PCOS Hidradenitis Suppurativa: Twice as Common, Slow to Diagnose

What is hidradenitis suppurativa, and why does it keep getting missed?

Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition that produces painful, recurring lumps, abscesses, and — in more advanced disease — connecting tunnels under the skin, almost always in areas where skin rubs against skin: the armpits, groin, under the breasts, and the buttocks. It is not an infection, not caused by poor hygiene, and not the same thing as acne, even though it starts in the same type of hair follicle and shares some of the same hormonal drivers. None of that is obvious from how it looks or feels at first, which is exactly why it gets misread. If you are still working out which of the full range of PCOS symptoms belong to you, HS is one that is genuinely easy to miss precisely because it looks so much like something else at the start.

The average time from first symptom to correct diagnosis is close to a decade: a multicentre study of 394 adults with HS in Germany found an average diagnostic delay of 10.0 years, during which patients saw more than three different physicians on average and collected more than three misdiagnoses each — most commonly told they had recurrent boils, folliculitis, or an infection from shaving. A separate study of 285 patients at a Portuguese tertiary hospital found an almost identical average delay of 10.1 years, with no meaningful improvement over the study period. If you have been treating what you were told was “just a boil” for years, with antibiotic creams or repeated lancing that never quite fixes it, HS is worth raising as a specific possibility at your next appointment — by name.

Part of why it is missed is that early HS genuinely can look like an ordinary boil, a shaving bump, or an ingrown hair, and a single early lesion often does resolve on its own the way those things do. What distinguishes HS is the pattern over time rather than any one lesion: lumps that keep returning to the same handful of spots, that leave small scars or firm nodules behind even after they heal, and that eventually start to feel connected under the skin rather than isolated. None of that is visible in a single GP appointment for a single new bump, which is part of why recognising the pattern usually falls to the patient noticing it first, over months, rather than to a single consultation catching it early.

Why are PCOS and hidradenitis suppurativa linked?

Having PCOS roughly doubles the odds of also having HS. A population-based analysis of nearly 23,000 people with HS across the United States found PCOS in 9.0% of them, compared with 2.9% of people without HS — 2.14 times the odds, after adjustment, a strength of association the study’s authors compared directly to the well-established links between PCOS and both diabetes and obesity. A second analysis using the All of Us research database, in 1,022 women with HS matched against 4,088 controls and additionally adjusted for socioeconomic status, found essentially the same pattern — PCOS in 8.8% of women with HS against 4.3% of controls, 1.71 times the odds, confirming the link holds even once income and access to care are accounted for.

The likely mechanism is the one running through most of this site’s coverage of PCOS and skin: androgens act on the hair follicle and its surrounding tissue, and HS begins with blockage and inflammation of exactly that follicular unit, in body-fold skin where friction and moisture make the process worse. The authors of the largest study put it directly — patients with HS who also have signs of androgen excess, such as irregular cycles, acne, or unwanted hair growth, should be screened for PCOS rather than having the two treated as unrelated coincidences.

Another chronic inflammatory skin condition, psoriasis, shows a similar overlap with PCOS for related metabolic reasons — see PCOS and psoriasis for that separate link. Weight and metabolic health add a second, overlapping layer. HS is independently more common in people with obesity and with type 2 diabetes, both of which are themselves more common in PCOS — so some of the PCOS-HS overlap likely runs through shared metabolic risk as well as through androgens directly, rather than one single pathway explaining all of it. That does not mean HS is caused by weight, and it is not a condition that improves reliably with weight loss alone; it means the same metabolic picture that makes PCOS harder to manage can also be part of what makes HS more likely, which is one more reason the two are worth managing as a connected picture with your clinician rather than as separate, unrelated complaints raised in different appointments.

How is HS staged, and does the stage matter?

HS is graded using the Hurley system, a three-stage scale created in 1989 that remains the most widely used severity tool despite being simple by design: Stage I is one or more abscesses without tunnels or scarring; Stage II is one or more widely separated, recurring abscesses with tunnel formation and scarring; Stage III is multiple interconnected tunnels and abscesses across a substantially affected area. A 2019 study testing how consistently 15 clinicians applied the Hurley system to 30 patient photographs found the tool reliable overall, and especially reliable for identifying Stage III disease specifically — the stage that typically indicates a need for surgery rather than medical management alone.

Staging matters because it changes the conversation with a clinician from “how do I stop this recurring” to a specific plan matched to how far the disease has progressed — which is also why the decade-long average delay above is not a minor inconvenience. Longer diagnostic delay is directly associated with more severe disease at the point of diagnosis, more surgical treatment, and more missed work, so the years lost to a wrong diagnosis are not neutral — they are years the underlying disease had to progress unmanaged.

Stage is also not fixed forever. Someone diagnosed early, at Stage I, has meaningfully more treatment options and a better chance of staying there than someone who reaches Stage III before anyone names the condition correctly — which is the practical argument for raising a suspicious, recurring pattern of lumps sooner rather than waiting to see if it settles down on its own. It usually does not, left alone, precisely because the tunnels and scarring that define Stage II and III form gradually, from repeated cycles of the same follicles becoming blocked and inflamed without ever being addressed at the root.

Does this mean my PCOS is more severe?

Not necessarily — HS tracks with androgen excess and with the metabolic overlap between PCOS and obesity or insulin resistance, not with how irregular your cycles are or how your ovaries look on ultrasound. If your PCOS bloodwork shows clearly elevated androgens, or if you also carry significant insulin resistance, the biological picture that makes HS more likely is the same one driving those results, and it is worth mentioning any recurring skin-fold lumps to whoever manages your PCOS care, not just to a dermatologist in isolation. If your PCOS is closer to the ovulatory or lean end of the spectrum with androgens near normal, HS is less likely to be androgen-driven in your case specifically, though it can still occur — the diagnosis and staging matter more than the theory of why it happened.

Why this needs dermatology-led care, not self-management

Treating HS as a hygiene problem or a stubborn acne problem is one of the most common ways it gets worse rather than better. General PCOS treatment aimed at lowering androgens — combined hormonal contraceptives or an anti-androgen such as spironolactone — are treatment options a dermatologist or GP may raise for some cases of milder HS, but neither is automatically appropriate: combined hormonal contraceptives carry a clotting risk that rules them out for smokers over 35, anyone with a history of blood clots or venous thromboembolism, or migraine with aura, and spironolactone is contraindicated in pregnancy and needs a potassium check in anyone with reduced kidney function or already taking an ACE inhibitor or ARB. Neither is a substitute for dermatology assessment, and neither will resolve Stage II or Stage III disease on its own. Addressing the insulin resistance that frequently accompanies both PCOS and HS is a reasonable, evidence-aligned part of a longer management plan, but it is not a fast fix and should not delay a dermatology referral while you wait to see if it helps. HS is a distinct diagnosis from PCOS acne, and while the two can share hormonal drivers, treating one is not the same as treating the other. If what you are noticing is more widespread oiliness, dryness, or patchy darkening rather than deep, recurring lumps in a fold, the broader picture of PCOS skin changes is the more accurate place to start, since it covers conditions with a very different course and treatment path from HS.

It is also worth saying plainly, because stigma is one of the documented reasons diagnosis takes so long: HS is not caused by poor hygiene, and it is not something to be embarrassed into hiding from a clinician. The pain and visible lesions are real, common, and treatable with the right diagnosis — the delay is the system’s failure to recognise it quickly, not a reflection on you.

PCOS was renamed polyendocrine metabolic ovarian syndrome (PMOS) in May 2026 by a global consensus of more than 50 medical organisations — the same condition and the same underlying mechanism, with only the label changed. This article uses PCOS because that is what most people still search, and the HS research above was conducted under that name.

Your next step

If you have recurring lumps in a skin fold that keep returning to the same spot, write down where, how often, and how long each one lasts, and ask specifically for a referral to dermatology for hidradenitis suppurativa — not just “recurring boils.” Naming the condition by name, and mentioning your PCOS diagnosis in the same conversation, is the single fastest way to close the decade-long gap this article describes.