Hidradenitis Suppurativa: The Inflammation Behind Recurring Boils

TL;DR: Hidradenitis suppurativa is a chronic inflammatory disease driven by the immune system, and it produces painful, deep lumps in the armpits, groin, buttocks, and under the breasts that come back in the same places and can leave scars and tunnels under the skin. It has nothing to do with how well you wash, and it is a poor fit for the word infection, which is why courses of antibiotics prescribed as if for a boil keep failing. The process starts when a hair follicle plugs and ruptures, spilling its contents into the surrounding skin and setting off an inflammatory cascade that keeps running. It travels closely with insulin resistance, metabolic syndrome, and PCOS, which is why this belongs in primary care as much as dermatology. People wait years for the diagnosis, commonly the better part of a decade, and that delay is the most fixable part of the whole story. Treatment ranges from anti-inflammatory antibiotics and hormonal medication to metformin and modern biologics, and it works far better when the metabolic drivers are treated at the same time.

If you have this, you have probably been told it was a boil. Then another boil. You may have had them drained more than once, taken courses of antibiotics that helped for a few weeks, and heard some version of a suggestion about hygiene. Meanwhile the lumps kept returning to the same spots, the scars built up, and sitting, walking, or raising your arm became something you plan around. Many people carry this for years without a name for it, and carry a quiet shame with it that the condition never deserved.

What I want you to know first is that this has a name, it is more common than the silence around it suggests, and it is an immune-driven disease rather than a hygiene failure or a run of bad luck with infections. Once that is clear, the treatments that work start to make sense.

What is hidradenitis suppurativa?

Hidradenitis suppurativa is a chronic inflammatory skin disease that produces painful nodules and abscesses in areas where skin meets skin: the armpits, the groin, the inner thighs, the buttocks, and under the breasts. The lumps sit deep, they hurt out of proportion to how they look, and they return to the same territory again and again.

Over time, the repeated inflammation can join separate spots together beneath the surface into narrow channels called sinus tracts, or tunnels, which drain and refuse to heal. Scarring follows, and in the areas worst affected the skin can become thickened and cord-like. Dermatologists grade severity with the Hurley stages: stage one is isolated lumps with no tunnels or scarring, stage two adds recurrent lesions with tunnels and scarring in separated areas, and stage three describes widespread involvement across an entire region.

The name is a historical accident worth undoing. It was assigned when the disease was believed to arise in the sweat glands, and the word suppurativa points at pus, which pushes everyone toward thinking about infection. Both parts of that picture turned out to be wrong. The disease begins at the hair follicle, and the pus is the debris of an inflammatory process rather than the sign of an ordinary infection.

Prevalence estimates vary depending on how cases are counted, from around 0.1 percent in United States insurance claims data to roughly 1 percent in European surveys, and there is wide agreement that the true figure is higher than the recorded one because so many cases go unnamed. It usually begins after puberty, most often in the 20s and 30s, and it affects women more often than men.

Why does this keep coming back?

Here is the mechanism, and it explains both why the lumps recur in the same places and why treating them as ordinary boils keeps failing.

The process starts at the hair follicle. In hidradenitis suppurativa, the lining of the follicle thickens and the follicle plugs, which traps keratin and its normal contents inside. Pressure builds, and the follicle ruptures into the surrounding skin. That spill puts keratin and skin bacteria into tissue where they have no business being, and the immune system responds the way it should to material in the wrong place: it mounts an aggressive inflammatory reaction.

What separates this disease from a one-off blocked follicle is what happens next. In hidradenitis suppurativa the immune response overshoots and then keeps running. Inflammatory signals including interleukin-1 and the interleukin-17 pathway draw in waves of neutrophils, the immune cells that produce pus, and this self-sustaining inflammation damages the surrounding tissue. As the cycle repeats, the body attempts to wall off the damage, which is how the tunnels and scars form. The follicles in that area remain primed, so new lesions rise in the same neighborhoods.

Two things follow from this that matter a great deal for how you are treated. The first is that washing has no bearing on it. The trigger sits inside the follicle and in the immune response to it, and no amount of scrubbing reaches either. Scrubbing an inflamed area adds friction, which makes things worse. If you have been carrying embarrassment about this, you can set it down.

The second is that this is a poor fit for the word infection. Bacteria are part of the story once a follicle has ruptured and later when tunnels are colonized, and the engine is immune rather than infectious. This is why a week of antibiotics for a boil gives partial relief and then the lumps return. It is also why the antibiotics that do help in this disease, such as the tetracyclines, are chosen largely for their anti-inflammatory effect and given for months rather than days.

Why does it take so long to get diagnosed?

The delay in this condition is one of the widest in medicine. Research across multiple countries found that people with hidradenitis suppurativa wait years longer for a diagnosis than people with other skin diseases, commonly around 7 years from the first symptoms.

Several forces stack up to produce that. The lesions appear in private areas, so people wait before showing anyone. When they do seek help, it is often during a flare at an urgent care or emergency department, where a single painful lump gets drained and treated as an isolated abscess, and nobody assembles the pattern across visits. The name itself is unfamiliar to many clinicians outside dermatology. And the disease has no confirmatory blood test or biopsy, so recognizing it depends on someone knowing the pattern: recurrent, painful, deep lesions, in skin folds, coming back in the same places.

That pattern is the whole diagnosis, and it is why I want people to know the name. Lesions in those locations, recurring twice or more within 6 months, is enough to raise this and start treatment. The years lost to not naming it are years when scarring accumulates, and scarring is the part that treatment cannot undo.

What is the link between hidradenitis suppurativa and insulin resistance?

This is where a skin condition becomes a whole-body one, and where primary care has more to contribute than most people are told.

Hidradenitis suppurativa travels with metabolic dysfunction at a rate too high to be coincidence. In case-control research, insulin resistance was found in roughly 46 percent of people with hidradenitis suppurativa compared with about 8 percent of controls, and metabolic syndrome in roughly 32 percent compared with about 5 percent. Broader reviews confirm strong associations with obesity, metabolic syndrome, cardiovascular disease, and higher all-cause mortality.

The relationship appears to run in both directions rather than in a simple line. Insulin resistance raises circulating insulin and androgens, both of which drive the follicular plugging that starts the process, and the low-grade inflammation that accompanies metabolic dysfunction feeds an immune system already inclined to overreact. Running the other way, living with a painful chronic inflammatory disease affects sleep, movement, and stress, and all of those feed back into metabolic health.

I want to be careful with this, because people with this condition have often been told their weight caused it, which is both unkind and inaccurate. Lean people get hidradenitis suppurativa, and the disease is not a verdict on anyone's habits. What the association does mean is practical: everyone with this diagnosis deserves screening for insulin resistance, blood sugar, lipids, and blood pressure, because the cardiovascular risk that travels alongside it is substantial and treatable, and because addressing the metabolic layer often improves the skin as well.

Is there a connection to PCOS and hormones?

Yes, and it is strong enough to be worth checking in every woman with this diagnosis.

Women with hidradenitis suppurativa have substantially higher odds of also having polycystic ovary syndrome, with pooled analyses putting the odds at roughly two and a half times that of women without it, and the relationship holds looking the other direction as well: women with PCOS are about twice as likely to develop hidradenitis suppurativa. The shared ground is androgens and insulin. Both conditions involve androgen effects on the follicle, both involve insulin resistance, and each amplifies the other.

The clinical timing points the same way. This disease typically begins after puberty, often flares in the week before a period, may improve or worsen in pregnancy, and tends to settle after menopause. That is the signature of a hormonally responsive condition, and it opens a line of treatment that gets overlooked when the problem is filed under skin infections.

What treatments work?

Treatment is chosen by severity, and the honest framing is that this is a condition we control well rather than one we cure. The goal is fewer flares, less pain, and above all preventing the scarring and tunneling that cannot be reversed.

For milder disease, topical clindamycin is a starting point, and oral tetracycline antibiotics such as doxycycline are used for months at a time for their anti-inflammatory effect. Antiseptic washes reduce bacterial load in affected areas. For flares, an injection of corticosteroid into a painful lesion settles it quickly, which is a far better option than the incision and drainage that people often receive repeatedly, since draining alone does nothing for the underlying process and adds scarring.

For women, hormonal treatment is frequently valuable and frequently skipped: spironolactone, an anti-androgen, and combined oral contraceptives both have a place, particularly when flares track with the menstrual cycle or PCOS is present.

Metformin deserves its own mention because it sits at the intersection of the two stories. It improves insulin sensitivity, and small open-label studies have found improvement in disease severity, with the strongest rationale in people who have insulin resistance or PCOS alongside their skin disease. The evidence base is modest rather than definitive, and I want to be clear about that, and given its safety and its independent value for the metabolic picture, it earns consideration in the right person.

For moderate to severe disease, the last decade transformed what is possible. Biologic medications that block specific inflammatory signals now have strong trial evidence: adalimumab, which blocks tumor necrosis factor, was the first approved, and secukinumab and bimekizumab, which block interleukin-17 signaling, followed on the strength of phase 3 trials. These do not work for everyone and they are a substantial step in care requiring specialist management, and for people with significant disease they have changed the trajectory in a way nothing before them did.

Surgery has a defined role. Established tunnels do not resolve with medication, and procedures such as deroofing, which opens a tunnel so it can heal from the base, or wider excision of a badly affected area can bring lasting relief in the right anatomy. Medical and surgical treatment work together rather than as alternatives.

What can you do yourself?

Several things help, and none of them involve washing harder.

Stopping smoking is the single most effective change available. Smoking is strongly linked to both developing hidradenitis suppurativa and to more severe disease, and quitting improves the course for many people.

Reducing friction in affected areas helps: looser clothing, breathable fabrics, and avoiding tight waistbands or seams over the areas that flare. Avoid shaving or waxing inflamed skin, and be gentle with the skin generally, since irritation and mechanical trauma provoke lesions.

Working on the metabolic layer supports everything else. Steadier blood sugar, treating insulin resistance, regular movement, and adequate sleep all reduce the inflammatory load the disease is drawing on. Some people find that reducing dairy and high-glycemic foods helps their flares, and the evidence for specific diets is limited, so this is worth testing individually rather than following a rule.

And treat the pain properly. Pain in this condition is frequently undertreated, and it drives the sleep loss and the mood effects that make everything harder. Depression and anxiety are more common here, which makes sense for a painful, visible, and often hidden disease, and they deserve attention rather than being framed as separate problems.

In my practice, the moment that changes things for people with this condition is not usually a prescription. It is the conversation where they learn it has a name, that it was never about being unclean, and that the years of being handed antibiotics for boils were a failure of pattern recognition rather than a failure of theirs. From there the plan gets built, and it works. What I hate is the delay, because the scarring that accumulates during those years is the part I cannot give back.

How Fishtown Medicine approaches hidradenitis suppurativa

At Fishtown Medicine, this condition gets treated as the whole-body inflammatory disease it is. The first job is naming it, which frequently means recognizing the pattern from a history of recurrent lumps that have been drained and dismissed for years.

From there we work both layers at once. On the skin side, we start treatment matched to severity, use targeted injections for flares rather than repeated drainage, add hormonal treatment when the pattern calls for it, and coordinate with dermatology for biologic therapy or with surgery for established tunnels when that is what the disease requires. On the systemic side, we screen every patient for the things that travel with this: fasting insulin and hemoglobin A1c, lipids, blood pressure, and a PCOS evaluation where relevant, because the cardiovascular and metabolic risk here is meaningful and treatable, and because addressing it improves the skin.

Because this is direct primary care, there is time for the parts that get skipped: talking openly about pain, about how this affects intimacy and work and clothing, and about the mental health load of a disease people hide. If you are in Philadelphia and have spent years being handed antibiotics for what you were told were boils, that pattern deserves a name and a plan. The fastest way to start is to tell Dr. Ash what has been happening.

Related at Fishtown Medicine

• PCOS - the hormonal condition that travels most closely with this one
• Understanding Insulin Resistance - the metabolic driver worth screening for at diagnosis
• Chronic Inflammation and Aging - why systemic inflammation matters beyond the skin
• Acne - another follicular condition with hormonal and metabolic drivers
• Prediabetes Reversal - treating the insulin resistance found alongside it
• Metabolic Health in Philadelphia - how the metabolic workup comes together

Scientific References

1. Sabat R, Jemec GBE, Matusiak Ł, Kimball AB, Prens E, Wolk K. Hidradenitis suppurativa. Nature Reviews Disease Primers. 2020;6(1):18.
2. Saunte DM, Boer J, Stratigos A, et al. Diagnostic delay in hidradenitis suppurativa is a global problem. British Journal of Dermatology. 2015;173(6):1546-1549.
3. Phan K, Charlton O, Smith SD. Hidradenitis suppurativa and metabolic syndrome: systematic review and adjusted meta-analysis. International Journal of Dermatology. 2019;58(10):1112-1117.
4. Garg A, Kirby JS, Lavian J, Lin G, Strunk A. Sex- and age-adjusted population analysis of prevalence estimates for hidradenitis suppurativa in the United States. JAMA Dermatology. 2017;153(8):760-764.
5. Kimball AB, Okun MM, Williams DA, et al. Two Phase 3 Trials of Adalimumab for Hidradenitis Suppurativa. New England Journal of Medicine. 2016;375(5):422-434.
6. Kimball AB, Zouboulis CC, Sayed CJ, et al. Bimekizumab in patients with moderate-to-severe hidradenitis suppurativa (BE HEARD I and BE HEARD II). The Lancet. 2024;403(10443):2504-2519.
7. Verdolini R, Clayton N, Smith A, Alwash N, Mannello B. Metformin for the treatment of hidradenitis suppurativa: a little help along the way. Journal of the European Academy of Dermatology and Venereology. 2013;27(9):1101-1108.