Hidradenitis Suppurativa

Hidradenitis suppurativa (HS), also called acne inversa, is a chronic inflammatory disease of the hair follicle and its associated structures, occurring in intertriginous, apocrine-gland-bearing skin - most often the axillae, groin, perianal/perineal region, and inframammary folds.^[1][2] The disease process begins with follicular occlusion: keratinous debris and sebaceous material plug the follicle, which then ruptures into the surrounding dermis and triggers an intense, self-perpetuating inflammatory response - recruiting neutrophils, then a chronic granulomatous infiltrate, and ultimately driving the abscesses, sinus tracts, and scarring that define the disease.^[1][2] This is a genuinely important framing point for pharmacists: despite the name "suppurativa" and the fact that established lesions frequently become secondarily colonized or infected with skin and gut flora, HS is not primarily an infectious disease - it is an inflammatory one. This is exactly why oral antibiotic combination therapy is dosed and continued for its anti-inflammatory rather than purely antimicrobial effect (see Choose Initial Treatment), and why treating every flare as a simple skin infection, with repeated short antibiotic courses and no attention to the underlying inflammatory process, is a common and consequential error (see Common Errors to Avoid).

HS is common enough to matter in routine pharmacy practice but its reported prevalence varies enormously by how it is measured: population-based studies using routinely collected US healthcare data estimate a prevalence around 0.1%, while European studies designed to also capture undiagnosed disease typically estimate 1% or more - a more than 10-fold discrepancy that reflects how often HS goes undiagnosed or misdiagnosed as recurrent boils.^[3] The Canadian Dermatology Association estimates that between 300,000 and over 1 million Canadians live with HS.^[1] Onset is typically soon after puberty, most often in the teens or twenties, and women are affected roughly 3 times more often than men in North American and European populations (a ratio that is reversed in some other populations, underscoring that HS epidemiology does not generalize perfectly across all groups).^[3][1] HS is a chronic, relapsing disease with a substantial, often underappreciated impact on quality of life, driven by chronic pain, malodorous drainage, and a genuinely significant psychosocial burden - see Risk Factors and Complications.

Hurley stage II hidradenitis suppurativa in the axilla - a recurrent abscess with early sinus tract formation and scarring, in an otherwise widely separated single lesion. (Alharbi Z, Kauczok J, Pallua N, Wikimedia Commons, CC BY 2.5)

What HS looks like

The hallmark lesions are deep, painful, inflamed nodules and abscesses in the sites listed above, which recur over months to years and progressively evolve into sinus tracts ("tunnels") that intermittently or continuously drain malodorous, purulent or serosanguinous fluid, and eventually into fibrotic scarring, contractures, and open or "double-headed" comedones characteristic of chronically involved skin.^[2][1] Lesions are typically painful out of proportion to their size and can meaningfully limit movement - axillary disease can restrict arm mobility, and perianal or inguinal disease can make sitting or walking painful.^[1] The disease is chronic and recurrent: a single episode that never returns is not HS.^[2]

Hurley staging - directly drives the treatment ladder

The Hurley staging system, first described in 1989, remains the most widely used clinical severity classification and is the framework this chapter's treatment ladder (see Choose Initial Treatment) is built around.^[2]

Hurley stage can differ by anatomic site in the same patient (for example, Stage III axillary disease alongside Stage I groin disease), so stage - and treatment - should be assessed and recorded separately for each affected region rather than assigned once for the whole patient.^[2]

• Female sex - roughly 3 times more common in women than men across North American and European cohorts.^[3][1]
• Obesity - one of the 2 strongest, and genuinely modifiable, risk associations in HS; higher body mass index is linked to both HS risk and greater disease severity.^[3] This is why weight management is treated as a disease-modifying intervention in this chapter, not generic health advice (see Non-Pharmacologic Management).
• Cigarette smoking - the other strongly and consistently replicated, modifiable risk association; smoking is linked to both HS onset and greater severity.^[3] Smoking cessation is likewise treated as disease-modifying, not generic counseling (see Non-Pharmacologic Management).
• Family history - an estimated 1 in 3 patients with HS has an affected first-degree relative, consistent with a genetic contribution to follicular occlusion susceptibility.^[1]
• Age and hormonal timing - onset is typically soon after puberty, when androgen-driven sebaceous and apocrine gland activity rises; whether menopause reliably induces remission remains unknown.^[3]

A substantial, often underappreciated comorbidity burden

HS is not "just a skin disease" - it carries a comorbidity burden that changes how it should be assessed and followed, and every patient benefits from proactive screening rather than waiting for symptoms to be volunteered.^[4]

• Metabolic syndrome and cardiovascular risk - HS is associated with type 2 diabetes and metabolic syndrome, and patients with HS have roughly double the risk of cardiovascular death compared with people without HS, and about 1.5 times the risk compared with patients with psoriasis.^[3] This overlaps directly with the obesity and smoking associations above.
• Inflammatory bowel disease and inflammatory arthritis - both are significantly associated with HS, and perianal HS specifically can be difficult to distinguish from fistulizing Crohn disease (see Diagnosis/Differential and Red Flags/Refer).^[3][5]
• Depression, anxiety, and suicide risk - a systematic review and meta-analysis found a pooled depression prevalence of 16.9% in patients with HS (odds ratio 1.84 versus comparison groups) and an anxiety prevalence of 4.9%.^[6] Separately, completed suicide rates in patients with HS are more than double the rate in controls.^[3] This psychosocial burden is frequently driven as much by chronic pain, malodour, and disfigurement as by disease severity on examination, and deserves the same explicit, proactive counseling attention as the physical disease (see Patient Education within Monitoring and Follow-Up).
• Other documented associations include pilonidal sinus disease, polycystic ovary syndrome, and obstructive sleep apnea.^[3]

Complications

Beyond the recurrent nodules and abscesses themselves, long-standing, poorly controlled HS carries real complication risk. Chronic scarring and repeated inflammation can cause lasting functional limitation - restricted arm mobility with axillary disease, or lymphedema and contracture in a chronically involved region.^[1] Perianal/perineal HS can develop true fistulous tracts and can be genuinely difficult to distinguish from, or can coexist with, fistulizing Crohn disease.^[5] The psychosocial complications introduced in Risk Factors - depression, anxiety, and an elevated suicide rate - are complications of the disease in their own right, not a separate issue, and deserve the same clinical attention as any physical complication.^[6][3] Most seriously, squamous cell carcinoma (SCC) can arise within chronic HS sinus tracts - a well-described though uncommon complication, reported in roughly 2-5% of long-standing cases in surgical/case series, more common in men, and typically arising after many years (often decades) of poorly controlled disease. Because chronic HS skin is already thickened, scarred, and malodorous, a new malignancy can be masked by the background changes and diagnosed late, which is part of why HS-associated SCC carries a disproportionately poor prognosis once it develops.^[7]

Diagnosis is clinical

HS is diagnosed clinically, without a confirmatory laboratory test, using a widely accepted 3-part definition: (1) typical lesions - painful nodules, abscesses, draining sinus tracts, and/or fibrotic scars/comedones; (2) typical topography - the axillae, groin, perianal/perineal region, inframammary folds, or buttocks; and (3) chronicity and recurrence - at least 2 episodes in a 6-month period.^[2] All 3 elements should genuinely be present; a single self-limited boil in a typical location is not, on its own, sufficient for a diagnosis of HS.

Differential diagnosis

Investigations

Most patients need no laboratory or imaging work-up to confirm the diagnosis. Routine bacterial culture of draining lesions is not required for diagnosis or initial management - established HS lesions are frequently colonized with mixed skin and gut flora that do not reflect a true, treatable infection - but culture is reasonable when a superimposed infection or antibiotic resistance is specifically suspected (see Choose Initial Treatment and Treatment Failure/Next Step).^[2] Skin biopsy is not routinely needed but should be pursued for a genuinely atypical presentation, to help distinguish HS from fistulizing Crohn disease when the distinction is unclear, or - importantly - for any atypical, indurated, non-healing, or rapidly growing area within long-standing, chronically scarred HS, to exclude squamous cell carcinoma (see Red Flags/Refer).^[7] Imaging (ultrasound or MRI) is not routine but can help delineate the extent of sinus tract involvement before surgical planning in complex Stage III disease.^[2]

• Reduce the frequency, severity, and duration of inflammatory flares - nodules, abscesses, and draining sinus tracts.
• Prevent progression to a more advanced Hurley stage, since Stage III disease is materially harder to control and more often needs definitive surgery.
• Control pain, which is frequently the most disabling day-to-day symptom and does not always track visible lesion count.
• Improve quality of life and address the psychosocial burden of HS directly - not as an afterthought once the skin is controlled.
• Actively address the genuinely modifiable disease-driving factors - smoking and excess weight - as therapeutic goals in their own right, not only general health advice.
• Screen for, and coordinate care around, the comorbidities (metabolic syndrome, inflammatory bowel disease, depression/anxiety) that meaningfully affect this population's overall health.

Genuinely disease-modifying, not just general health advice

• Smoking cessation - one of the 2 strongest modifiable risk factors for both HS onset and severity; counsel and support cessation with the same priority given to it in other genuinely smoking-driven diseases, not as generic health messaging.^[3]
• Weight management - obesity is likewise strongly, and modifiably, associated with both HS risk and severity; even modest, sustained weight loss is a reasonable, evidence-supported therapeutic goal alongside pharmacologic treatment, not a separate lifestyle conversation.^[3]

Supportive local measures

• Warm compresses to an acutely inflamed nodule can ease pain and may help a superficial lesion drain spontaneously.
• Loose-fitting, breathable clothing over affected areas reduces friction and sweat retention, both of which can provoke flares.
• Antiseptic washes (chlorhexidine or benzoyl peroxide wash) to affected areas can reduce secondary bacterial colonization as an adjunct to medical therapy.^[8]
• Avoid tight or occlusive dressings and harsh mechanical exfoliation over active lesions, which can worsen follicular trauma and inflammation.

Psychosocial support

Given the depression, anxiety, and elevated suicide risk documented in this population (see Risk Factors), proactively ask about mood, coping, and quality-of-life impact rather than waiting for a patient to raise it, and have a concrete pathway ready for referral to mental health support when needed.^[6][3] Patient support organizations, including the Canadian Hidradenitis Suppurativa Foundation, can be a valuable adjunct for peer support and practical coping strategies.^[14]

Pregnancy

Breastfeeding

Topical and oral clindamycin are compatible with breastfeeding. Avoid prolonged tetracycline-class therapy. Spironolactone requires individualized discussion given limited infant safety data at HS doses. Adalimumab is generally considered compatible with breastfeeding given minimal transfer into breast milk.

Adolescents

HS onset soon after puberty means adolescent presentations are not rare; the same clinical diagnostic approach applies. Involve a parent/guardian and, where available, pediatric dermatology in staging and treatment decisions, particularly before starting a biologic or an oral antibiotic combination course, and pay particular attention to the psychosocial impact - HS at this age can meaningfully affect school attendance, activity participation, and self-esteem during a formative period (see Non-Pharmacologic Management).

Obesity and metabolic comorbidity

Given the strength of the obesity association (see Risk Factors), actively support weight management as part of the treatment plan rather than treating it as a separate issue, and consider referral for bariatric surgery assessment in a patient with severe, refractory, obesity-associated Stage III disease and no adequate response to medical therapy, in coordination with their broader care team.^[3][4]

Reassess disease activity at each visit by lesion count, drainage, pain, and functional impact (not appearance alone), and confirm genuine adherence before labelling a regimen a failure - see Treatment Failure/Next Step.^[8]

Patient education

• HS is a genuine chronic inflammatory disease, not a hygiene problem - explicitly correct the common and hurtful misconception that HS results from poor hygiene or is contagious; it is neither.^[1]
• Set realistic expectations: HS is a relapsing-remitting condition best managed as a long-term program (often combining medical and, eventually, surgical treatment) rather than something cured by a single antibiotic course or a single drainage procedure.
• Explain clearly that incision and drainage relieves an acute abscess but does not address the underlying sinus tract, so recurrence at or near the same site is expected without more definitive treatment.^[2]
• Reinforce that smoking cessation and weight management are genuinely disease-modifying interventions, not just general wellness advice, and connect the patient with concrete support for both when there is interest.
• Normalize and proactively ask about the emotional impact of HS - pain, malodour, and visible disease meaningfully affect mood and relationships for many patients, and support is available and worth accessing (see Non-Pharmacologic Management).

1. Confirm the diagnosis and current Hurley stage are both still accurate, and confirm genuine adherence to the current regimen (topical technique, oral antibiotic completion, hormonal therapy timing) before calling it a failure.
2. Stage I disease not controlled by topical clindamycin and antiseptic washes after a reasonable trial: add a short oral antibiotic course, or reassess whether the disease has actually progressed to Stage II.^[8]
3. Stage II disease not controlled by an adequate 10-12 week course of clindamycin plus rifampin (or a tetracycline-class alternative): add hormonal therapy in women with a plausible hormonal pattern, and pursue deroofing for a persistent, localized sinus tract.^[8][2]
4. Stage II/III disease inadequately controlled by the combination of oral antibiotics, hormonal therapy, and targeted procedures: proceed to biologic therapy, with adalimumab (at its weekly HS-specific dose) as the preferred first agent.^[11]
5. Inadequate response to, or loss of response to, adalimumab: switch to an alternative biologic (secukinumab or bimekizumab) rather than repeatedly extending or re-trialling the same agent.^[12][13]
6. Extensive Stage III disease, or a persistent localized area not responding to medical therapy: refer for surgical assessment - deroofing for a discrete area, or wide local excision for extensive, interconnected disease - generally alongside, not instead of, continued medical therapy.^[2]
7. At any point where GI symptoms raise concern for coexisting Crohn disease, or where a chronic lesion looks atypical, refer appropriately (gastroenterology, or biopsy to exclude squamous cell carcinoma) rather than continuing to escalate HS-directed therapy alone.^[5][7]

• Treating HS purely as recurrent "boils" or skin infections, with repeated short antibiotic courses aimed at an infection rather than addressing the underlying follicular-occlusion and inflammatory process — this both under-treats the disease and needlessly escalates antibiotic exposure.
• Using clindamycin or another antibiotic as extended HS monotherapy rather than as part of the evidence-based clindamycin-plus-rifampin combination.
• Treating incision and drainage of an abscess as if it were curative, without explaining to the patient that recurrence at the same site is expected without more definitive medical or surgical therapy.
• Dosing adalimumab at the every-other-week schedule used for rheumatoid arthritis or psoriasis rather than the weekly maintenance dose specific to HS.
• Treating smoking cessation and weight management as optional lifestyle advice rather than genuinely disease-modifying interventions worth the same counseling priority as any prescribed medication.
• Missing the opportunity to screen for depression, anxiety, and the broader comorbidity burden (metabolic syndrome, inflammatory bowel disease) because the visit focused solely on the skin.
• Failing to consider hormonal therapy (spironolactone or a combined oral contraceptive) in a woman with an obvious menstrual-cycle-linked flare pattern.
• Missing a new, atypical, non-healing, or rapidly growing area within long-standing, chronically scarred HS as "just another flare" rather than biopsying to exclude squamous cell carcinoma.
• Delaying biologic escalation in genuinely Stage III disease by repeatedly cycling through further oral antibiotic courses instead of moving to adalimumab or an alternative biologic.

How to use this table: doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment and pregnancy status. Surgical management (incision and drainage, deroofing, wide excision) is covered in Choose Initial Treatment and is not a pharmacotherapy, so it is not repeated here. Select any drug name to open its complete Pharmasist Drug Database page.

Topical Therapy — Hurley Stage I / Mild Disease

First-line for genuinely mild or localized disease; also used as an ongoing adjunct at every stage.

Oral Antibiotic Therapy — Hurley Stage II (or a more inflamed Stage I flare)

Dosed and continued for an anti-inflammatory, not purely antimicrobial, effect — this is not treatment of a simple skin infection.

Hormonal Therapy — Women, Adjunct or Alternative

Consider specifically for a woman with a menstrual-cycle-linked flare pattern.

Biologic Therapy — Hurley Stage III or Refractory Moderate-Severe Disease

Adalimumab is the preferred first biologic given the depth of its trial evidence base in HS; secukinumab and bimekizumab are reasonable alternatives, particularly after an inadequate response.