanding its pathophysiology have led to new and emerging treatment options, including targeted biologics and minimally invasive surgical techniques. A multidisciplinary approach is essential to optimize outcomes and improve quality of life for patients with HS.
References
Del Rosso JQ, Tanghetti EA. Folliculitis and Other Follicular Disorders. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:671-684.
Sabat, R., Alavi, A., Wolk, K., Wortsman, X., McGrath, B., Garg, A., & Szepietowski, J. C. (2025). Hidradenitis suppurativa. The Lancet, 405(10476), 420-438.
Frew, J. W. (2025). Unravelling the complex pathogenesis of hidradenitis suppurativa. British Journal of Dermatology, 192(Supplement_1), i3-i14.
Ballard, K., & Shuman, V. (2024). Hidradenitis suppurativa. StatPearls.
Krueger, J. G., Frew, J., Jemec, G. B., Kimball, A. B., Kirby, B., Bechara, F. G., ... & Wolk, K. (2024). Hidradenitis suppurativa: new insights into disease mechanisms and an evolving treatment landscape. British Journal of Dermatology, 190(2), 149-162.
Calabrese, L., Cartocci, A., Rubegni, P., French, L. E., & Kendziora, B. (2025). Efficacy and safety of biologics for hidradenitis suppurativa: A network meta‐analysis of phase III trials. Journal of the European Academy of Dermatology and Venereology.