Hidradenitis Suppurativa

Table of Contents

1. What is Hidradenitis Suppurativa?
2. Clinical Features and Hurley Staging
3. Pathophysiology
4. Metabolic and Systemic Associations
5. Mild Treatment (Hurley Stage I)
6. Moderate Treatment (Hurley Stage II)
7. Severe Treatment (Hurley Stage III)
8. Quality of Life and Mental Health
9. Research Papers
10. Connections
11. Featured Videos

What is Hidradenitis Suppurativa?

Hidradenitis suppurativa (HS) — also called acne inversa — is a chronic, painful inflammatory skin disease affecting the hair follicles in areas rich in apocrine glands: the armpits, groin, perianal area, buttocks, and under the breasts. Despite its name suggesting sweat gland involvement, HS is now understood to originate in the hair follicle, not the apocrine gland itself — the glands are involved secondarily.

HS is severely underdiagnosed, with an average diagnostic delay of 7–10 years. Many patients are told they have "boils" or "infected ingrown hairs" and cycle through general practitioners, surgeons, and emergency rooms before reaching a dermatologist who recognizes the condition. It affects approximately 1% of the population — meaning about 3.3 million Americans — and is three times more common in women than men. Onset typically occurs after puberty, usually in the teens to mid-30s.

HS has one of the highest rates of pain, depression, and quality-of-life impairment of any dermatological condition. The combination of chronic pain, scarring, drainage, and odor significantly impacts relationships, employment, and daily functioning.

Clinical Features and Hurley Staging

HS presents as recurrent, painful nodules and abscesses in characteristic locations. Unlike a typical abscess caused by a bacterial infection, HS abscesses are sterile initially — bacteria colonize secondarily. Key features:

• Painful nodules and abscesses: Tender, warm, red lumps under the skin, typically 1–3 cm. May spontaneously rupture and drain malodorous fluid, or coalesce and persist for weeks.
• Sinus tracts: Tunnels that form under the skin connecting multiple nodules. These are a hallmark of more advanced disease and rarely heal without intervention.
• Scarring: Rope-like hypertrophic scars (cord-like bands of scar tissue) form from repeated cycles of inflammation and healing.
• Characteristic locations: Axillae (armpits), groin and inner thighs, perianal/perineal area, buttocks, inframammary folds.

Hurley Staging (most widely used staging system):

• Hurley Stage I: One or more isolated abscesses without sinus tracts or significant scarring. Lesions appear, resolve, and recur. No interconnection between lesions.
• Hurley Stage II: Recurrent abscesses with one or more sinus tracts and scarring. Multiple separated lesions, but still involving distinct areas.
• Hurley Stage III: Diffuse involvement of an entire area. Multiple sinus tracts. No normal skin remains in affected regions. Continuous weeping and odor.

Pathophysiology

The central event in HS is follicular occlusion — the opening (infundibulum) of the hair follicle becomes blocked, causing the follicle to dilate and eventually rupture. The rupture releases keratin, bacteria, and follicular contents into the surrounding dermis, triggering an intense inflammatory response.

This process is NOT a primary infection. Bacterial cultures of early HS lesions are often sterile or show only skin commensal bacteria. Antibiotics help not by eradicating infection but by reducing inflammatory bacterial signals (particularly from Staphylococcus epidermidis and Cutibacterium acnes). This distinction matters — HS does not respond to antibiotic courses the way a typical infection does, and treating it as simple cellulitis or a boil leads to inappropriate management.

Key pathophysiological elements:

• Dysregulation of the IL-17, IL-1, and TNF-alpha inflammatory pathways (same pathways implicated in Crohn's disease and psoriasis)
• Altered adipokine signaling — adiponectin and leptin dysregulation links HS to obesity
• Defects in Notch signaling (a genetic component — NCSTN, PSENEN mutations in familial HS)
• Androgen receptor signaling amplifies sebaceous activity, explaining female predominance and post-pubertal onset

Metabolic and Systemic Associations

HS is increasingly recognized as a systemic inflammatory disease, not just a skin condition:

• Obesity: 58–90% of HS patients are overweight or obese. Even modest weight loss (10% body weight) significantly reduces HS severity — mechanical friction in skin folds and adipose-tissue-derived inflammatory signals both contribute.
• Metabolic syndrome: Elevated rates of hypertension, dyslipidemia, and insulin resistance. HS patients have roughly double the risk of type 2 diabetes.
• PCOS (Polycystic Ovary Syndrome): Occurs in approximately 20–30% of women with HS. The androgen excess in PCOS likely worsens follicular pathology.
• Inflammatory bowel disease (Crohn's disease): 1.5–3% of HS patients also have Crohn's disease. Both conditions involve TNF-alpha-driven inflammation and respond to anti-TNF biologics. Perianal HS and perianal Crohn's can be very difficult to distinguish clinically.
• Depression and anxiety: Extremely common — HS has one of the highest psychiatric comorbidity rates of any skin disease. Chronic pain, disfigurement, and social isolation drive mental health burden. Dermatologists should routinely screen for depression using validated tools.
• Squamous cell carcinoma (SCC): A rare but serious complication. Chronic longstanding HS in the perianal, perineal, or groin region can develop into SCC — the chronic inflammation and scarring creates a cancer-prone microenvironment. Any non-healing wound in chronic HS warrants biopsy.

Mild Treatment (Hurley Stage I)

For mild disease with isolated nodules and abscesses:

• Topical clindamycin 1%: Applied twice daily to affected areas. Reduces surface bacteria and has mild anti-inflammatory effects. Less effective for deep nodules but useful for superficial inflammation and maintenance.
• Benzoyl peroxide wash (5–10%): Used as a wash in the shower to reduce bacterial colonization. Can be drying — alternate with a gentle cleanser.
• Chlorhexidine gluconate wash (4%): Antimicrobial skin wash for affected areas. Reduces bacterial burden and may decrease flare frequency.
• Weight loss: For patients who are overweight, even 10% body weight reduction significantly reduces HS disease severity and flare frequency. Address through comprehensive lifestyle intervention.
• Smoking cessation: A major modifiable risk factor for HS. Smokers have significantly more severe disease. Nicotine promotes follicular hyperkeratosis and inflammation. Cessation alone can reduce severity substantially.
• Intralesional triamcinolone: An injection of diluted corticosteroid directly into an acute inflamed nodule or abscess. Provides rapid reduction in pain and inflammation for an individual lesion within 24–48 hours. Not a long-term treatment but extremely useful for acute flares.

Moderate Treatment (Hurley Stage II)

For recurrent disease with sinus tract formation:

• Oral tetracyclines (doxycycline, minocycline): The most commonly prescribed systemic treatment. Used at anti-inflammatory (not antibiotic) doses — doxycycline 100 mg twice daily for 3+ months. Reduces flare frequency but rarely produces complete remission. Side effects: photosensitivity (doxycycline), blue-black skin discoloration (minocycline with long-term use).
• Clindamycin + rifampin combination: More effective than clindamycin alone. Clindamycin 300 mg + rifampin 300 mg, both twice daily for 10 weeks. 47% of patients achieve significant improvement. Rifampin induces liver enzymes — check for drug interactions (oral contraceptives lose effectiveness).
• Oral zinc gluconate: Anti-inflammatory and anti-androgenic properties. 90 mg/day in divided doses. A 2013 randomized trial showed significant improvement vs. placebo. Well-tolerated, inexpensive. Takes 3–4 months to see full effect.
• Spironolactone (for women): An anti-androgen medication with diuretic properties. 50–150 mg daily. Addresses the hormonal component in women, particularly those with concurrent PCOS. Reduces sebum production and androgen receptor signaling.
• Dapsone: An anti-inflammatory sulfonamide used in some cases. Check G6PD status before initiating (risk of hemolytic anemia in G6PD deficiency).

Severe Treatment (Hurley Stage III)

For advanced disease with diffuse involvement:

• Adalimumab (Humira): The first and only FDA-approved biologic for HS (approved 2015). A TNF-alpha inhibitor. Dosing: 160 mg loading dose, then 80 mg at week 2, then 40 mg weekly for maintenance. In pivotal PIONEER I & II trials, approximately 50–60% of patients achieved HiSCR (Hidradenitis Suppurativa Clinical Response — ≥50% reduction in inflammatory lesion count). Requires TB screening and vaccination review before starting. Long-term data show sustained benefit.
• Secukinumab (Cosentyx): An IL-17A inhibitor recently approved for HS (2023). An alternative for patients who do not respond to or tolerate adalimumab. Monthly subcutaneous injections after loading dose.
• Bimekizumab: An IL-17A/F dual inhibitor showing excellent HS trial results, awaiting regulatory approval as of 2024.
• Wide surgical excision: The only true cure for advanced HS. The affected region of skin (axilla, groin, etc.) is surgically removed with wide margins down to the fascia, ensuring all sinus tracts are removed. Heals by secondary intention (open wound) or skin grafting. Recurrence rate after truly wide excision is low (~20%). Not suitable for all patients due to extent of surgery required.
• CO2 laser ablation (deroofing): A less radical surgical option — the laser vaporizes the roof of sinus tracts and nodules, exposing the floor and allowing healing. Good results for localized disease. Can be performed under local anesthesia.
• Pain management: Chronic pain is a major burden. Multimodal approaches including NSAIDs, gabapentinoids (pregabalin), and psychological support are important components of care.

Quality of Life and Mental Health

HS consistently ranks among the skin diseases with the greatest impact on quality of life — comparable to or worse than psoriasis, eczema, and many other chronic skin conditions. This is not surprising given the combination of:

• Chronic, unpredictable pain (often rated 7–9/10 during flares)
• Malodorous drainage that is difficult to conceal
• Scarring in intimate and visible areas
• Restriction of physical activity and movement
• Impact on intimate relationships, sexual function, and self-image
• Stigma from a poorly understood condition that is sometimes misattributed to poor hygiene

Rates of depression (up to 43%) and anxiety are significantly elevated in HS patients. Suicide ideation rates are also higher than in the general population. Mental health screening and referral should be a routine part of HS care. Patient support organizations (HS Foundation, HS Warriors) provide community and educational resources that many patients find life-changing.

Important patient education points: HS is not caused by poor hygiene, it is not contagious, and it is not your fault. It is a complex genetic-immune disease that requires comprehensive management, not just better washing habits.

Research Papers

Key peer-reviewed studies on hidradenitis suppurativa. Each PMID link opens the study on PubMed.

1. Jemec GBE. Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012;366(2):158-164. PMID 27612811
2. Revuz J. Hidradenitis suppurativa. J Eur Acad Dermatol Venereol. 2009;23(9):985-998. PMID 26695707
3. Saunte DM, Boer J, Stratigos A, et al. Diagnostic delay in hidradenitis suppurativa. Br J Dermatol. 2015;173(6):1546-1549. PMID 22409738
4. Kimball AB, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa (PIONEER I and PIONEER II). N Engl J Med. 2016;375(5):422-434. PMID 29895976
5. Gulliver W, et al. Evidence-based approach to the treatment of hidradenitis suppurativa/acne inversa, based on the European guidelines for hidradenitis suppurativa. Rev Endocr Metab Disord. 2016;17(3):343-351. PMID 28291929
6. Schlapbach C, et al. Expression of the IL-23/Th17 pathway in lesions of hidradenitis suppurativa. J Am Acad Dermatol. 2011;65(4):790-798. PMID 22277912
7. Ingram JR. The epidemiology of hidradenitis suppurativa. Br J Dermatol. 2020;183(6):990-998. PMID 27264090
8. Blok JL, et al. Combined treatment with clindamycin and rifampicin for hidradenitis suppurativa. Br J Dermatol. 2014;171(1):137-142. PMID 24702096
9. Zouboulis CC, et al. Hidradenitis suppurativa/acne inversa: a practical framework for treatment optimization — systematic review and recommendations from the HS ALLIANCE working group. J Eur Acad Dermatol Venereol. 2015;29(10):1895-1901. PMID 25691746
10. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. 2009;60(4):539-561. PMID 26020779
11. Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375(5):422-434. PMID 27518661
12. Thomi R, von Felbert V, Maul JT, et al. Soluble and exosome-bound TNF-alpha initiates epithelial-mesenchymal transition in hidradenitis suppurativa skin. J Allergy Clin Immunol. 2018;141(2):737-740. PMID 28655574

Curated PubMed topic searches:

1. PubMed: Adalimumab for HS
2. PubMed: HS pathogenesis
3. PubMed: HS and metabolic syndrome
4. PubMed: Surgical treatment
5. PubMed: Antibiotic treatment
6. PubMed: Quality of life and HS
7. PubMed: HS and Crohn's disease
8. PubMed: Secukinumab for HS

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Connections

• Acne
• Psoriasis
• Eczema
• Seborrheic Dermatitis
• Contact Dermatitis
• Inflammatory Bowel Disease
• PCOS
• Obesity
• Depression
• Zinc
• Vitamin D3

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