Hidradenitis suppurativa

Meet the patient

A 29-year-old woman has spent seven years being treated for "recurrent boils" in her axillae and groin — courses of flucloxacillin, repeated incisions, and a growing dread of summer. Now her axillae are crossed by rope-like scars and draining sinus tracts, the pain stops her exercising, and she has stopped socialising. She smokes twenty a day and her BMI is 33. She has never heard the name of her disease.[1][6]

Two questions reframe her care: is this really recurrent staphylococcal boils? — no, and the seven-year delay is the textbook HS story — and what stage is she, and what drives her severity? Smoking and obesity are modifiable, and the Hurley stage decides whether she needs a biologic and surgery, not another antibiotic.[1][4]

Not a boil — the follicular occlusion cascade

HS is a disease of the hair follicle, not the apocrine gland and not an infection. The name (hidro-, sweat; suppurativa, pus-forming) is a 170-year-old misnomer that still misleads: cultures from active lesions are usually sterile or grow only commensals, and repeated antibiotics alone rarely induce remission.[1][6]

The primary event is occlusion of the follicular infundibulum by hyperkeratosis, compounded in the folds by friction, heat, occlusion and hormones (insulin, IGF-1, androgens) — and powerfully by nicotine, which drives follicular hyperkeratosis and cripples neutrophils. The occluded follicle distends with keratin, sebum and commensals, then ruptures, spilling its contents into the dermis.[1][6]

That rupture lights the fire: an innate neutrophil-rich response (IL-1-beta, IL-17, complement) amplified by an adaptive IL-23/Th17 and TNF-alpha cascade. The consequences are the disease's signature — abscess, epithelialised sinus tract (the permanent reservoir), and rope-like fibrosis. Every biologic you will name targets a node on that cascade (TNF, IL-17, IL-23).[4][6]

Etymology for viva gold: hidradenitis (Greek hidros, sweat, plus aden, gland) and apocrinitis both imply the apocrine gland is the culprit — it is not; it is a bystander caught in follicular inflammation. Acne inversa, the modern synonym, is the honest name: the lesion is an inverted, follicular occlusion process in the folds. Verneuil disease honours the French surgeon who described it in 1854, when the apocrine theory was plausible.[1]

Hurley staging — the bedrock that decides everything

Hurley stage at presentation is the single most important fact about an HS patient: it sets the treatment, predicts the prognosis, and decides who needs a biologic or surgery. Memorise the three stages as a ladder of irreversible change.[1]

Hurley's limitation: it is static and weighted toward late scarring, so it does not capture activity or response. The dynamic IHS4 (nodules x1, abscesses x1, draining tunnels x2, inflammatory skin lesions x4; mild under 4, moderate 4-10, severe 11 or more) and HiSCR (at least 50 percent reduction in abscess and inflammatory nodule count with no rise in abscesses or draining tunnels) do — the latter is the trial endpoint.[2][7]

How common, who, and the seven-year delay

[1] [6]

HS is not rare — about 1-4 percent of adults — with onset typically post-pubertal, a late-teens-to-early-30s peak (and a second postmenopausal peak in women), and a roughly three-to-one female predominance that flips to male in perianal disease. Prevalence and severity run higher in Black and Afro-Caribbean populations, partly genetic, partly under-recognition.[1][6]

The seven-to-twelve-year diagnostic delay is itself a morbidity — years of mislabelled "boils", repeated incision-and-drainage, and short antibiotic courses that were never going to work. Spotting the disease early changes a life, because Hurley I is largely reversible and Hurley III largely is not.[1][4]

The comorbidities that change the plan

HS is a systemic inflammatory disease, not a skin complaint, and its comorbidities are examinable because they change therapy. Three deserve a named screen at baseline: inflammatory bowel disease, spondyloarthropathy, and depression.[1][6]

• Inflammatory bowel disease — a three- to five-fold increased risk, overwhelmingly Crohn's; screen with symptoms, faecal calprotectin and gastroenterology referral, because perianal disease overlaps and adalimumab treats both.[1][6]
• Spondyloarthropathy and sacroiliitis in 10-20 percent, on a shared IL-23/IL-17 axis.[4]
• Depression and anxiety in 30-50 percent, with elevated suicide rates — screen with PHQ-9 at every visit. HS has one of the lowest DLQI scores in dermatology.[4][6]
• Metabolic syndrome, type 2 diabetes and cardiovascular disease track with the chronic inflammation and obesity.[1]
• Down syndrome — markedly over-represented, through Nicastrin copy-number on chromosome 21.[5]

The follicular occlusion tetrad — HS, acne conglobata, dissecting cellulitis, pilonidal sinus — shares the same follicular occlusion mechanism and can coexist in one patient.[1]

Read the lesions — the cardinal six and the diagnostic criteria

Painful deep nodules and abscesses in the axillae, groin, buttocks or inframammary folds, with double-headed comedones, sinus tracts and rope-like scarring, recurring for over six weeks, is HS until proven otherwise. The international diagnostic criteria need typical lesions, typical sites, and chronicity — all three.[1]

The classic trap: treating this as recurrent staphylococcal boils. The discriminators are the double-headed (paired) comedones, the sinus tracts and bridging scars, the intertriginous distribution, and the chronicity — none of which belong to furunculosis, which responds to antibiotics, grows Staphylococcus aureus, and resolves in days to weeks.[1]

The cardinal six (ABSCDR): abscess, bridging rope-like scars, comedones double-headed, sinus tracts, draining fistulae, recurrent nodules. Double-headed comedones are highly specific but not sensitive.[1]

Face-off — HS versus its closest mimics

[1]

The discriminator line: comedones that come in pairs, sinus tracts that bridge, and scars that rope across a fold, in apocrine skin, recurring for months — that is HS, not boils, not Crohn's, not acne conglobata.[1]

Investigations — clinical first, biopsy for the danger sign

HS is a clinical diagnosis. Document the Hurley stage and IHS4 with a dated photograph, screen the comorbidities, and reserve tests for staging, surgical planning and excluding mimics or complications.[1][7]

• Swabs during flares grow polymicrobial flora and do not change management — culture only at first presentation, when cellulitis is suspected, or when antibiotics are failing (to catch resistant organisms).[1]
• High-frequency ultrasound (15-20 MHz) is the bedside gold standard for counting subclinical lesions and mapping tunnels before surgery; MRI pelvis separates perianal HS from Crohn's fistulation and stages suspected squamous cell carcinoma.[4][6]
• Biopsy is mandatory when a chronic sinus tract becomes proliferative, ulcerated, bleeding or painful — exclude squamous cell carcinoma (Marjolin ulcer). It is also needed if Crohn's, atypical infection or lymphoma is in the differential.[6]

At baseline screen BMI, fasting glucose, HbA1c, lipids and blood pressure; screen for IBD symptoms and faecal calprotectin, spondyloarthropathy symptoms, and depression (PHQ-9); and check pregnancy and contraception before any retinoid.[1]

Management — four pillars, staged by Hurley

Pillar 1 — lifestyle for everyone (and the smoker is the highest-yield patient)

Smoking cessation is the single highest-yield intervention in HS, and offering advice without prescribing nicotine replacement is a recurring failure point. Use the 5 As plus nicotine replacement, varenicline or bupropion; document it. Weight loss (BMI optimisation, GLP-1 agonists, bariatric surgery in severe obesity), loose cotton clothing, no shaving or waxing of folds, antiseptic washes (chlorhexidine 4 percent, benzoyl peroxide 5-10 percent), wound care and analgesia complete the foundation.[1][7]

Pillar 2 — topical and intralesional (Hurley I; adjunct in II)

Pillar 3 — oral systemic therapy (Hurley II; adjunct in III)

[1] [7]

Pillar 4 — biologics and surgery (Hurley III, refractory II)

HS biology is dominated by TNF-alpha, IL-17A/F and IL-23, and these are the targets — adalimumab first, secukinumab and bimekizumab next.[4][7]

Adalimumab is dosed more intensively in HS than in psoriasis or Crohn's (weekly, not alternate-weekly, from week 4) — a viva trap. Screen for tuberculosis before starting, and avoid in active infection, severe heart failure, or demyelinating disease. A paradox: anti-TNF drugs can themselves trigger HS-like lesions, especially in IBD — switch to an anti-IL-17.[1][6]

Surgery is integral to Hurley III. Four approaches: incision and drainage (acute abscess relief only — does not prevent recurrence), deroofing (unroofing individual tunnels to heal by secondary intention, ideal for localised Hurley II), wide local excision down to fascia with a 1-2 cm margin (definitive; recurrence 2-5 percent versus 50-100 percent after drainage alone), and laser (CO2 ablation of tracts; Nd:YAG hair reduction to prevent re-occlusion). The best outcomes come from medical stabilisation first (3-6 months of biologic), then surgical extirpation, then continued biologic — and smoking cessation 4-6 weeks pre-op to cut wound complications.[1][4][7]

How patients with HS come to harm (the preventable list)

• Squamous cell carcinoma (Marjolin ulcer) in a chronic sinus tract after 20-30 years — biopsy any non-healing, bleeding or proliferative tract; metastasis in up to 50 percent[6]
• Years of misdiagnosis as boils, treated with incision-and-drainage and short antibiotics that were never going to work[1]
• Untreated depression and suicidality — PHQ-9 never screened in a disease with the lowest dermatology quality-of-life scores[4][6]
• Smoking cessation advised but never prescribed — the single highest-yield intervention left on the table[1][7]
• Adalimumab started without a TB screen, or dosed at the psoriasis (alternate-weekly) schedule rather than the HS weekly schedule[1]
• Rifampicin added without checking interactions — OCP failure, methadone withdrawal, warfarin destabilisation[1]
• Retinoid given in pregnancy — teratogenic; contraception and pregnancy test first[1]

Special populations

Pregnancy: topical clindamycin is safe (category B); oral tetracyclines, acitretin and isotretinoin are contraindicated; adalimumab is generally compatible but discontinue in the third trimester if possible; defer wide excision until postpartum.[1]

Paediatric HS (about 2 percent of cases, often pre-menarche): screen for early PCOS or androgen excess, and for Down syndrome in prepubertal children; avoid tetracyclines under 12 years; weight-based dosing; family education on smoking and weight is pivotal.[5]

HS with IBD: adalimumab treats both HS and Crohn's and is often first-line; avoid secukinumab in active ulcerative colitis (it can worsen it); biopsy perianal tracts to separate HS, Crohn's and squamous cell carcinoma.[1]

HS with PCOS or hyperandrogenism: hormonal therapy is central — combined OCP, spironolactone 50-100 mg, finasteride 5 mg, metformin; refer to endocrinology or gynaecology.[1]

Prognosis and quality of life

HS is chronic and lifelong; spontaneous remission is uncommon (about 15 percent at 10 years, mostly in mild disease). Hurley stage at presentation is the principal prognostic factor — Stage I rarely progresses, Stage III is largely irreversible without surgery. Quality of life is among the worst in dermatology, comparable to or worse than psoriasis and atopic dermatitis; depression affects 30-50 percent, sexual dysfunction over half of those with perineal disease, and work absenteeism is high. Screen PHQ-9 at every visit and treat the person, not just the skin.[4][6]

The mantra, and the memory device

[1] [6]

The mantra: not a boil — it is follicular occlusion; stage by Hurley, treat the smoker, escalate topical to oral to biologic to surgery, and biopsy the changing sinus.[1][7]

Ward-round test — three stems, thirty seconds each

Stem 1 — seven years of recurrent boils (answer)

A 29-year-old smoker with BMI 33 has recurrent axillary and groin abscesses, double-headed comedones and rope-like scarring for seven years, treated as boils. What is it, and what is the first conversation? Model: Hidradenitis suppurativa, Hurley II-III — the double-headed comedones, sinus tracts and bridging scars in apocrine folds are diagnostic, and the seven-year delay is typical. The first conversation names the disease and reframes it: it is follicular, not infectious, so antibiotics alone will not work. Document Hurley stage and IHS4, screen for IBD, depression (PHQ-9) and metabolic syndrome, and — the highest-yield single intervention — prescribe smoking cessation with nicotine replacement, not just advise it. Then stage therapy: clindamycin-rifampicin or a tetracycline now, with a biologic and surgical pathway for Stage III disease.[1][6][7]

Stem 2 — the changing sinus tract (answer)

A 55-year-old with 25 years of Hurley III HS has a chronic perianal sinus that has become raised, bleeding and painful over two months. Next step? Model: Urgent biopsy to exclude squamous cell carcinoma (Marjolin ulcer) — a chronic non-healing sinus tract that turns proliferative, ulcerated or bleeds after decades of HS is the can't-miss complication, with metastasis in up to 50 percent. Stage with MRI pelvis for depth, and involve surgery and oncology. Do not keep dressing it. Also separate it from perianal Crohn's with endoscopy if the biopsy is granulomatous rather than malignant.[6]

Stem 3 — HS plus bloody diarrhoea (answer)

A 34-year-old with Hurley II HS develops chronic bloody diarrhoea and perianal fistulae. How does this change the plan? Model: Screen for inflammatory bowel disease — HS carries a three- to five-fold increased risk, overwhelmingly Crohn's, and perianal disease overlaps. Send faecal calprotectin and refer to gastroenterology for endoscopy and biopsy. The therapeutic point examiners want: adalimumab treats both HS and Crohn's, so it becomes first-line; avoid secukinumab if there is active ulcerative colitis. Biopsy the perianal tracts to separate HS, Crohn's and squamous cell carcinoma.[1][6]

References

1. [1]Goldburg SR, Strober BE, Payette MJ. Hidradenitis suppurativa: Epidemiology, clinical presentation, and pathogenesis J Am Acad Dermatol, 2020.PMID 31604104
2. [2]Jenkins T, Isaac J, Edwards A, et al. Hidradenitis Suppurativa Dermatol Clin, 2023.PMID 37236715
3. [3]González-López MA. Hidradenitis suppurativa Med Clin (Barc), 2024.PMID 37968174
4. [4]McCarthy S. Hidradenitis Suppurativa Annu Rev Med, 2025.PMID 39869430
5. [5]Cotton CH, Chen SX, Hussain SH, et al. Hidradenitis Suppurativa in Pediatric Patients Pediatrics, 2023.PMID 37102307
6. [6]Sabat R, Alavi A, Wolk K, et al. Hidradenitis suppurativa Lancet, 2025.PMID 39862870
7. [7]Zouboulis CC, Bechara FG, Benhadou F, et al. European S2k guidelines for hidradenitis suppurativa/acne inversa part 2: Treatment J Eur Acad Dermatol Venereol, 2025.PMID 39699926