Can hidradenitis suppurativa turn into cancer?
Rarely, squamous cell carcinoma has been reported arising within areas of long-standing HS, particularly gluteal, perineal and perianal disease. This is a recognised but uncommon complication.
Long-term complications
Most hidradenitis suppurativa wounds are not cancer. This guide explains the rare exception, and the one signal worth acting on: persistent change from your own baseline.
Do not inspect every HS lesion anxiously. Instead, learn what is normal for you, and notice when something departs from it persistently.
Long-standing HS does not automatically become cancer. Most people with HS will never develop SCC, and the absolute individual risk remains uncertain but appears low.
Squamous cell carcinoma, usually abbreviated SCC or cSCC, is a form of skin cancer arising from squamous cells in the epidermis. In the general population it is commonly associated with cumulative ultraviolet exposure and usually develops on sun-exposed skin.
HS-associated SCC is unusual because it has repeatedly been reported in chronically inflamed, scarred and wounded areas that may receive little or no sun exposure — particularly the gluteal, perineal and perianal regions. That is why generic sun-safety advice does not adequately address this HS-specific issue: SCC arising in HS does not generally start from a mole, and can present as an enlarging growth, an ulcer, or a nodule.
We do not have a reliable single percentage. Older reviews and patient resources have quoted estimates up to approximately 4.6%, but those figures come from limited historical case literature and selected populations rather than a clean estimate of risk for every person with HS. Even the patient organisation that popularised that figure has stressed that the true frequency is difficult to establish because the complication is rare.
A much larger 2026 systematic review and meta-analysis illustrates the uncertainty. It included 11 studies, 624,721 people with HS and approximately 394 million controls. The pooled crude odds ratio for overall cancer was 1.82 (95% CI 1.13–2.93) — but the SCC-specific analysis was far less certain: crude OR 2.80 (95% CI 0.64–11.76), which was not statistically significant and showed very high heterogeneity between studies.
An analysis of adjusted estimates suggested roughly a 2.5-fold increased SCC risk, but that finding relied on only two studies, and the authors explicitly advise caution. The responsible conclusion is that SCC is a recognised, rare complication of HS, but current evidence does not allow a precise individual percentage to be given confidently.
Most published cases share several characteristics: long-standing HS, severe or chronically damaged tissue, gluteal, perineal or perianal disease, and years of recurrent wounds, tunnels and scarring.
A 2025 review summarising reported cases found a mean HS duration of approximately 25.8 years, and that 94.6% of reported SCC cases occurred in the gluteal/perianal region.
These observations are useful for identifying the group in whom vigilance is most relevant. They are not a risk calculator: someone who has had HS for 25 years has not crossed a biological cancer threshold, and someone with shorter disease duration cannot be guaranteed zero risk.
Because ordinary HS already produces many of the features that would be unusual in healthy skin: non-healing wounds, drainage, crusting, bleeding, painful nodules, irregular scars, chronic tunnels and recurring ulcers.
A 2025 cancer review explicitly notes that SCC arising in HS can look like a tumour, ulcer or nodule and can be difficult to distinguish from chronic HS lesions. So the useful question is not "does this lesion look bad?" — HS already produces lesions that look concerning. It is: "is this area behaving differently from the way my HS normally behaves?"
None of the following proves cancer. They are reasons to stop automatically assuming that a chronic lesion is merely ordinary HS, and to have it examined directly instead.
HS areas typically swell during flares and settle again afterwards. An area that instead keeps enlarging steadily over weeks to months, rather than returning to its usual baseline, is different from an ordinary flare.
Historical case literature on HS-associated SCC includes reports of rapidly enlarging chronic ulcers.
How you might describe it: "This wound has existed for years, but over the last two months it has become noticeably larger rather than returning to its normal baseline."
SCC does not always present as a flat wound. Reported HS-associated SCC has also presented as tumour-like or nodular growth.
This description is not a home diagnostic criterion. Show the change rather than trying to interpret it yourself.
How you might describe it: "At the site that has drained for a long time, a firm, raised growth has appeared over the last few weeks that wasn't there before."
HS wounds can remain open for long periods — that alone is not evidence of cancer. What matters is an ulcer that develops a new, persistent trajectory: enlarging steadily, becoming structurally different, developing a new raised margin, or repeatedly changing despite the usual treatment pattern.
The key word is new.
How you might describe it: "The ulcer has looked different for a few months — the margin is raised and it is no longer responding to treatment the way it used to."
Bleeding can happen in ordinary HS wounds, particularly with friction or dressing changes — that alone does not mean cancer.
But if an established lesion begins bleeding spontaneously or repeatedly in a way that is unusual for that area, that is worth reporting.
How you might describe it: "This area has never bled spontaneously in years, but recently it has started bleeding without an obvious cause and crusting over in an unusual way afterwards."
Pain is already common in HS. An isolated increase is much more likely to have benign explanations such as inflammation.
But if a long-standing area develops a persistent change in pain together with structural change, it is worth naming explicitly at review.
How you might describe it: "The pain at this site has felt different for several weeks from the pain I usually know from my HS — and the area looks different too."
A chronic HS area may never fully disappear. But if it previously became quieter after treatment and now continues to enlarge or change despite the usual management, that difference is worth showing.
This does not mean treatment resistance equals cancer. It means "this no longer behaves like the same lesion I have known for years" is useful clinical information.
How you might describe it: "This area always used to respond to my treatment. For the last few months it has kept growing regardless."
Most reported SCC cases arising in HS involve chronic gluteal, perineal or perianal disease. The American Academy of Dermatology likewise specifically tells HS patients that SCC can arise in unusual sites around the anus and groin.
These areas are also difficult to monitor: they are hard to see, chronic tunnels may already distort the anatomy, drainage and wounds may have been present for years, and many people feel uncomfortable repeatedly asking a clinician to inspect intimate areas. That last barrier is practical, not biological — and this page exists partly to remove it.
You could say: "I cannot monitor this area reliably myself. Because my HS there is long-standing, could you check whether anything looks materially different from the surrounding chronic disease?"
There is no established HS-specific population screening programme equivalent to cervical or colorectal cancer screening. The 2026 meta-analysis itself concludes that more evidence is needed to determine surveillance strategies and to separate HS-related effects from confounders such as smoking, BMI and other conditions.
The American Academy of Dermatology nevertheless notes that dermatologists can watch for skin-cancer signs in patients with HS. The practical takeaway: regular dermatology follow-up creates an opportunity for chronic HS areas to be examined, especially in long-standing severe disease — not an annual biopsy or imaging schedule, which no current guidance supports.
No. If every chronic HS wound were automatically biopsied, many people with severe disease would undergo repeated unnecessary procedures.
Biopsy is a clinician decision based on the lesion's appearance, its history, change over time, anatomical site, examination and broader clinical context. The useful patient action is to point out the changed lesion — the clinician decides whether biopsy is warranted.
Yes, but only for documenting change. A photograph cannot rule SCC in or out. A useful series might show the lesion two months ago, one month ago, and today — used to demonstrate "this area is steadily enlarging", not to ask an app or a clinician to diagnose cancer from an image.
This is deliberately not an automated task. No image-recognition tool on this site attempts to classify a lesion as safe or suspicious, because SCC may resemble ordinary chronic HS and diagnosis can require histopathology.
The next step depends on what the clinician sees. They may consider direct examination, dermoscopy where appropriate, biopsy, imaging if deeper involvement is suspected, or referral to dermatologic surgery, oncology or another relevant specialty.
There is no fixed pathway such as "changed lesion → CT scan." A biopsy is what establishes a histological diagnosis of SCC when clinically indicated.
Current evidence does not support telling patients that modern HS biologics are the explanation for HS-associated SCC. SCC in HS was documented decades before current biologic therapy, and the current literature does not demonstrate a consistent HS-specific skin-cancer signal attributable to biologics alone.
So do not stop a biologic because of this page. If a lesion is suspicious, investigate the lesion — treatment decisions come afterwards, and only with your prescribing clinician.
Smoking is common in HS populations and is independently associated with multiple cancers. Older HS-associated SCC case series also identify smoking frequently among affected patients, with chronic inflammation and smoking both proposed as contributors.
The available SCC evidence does not allow a calculation such as "if you smoke, your SCC risk is X." The appropriate message is simpler: smoking adds a separate, well-established cancer risk and is already one of the strongest modifiable HS-associated risk factors.
HPV has been proposed as one contributor to some anogenital SCC cases arising in HS, but the evidence is incomplete and not every HS-associated SCC is HPV-driven. Routine vaccination and cervical/other cancer-prevention recommendations should follow national guidance, not an invented HS-specific schedule.
This is not a validated cancer-screening instrument — it is a memory prompt. Once every few months, or during routine care, ask four questions about chronically affected areas:
If the answer is clearly yes to any of these: show it, rather than trying to interpret it yourself.
You do not need to say "I think I have skin cancer." A calmer, more useful message describes what has changed and asks for it to be examined.
You could say: "I have long-standing HS in this area. One chronic lesion has changed persistently over the last several weeks or months and is behaving differently from my normal HS. I would like it examined."
If applicable, add: "I have photographs showing the change over time." That is enough.
Squamous cell carcinoma arising in hidradenitis suppurativa is rare but recognised. The strongest pattern in the published case literature is long-standing disease, chronic tissue damage, gluteal/perineal/perianal involvement, and a lesion that becomes persistently atypical.
Current large-scale evidence confirms that cancer risk in HS deserves further study, but it does not give a trustworthy universal percentage for an individual's SCC risk. So the practical rule stays simple: most HS wounds are not cancer. But when an old lesion starts behaving differently and keeps doing so, show it.
Rarely, squamous cell carcinoma has been reported arising within areas of long-standing HS, particularly gluteal, perineal and perianal disease. This is a recognised but uncommon complication.
The precise risk is uncertain. Older, selected literature produced estimates up to 4.6%, but a much larger 2026 meta-analysis found substantial between-study heterogeneity and did not find a statistically significant crude increase in SCC risk (OR 2.80, 95% CI 0.64–11.76). An adjusted estimate suggested a roughly 2.5-fold increase, but relied on only two studies.
Published cases predominantly involve long-standing, severe disease around the buttocks, perineum and anus. In a 2025 review of reported cases, mean HS duration was approximately 25.8 years and 94.6% of SCC cases occurred in the gluteal/perianal region. These figures come from accumulated case reports, not a predictive risk calculator for any individual.
No. Chronic wounds are themselves part of HS. The concern is a persistent change from the lesion's established behaviour rather than non-healing alone.
Examples include progressive enlargement, a new persistent raised or wart-like growth, a chronic ulcer that develops a new behaviour, unexplained persistent bleeding or crusting, or another structural change clearly different from your normal HS pattern. None of these proves cancer.
No. Photographs can document change but cannot reliably establish SCC. Suspicious lesions require clinical assessment and may require biopsy.
No. Biopsy is guided by the clinical appearance, history and change in the lesion. The purpose of this page is to help patients identify which changes deserve examination, not to encourage routine biopsy of every HS wound.
Current evidence does not establish modern HS biologics as the cause of SCC arising within chronic HS lesions. The complication was described long before current biologic therapies, and treatment-specific cancer-risk data remain incomplete.
Regular dermatology follow-up provides an opportunity to examine chronic disease areas, and the American Academy of Dermatology recommends dermatologic monitoring for skin-cancer signs in people with HS. There is not, however, a universally established HS-specific annual cancer-screening protocol requiring a fixed schedule or routine biopsy.
Last editorially reviewed: · Next review due:
This page describes SCC as a rare recognised complication of long-standing HS. Current population-level risk estimates remain uncertain and heterogeneous between studies, which is why this page deliberately avoids quoting a single universal risk percentage and focuses on persistent change from baseline rather than numerical risk or visual self-diagnosis.
Any lesion suspected clinically of malignant transformation requires clinician assessment, and histopathology is required to establish a diagnosis of SCC. Content on this page is source-linked and reviewed on a schedule, or earlier if updated HS-specific surveillance guidance or incidence data become available.