Dermatology · PANCE / PANRE

Hidradenitis Suppurativa

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Chronic recurrent follicular occlusive disease of intertriginous areas with painful nodules, abscesses, sinus tracts, and scarring.

Also known as: hidradenitis suppurativa, HS, acne inversa, Verneuil disease

Overview

A chronic, recurrent, inflammatory follicular occlusive disorder presenting with painful deep-seated nodules, abscesses, sinus tracts, and dermal scarring in intertriginous areas (axillae, inguinal, gluteal, inframammary, perianal).

Epidemiology

Prevalence ~1% (likely underestimated; often misdiagnosed for years). Female predominance 3:1. Onset typically after puberty, peak ages 20-40. Higher prevalence in African American populations and patients with obesity, smoking, and metabolic syndrome.

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Question 1DermatologyMedium
A 35-year-old male presents with a 3-year history of recurrent painful nodules in his bilateral axillae and groin that rupture and form interconnecting sinus tracts, with numerous scars from prior lesions. Hurley stage II. Which of the following is the most likely diagnosis?
  • AEpidermoid cysts
  • BLymphogranuloma venereum
  • CHidradenitis suppurativa
  • DRecurrent furunculosis
Reveal answer & full explanation
Correct answer: C — Hidradenitis suppurativa
  • AEpidermoid cysts
  • BLymphogranuloma venereum
  • CHidradenitis suppurativa✓
  • DRecurrent furunculosis

Why hidradenitis suppurativa is correct

  • Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition of hair follicles in apocrine gland-bearing areas (axillae, groin)
  • Hurley staging: I = abscesses without sinuses; II = recurrent abscesses with sinus tracts and scarring (limited); III = diffuse involvement
  • This patient's bilateral axillary and groin involvement with interconnecting sinus tracts and scarring is Hurley stage II

Why the others are wrong

  • Epidermoid cysts — present as discrete, mobile subcutaneous nodules with a central punctum that may rupture, but they do not form interconnecting sinus tracts or the chronic recurrent scarring pattern across apocrine-bearing regions seen here
  • Lymphogranuloma venereum — a sexually transmitted Chlamydia trachomatis (serovars L1–L3) infection causing a transient genital ulcer followed by tender inguinal buboes, not a years-long recurrent process of axillary/groin nodules with sinus tracts and scarring
  • Recurrent furunculosis — repeated Staphylococcus aureus follicular abscesses (boils) that are typically self-limited and resolve between episodes, lacking the chronic interconnecting sinus tracts, bridging scars, and bilateral apocrine distribution that define this presentation

Additional high-yield points

  • Hurley II–III treatment: adalimumab (Humira) was the first FDA-approved biologic for moderate-severe HS (PIONEER I/II trials); secukinumab (interleukin-17A (IL-17A) inhibitor) is also FDA-approved for HS
  • Adjunctive therapies: topical clindamycin, tetracycline antibiotics, zinc, hormonal therapy (spironolactone in females), smoking cessation (strong exacerbating factor), weight loss, hair laser removal
  • Surgery (wide local excision): for chronic fibrotic lesions
Question 2DermatologyMedium
A 27-year-old woman presents with a 4-year history of painful, recurrent boils in both axillae and the groin. Exam shows tender deep-seated nodules, several draining sinus tracts, double-headed open comedones, and bridged hypertrophic scars in the axillae and inguinal folds, separated by areas of normal skin. She has smoked one pack daily for 10 years and has a BMI of 34. A wound culture is sterile, and a diagnosis of hidradenitis suppurativa is made. Which of the following best explains these findings?
  • AAutoantibodies directed against desmoglein in the epidermal layer
  • BGranulomatous inflammation centered on the eccrine sweat ducts
  • CPrimary bacterial infection of the apocrine sweat glands of the skin
  • DFollicular occlusion with rupture of the follicle into the dermis
Reveal answer & full explanation
Correct answer: D — Follicular occlusion with rupture of the follicle into the dermis
  • AAutoantibodies directed against desmoglein in the epidermal layer
  • BGranulomatous inflammation centered on the eccrine sweat ducts
  • CPrimary bacterial infection of the apocrine sweat glands of the skin
  • DFollicular occlusion with rupture of the follicle into the dermis✓

Why Follicular occlusion with rupture of the follicle into the dermis is correct

  • Hidradenitis suppurativa begins with hyperkeratinization and dilatation of the terminal follicle in apocrine gland-bearing skin, leading to follicular occlusion.
  • The occluded, distended follicle ruptures into the dermis, releasing keratin and bacteria that trigger a robust neutrophilic inflammatory response, sinus tract formation, and bridged scarring.
  • TNF-alpha, IL-17, and IL-1beta drive the inflammation, and the gamma-secretase/Notch pathway is implicated in familial forms. The double-headed comedones, sinus tracts, and intertriginous distribution all follow from this follicular occlusive process.

Why the others are wrong

  • Primary bacterial infection of the apocrine sweat glands of the skin — this is the obsolete "apocrinitis" concept; HS is a follicular occlusive disease, not a primary apocrine gland infection, and cultures are frequently sterile or polymicrobial.
  • Autoantibodies directed against desmoglein in the epidermal layer — describes pemphigus vulgaris, which causes flaccid bullae and erosions with a positive Nikolsky sign, not recurrent intertriginous nodules and sinus tracts.
  • Granulomatous inflammation centered on the eccrine sweat ducts — HS involves apocrine gland-bearing skin via follicular occlusion, not granulomatous eccrine duct disease; eccrine pathology underlies conditions such as miliaria, not HS.
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Risk factors

  • Smoking (90% of patients are current or former smokers) — strongest modifiable risk factor
  • Obesity (mechanical friction, hormonal milieu)
  • Family history (~30%) — autosomal dominant with variable penetrance in some kindreds (γ-secretase mutations)
  • Female sex; menstruation may worsen flares
  • Metabolic syndrome, type 2 diabetes, PCOS
  • Acne, inflammatory bowel disease (Crohn > UC), spondyloarthropathy associations

Pathophysiology

Follicular hyperkeratinization and dilatation in apocrine gland-bearing skin → follicular occlusion → rupture into dermis → robust neutrophilic inflammation, sinus tract formation, and scarring. NOT a primary apocrine gland disease (older name 'apocrinitis' is incorrect). TNF-α, IL-17, IL-1β drive inflammation; γ-secretase / Notch pathway implicated in familial forms.

Clinical presentation

Symptoms

  • Painful recurrent nodules and abscesses, often draining purulent foul-smelling discharge
  • Pruritus, burning, stinging
  • Sleep disturbance, dyspareunia, gait disturbance, work absences
  • Significant pain — worst-rated chronic dermatologic disease in quality of life surveys

Signs / physical exam

  • Primary lesions: tender, deep-seated, dermal/subcutaneous inflammatory nodules and abscesses
  • Secondary lesions: open comedones (double-headed 'tombstone' comedones — pathognomonic), sinus tracts (interconnecting tunnels), hypertrophic and atrophic scars, contractures, lymphedema
  • Distribution: axillae (most common), inguinal folds, perianal/perineal, buttocks, inframammary, submammary; less commonly nape, retroauricular, scalp
  • Lesions tend to be bilateral and symmetric
  • Hurley staging (clinical):
  • • I: solitary or multiple abscesses, NO sinus tracts or scarring
  • • II: recurrent abscesses with sinus tracts and scarring, separated by normal skin
  • • III: diffuse or near-diffuse involvement, multiple interconnected sinus tracts and abscesses across entire area

Classic findings

Recurrent abscesses + sinus tracts + bridged scarring in axillae and groin; double-comedones.

Differential diagnosis

  • Cutaneous abscess / furunculosis — Single acute abscess, not recurrent in same site, no sinus tracts; staphylococcal
  • Cystic acne / acne conglobata — Comedones present (HS lacks except 'double comedones'), trunk/face distribution
  • Crohn disease (metastatic / fistulating) — Perianal fistulas + GI symptoms; can overlap with HS
  • Pilonidal disease — Sacrococcygeal area, with hair tuft; not symmetric or multifocal
  • Granuloma inguinale (donovanosis) — Genital ulcers, slow growth, geographic exposure; Donovan bodies on smear
  • Lymphogranuloma venereum — Groove sign with bubo formation; serotype L1-L3 chlamydia
  • Steatocystoma multiplex — Multiple small cysts on chest/axillae, no inflammation or sinus tracts
  • Actinomycosis — Chronic sinus tracts with 'sulfur granules'; Actinomyces israelii

Diagnostic workup

Diagnostic criteria

All three required (Dessau criteria): (1) typical lesions (nodules, abscesses, sinus tracts, scars), (2) typical locations (intertriginous), (3) chronic relapsing course.

Labs

  • Clinical diagnosis — no required labs
  • CBC, CRP, ESR (elevated during flares)
  • Bacterial culture if secondary infection or atypical presentation (cultures often polymicrobial or sterile; routine antibiotics target empirically)
  • Screen comorbidities: metabolic syndrome (lipid panel, HbA1c), depression
  • Skin biopsy in atypical cases; rule out Crohn-related disease

Imaging

  • Ultrasound (high-frequency) — assesses sinus tract extent, often used to plan surgery
  • MRI for complex perineal/perianal disease and Crohn overlap
  • Sinography in selected presurgical cases

Diagnostic algorithm

Hurley StageClinical FeaturesPreferred Therapy
I (mild)Solitary/multiple abscesses; NO sinus tracts/scarringTopical clindamycin; doxycycline; antiseptic washes; lifestyle
II (moderate)Recurrent abscesses + sinus tracts/scars, separated by normal skinClindamycin + rifampin; adalimumab/secukinumab; localized excision/deroofing
III (severe)Diffuse interconnected sinus tracts and abscessesBiologic therapy + wide local excision; multidisciplinary care
Hurley staging of hidradenitis suppurativa and preferred therapy.

Treatment

First-line

  • Lifestyle: smoking cessation (most impactful intervention), weight reduction, loose breathable clothing, avoid friction/shaving
  • Daily antiseptic wash: chlorhexidine 4%, dilute bleach baths, benzoyl peroxide 5-10%
  • Topical clindamycin 1% solution BID for mild Hurley I disease
  • Hurley I-II: oral tetracycline antibiotic — doxycycline 100 mg BID × 12 weeks (anti-inflammatory dose) OR minocycline
  • Hurley II refractory or moderate-severe: combination oral clindamycin 300 mg BID + rifampin 300 mg BID × 10-12 weeks
  • Biologic therapy (Hurley II-III or refractory): adalimumab 160 mg loading → 80 mg week 2 → 40 mg weekly (FDA-approved); secukinumab (FDA-approved 2023); bimekizumab (recent approval)
  • Hormonal therapy in women: combined oral contraceptive (anti-androgenic — drospirenone/EE), spironolactone 50-200 mg/day, metformin
  • Intralesional triamcinolone 5-10 mg/mL for individual acute nodules
  • Pain control: acetaminophen, NSAIDs, gabapentin/pregabalin for neuropathic component; avoid chronic opioids

Severe Hurley III / extensive sinus disease

  • Wide local excision of involved areas with secondary intention healing or split-thickness grafting — definitive for Hurley III in affected region
  • Deroofing of sinus tracts (preferred over excision when possible)
  • Combine with biologic therapy preoperatively to reduce inflammation
  • Multidisciplinary care: dermatology, plastic surgery, pain, mental health

Acute abscess

  • Incision and drainage for relief (recognize recurrence is the rule; not curative)
  • Intralesional triamcinolone immediately after I&D
  • Punch debridement of inflamed nodules

Second-line / adjunct

  • Oral retinoids: acitretin or isotretinoin (limited evidence for HS but used in some)
  • Dapsone, colchicine, zinc supplementation (limited evidence)
  • Cyclosporine, methotrexate for refractory cases
  • JAK inhibitors (upadacitinib) — emerging data
  • Laser hair removal (Nd:YAG) reduces follicular occlusion in affected sites

Complications

  • Severe pain, depression, suicidality (rates exceed other chronic dermatoses)
  • Sexual dysfunction, infertility (genital scarring)
  • Lymphatic obstruction, lymphedema
  • Fistulas to urethra, bladder, rectum
  • Cutaneous squamous cell carcinoma in long-standing perianal/buttock disease (~3% lifetime, often aggressive)
  • Anemia of chronic disease, hypoproteinemia
  • Cardiovascular disease (independent risk factor), metabolic syndrome

PANCE pearls

  • Recurrent painful boils in the axillae or groin = HS until proven otherwise; not 'staph infections.'
  • Smoking cessation is the single most impactful lifestyle intervention — strongly counsel at every visit.
  • Double-headed open comedones in affected areas are pathognomonic.
  • Antibiotics work via anti-inflammatory mechanisms, not antimicrobial — failure to respond does not mean culture-directed therapy is needed.
  • Long-standing perineal/buttock HS carries a real risk of cutaneous SCC — biopsy any chronic non-healing lesion.

References

  • USCMS 2019 — North American Clinical Management Guidelines for Hidradenitis Suppurativa (Alikhan et al., J Am Acad Dermatol 2019)
  • EHSF 2019 — European S1 Guideline for the Treatment of Hidradenitis Suppurativa (Zouboulis et al., J Eur Acad Dermatol Venereol 2015; updates ongoing)
  • AAD 2024 — Joint AAD-HS Foundation Clinical Care Updates on Biologics and Surgical Options

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Commonly confused with

vs Folliculitis

Related Dermatology diagnoses

Acne VulgarisRosaceaAtopic Dermatitis (Eczema)Allergic and Irritant Contact DermatitisSeborrheic DermatitisPsoriasisLichen PlanusPityriasis RoseaTinea Infections (corporis, capitis, pedis, cruris, versicolor)Cutaneous CandidiasisScabiesPediculosisImpetigoHerpes Zoster (Shingles)

Differentials & related conditions

Crohn DiseasePilonidal Disease (Cyst, Abscess, Sinus)

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