Hidradenitis Suppurativa: The Recurrent 'Boils' That Have a Name and a Staging System

Seven years of being told it's boils

There is a specific kind of medical exhaustion that comes from a condition everyone recognises and nobody names. A painful lump appears in the armpit, groin, or under the breast. It is lanced, or it drains on its own. Antibiotics are prescribed. It heals, and then it comes back — same place, or a new one an inch over — and the cycle restarts. Somewhere in the second or third year the word "hygiene" enters the conversation, usually gently, and it lands like an accusation.

The published numbers on this are stark. Studies of diagnostic delay in hidradenitis suppurativa put the gap between first symptom and correct diagnosis at roughly seven to ten years, with one cohort reporting a mean of over ten. In that window people typically pass through three or more different specialties — general practice, dermatology, surgery, gynaecology — and collect three or more incorrect labels along the way. The delay is not evenly distributed either: it runs longer in people whose disease starts young, and it correlates with how severe the disease is by the time anyone gets it right.

That last point is the one worth sitting with. This is not a condition where waiting is neutral.

The name is wrong, and the wrong name is the problem

"Hidradenitis suppurativa" translates roughly to inflammation of the sweat glands with pus. Both halves of that are misleading, and the misdirection is not academic — it is the reason so many people are handed an antibacterial wash and sent home.

The disease starts in the hair follicle. Current understanding places the primary event at occlusion of the folliculopilosebaceous unit: the follicular opening keratinises and thickens, debris accumulates behind the plug, the follicle distends and eventually ruptures into the surrounding dermis. What follows is the part people actually see — a violent immune response to follicular contents where they do not belong. Sweat glands are bystanders. Bacteria colonise the mess, and can worsen it, but they are not the initiating event.

This matters because it explains the treatment failures. If the problem were bacterial, antibacterial soap would fix it, and it does not. If it were hygiene, it would track with washing, and it does not. What the mechanism actually predicts is that anything reducing follicular occlusion or damping the inflammatory response will help, and anything aimed purely at surface bacteria will not — which is precisely the pattern the evidence shows.

The condition is also more common than its obscurity suggests. Prevalence estimates range widely depending on how cases are ascertained, from well under one percent to several percent, with a consistent female predominance. Even the conservative end of that range describes a very large number of people being told to wash more.

Hurley I, II, III — architecture, not activity

Hurley staging is the shorthand every HS patient eventually hears, and it is worth understanding precisely because it is so often misread as a severity score.

Stage I is abscesses — single or multiple — without sinus tracts and without scarring. Stage II is recurrent abscesses with tract formation and scarring, in separated lesions. Stage III is diffuse involvement of an entire area, with multiple interconnected tracts and abscesses across it.

Read the definitions again and notice what they describe: structure. A tunnel is a physical channel lined with epithelium. A scar is fibrosis. Neither of these is a measure of how inflamed you are this month, and neither of them goes away when the inflammation is controlled. This is why a person can be doing genuinely well on treatment and still be Stage II — and why "you're still Stage II" is not the same statement as "the treatment isn't working."

It is also the clearest argument for early intervention that dermatology has. Medication can quiet inflammation and prevent new tracts from forming. It cannot un-tunnel skin. Everything that gets built during a diagnostic delay stays built, and the only thing that removes it afterwards is surgery. If you want a number for how much of you is involved and how that changes over time, the HS severity check and the body surface area painter are both more reliable than a memory of last month.

What the shelf can honestly do

Supportive care in HS is real, underrated, and frequently oversold — usually by people who have nothing better to offer.

Antiseptic washing is the piece with the most support. Benzoyl peroxide washes are recommended in the North American management guidelines as adjunctive care, and the logic is sound: ↗benzoyl peroxide reduces bacterial colonisation without driving resistance, which matters enormously in a condition treated with repeated courses of antibiotics. A gentler formulation like PanOxyl's 4% creamy wash is usually the right starting point for intertriginous skin, where a 10% foaming version such as PanOxyl 10% can be more than thin, occluded folds will tolerate. Use it as a wash with genuine contact time, not as a scrub — and expect it to reduce flare frequency at the margins, not to clear disease.

On the days when skin is raw from treatment, a bland non-medicated cleanser like Aveeno's Restorative Skin Therapy wash is a better choice than pushing through with a keratolytic, and friction management — loose fabric, seams away from lesions, an emollient barrier such as CeraVe Moisturizing Cream where clothing rubs — does more than most people expect for a mechanism driven by follicular trauma.

What none of this does is treat the disease. Supportive care lowers the noise floor. The ceiling is low and it arrives fast, and continuing to shop past it is the most common way another year disappears.

The ladder that starts where the shelf stops

The treatment sequence in HS is well documented, and the useful thing to know is that it is a genuine ladder — each rung exists because the one below it has a known limit.

Topical clindamycin 1% is the first prescription rung, and it is the only topical with randomised support: a double-blind trial in the early 1980s found it significantly better than placebo across abscesses, nodules and pustules, and a later head-to-head found topical clindamycin performed comparably to systemic tetracycline in mild-to-moderate disease. That is a meaningful result — it means many people at Hurley I do not need to start systemically.

Above that sit oral tetracyclines, then combination clindamycin and rifampicin, then hormonal approaches in appropriate candidates, then the biologics. The biologic rung is where the last decade actually changed something. Two phase 3 trials of adalimumab established that a targeted therapy could move the needle in moderate-to-severe disease, with roughly 42% and 59% of weekly-dosed patients hitting the response threshold at week 12 against 26% and 28% on placebo. More recently, two identical phase 3 trials of secukinumab demonstrated rapid improvement with response sustained through 52 weeks, opening a second mechanism for people who fail or lose response to the first.

These are not cure rates, and it is worth being blunt about that. A trial endpoint of a 50% reduction in inflammatory lesions is a real improvement in a disease this painful, and it is not remission. Surgery — deroofing for individual tracts, wider excision for established Stage III — remains part of the plan for architecture that medication cannot reach.

The words that get you taken seriously

If you recognise yourself in this, the single most useful thing you can do is change what you present at the appointment. "I keep getting boils" invites the treatment you have already had. "I get recurrent painful lumps in the same flexural sites, they have been coming back for years, some have left scars, and I think this may be hidradenitis suppurativa" is a different consultation. Recurrence, typical sites, and duration are the three features that distinguish HS from an isolated abscess, and stating all three is what moves you from the wrong list to the right one.

Bring evidence rather than recall. Photograph lesions when they are active, because they will not be active on the day you are seen, and keep a dated record of flares, sites and pain — a flare diary makes a pattern legible in a way that memory reliably fails to. If a clinician suggests you are simply prone to infections, the question worth asking directly is whether this could be hidradenitis suppurativa and what would rule it out.

Some things justify moving faster than a routine referral: a lesion that will not stop draining, rapidly worsening pain, fever with a spreading area of redness, or any long-standing tract that changes in character. And because HS travels with metabolic, inflammatory and psychiatric comorbidities, a first appointment should include screening for them rather than treating the skin in isolation.

The honest summary is that this is a chronic disease with imperfect treatments, all of which work better the earlier they start. Nobody gets those years back, but the ones ahead are still negotiable — and none of it starts until the condition is called by its name.