Recognizing Hidradenitis Suppurativa Before It Progresses

Written by Dr. rer. nat. Dennis Alexander Kwiatkowski

Hidradenitis suppurativa (HS) takes an average of 7 to 10 years to diagnose, making early recognition one of dermatology’s most urgent patient-education challenges. This chronic inflammatory skin condition affects roughly 1 in 300 people, producing painful, deep-seated nodules and abscesses in the armpits, groin, and under the breasts — areas where it is routinely misdiagnosed as ordinary boils, ingrown hairs, or folliculitis. Because three biologic therapies are now approved and early intervention can prevent irreversible tissue damage, the clinical stakes of recognizing HS sooner have never been higher. Here is what the current medical evidence says about how HS begins, what it looks like, and how to tell it apart from conditions it mimics.

What the Earliest Signs of HS Actually Look and Feel Like

HS does not arrive without warning. Research shows that up to 83% of patients experience a prodromal phase 12 to 48 hours before a visible lesion appears, marked by localized skin redness (75% of patients), tingling or burning sensations (63%), itching (20%), warmth, and sometimes excessive sweating at the site. Some patients also report systemic symptoms including fatigue (32%) and a general feeling of malaise (23%). These prodromal signals, though nonspecific on their own, become diagnostically meaningful when they repeatedly precede lesions in the same skin-fold locations.

The first visible sign is typically a single, deep-seated, firm nodule roughly the size of a pea — between 0.5 and 2 centimeters in diameter — located in an intertriginous area (where skin rubs against skin). Unlike a superficial pimple or folliculitis pustule, the HS nodule sits deep in the subcutaneous tissue. It does not form a central white “head,” does not point toward the surface, and is not centered on a visible hair follicle. Patients rate the pain between 4 and 10 out of 10 on a numerical scale. Individual nodules persist for roughly 7 to 15 days on average, and patients typically develop one to two new inflammatory lesions per month. For a closer look at how these early signs to watch for evolve, see our dedicated overview.

As individual nodules evolve, they may spontaneously rupture — yielding serosanguinous or purulent discharge that can be malodorous — then partially heal with fibrosis before recurring in an adjacent area. This cycle of nodule formation, rupture, and fibrotic healing is “highly diagnostic” for HS and distinguishes it from one-off boils. At this early stage, the disease has not yet produced sinus tracts (subcutaneous tunnels) or permanent scarring, which is what defines it as Hurley Stage I — the mildest and most treatable form.

How HS Presents Differently in the Armpits, Groin, and Under the Breasts

The three most clinically important HS sites do not behave identically. Understanding their differences matters for both diagnosis and patient self-monitoring.

The axillae (armpits) are the single most common HS location and frequently the first site affected. Early axillary HS presents as deep, round nodules that characteristically lack the central necrosis or “pointing” seen in staphylococcal furuncles — an important distinguishing feature. Involvement is often bilateral, reflecting the systemic inflammatory nature of the disease. Open double-headed comedones (paired blackheads connected by a subcutaneous tract), considered pathognomonic for HS, are most visible in this location. If disease progresses unchecked, axillary scarring can produce fibrotic contractures that restrict arm movement. Approximately 43% of HS surgical procedures involve axillary sites. Our guide to HS under the armpits covers what to look for at this site in more detail.

The inguinal (groin) region is the second most common location and is often one of the first sites affected in women, extending along the inner thighs and genitofemoral folds. In men, groin HS more commonly extends toward the perineal and perianal regions. Inguinal HS carries a particularly high risk of misdiagnosis — it may be mistaken for sexually transmitted infections, enlarged lymph nodes, Bartholin’s cysts in women, or even Crohn’s disease when perianal extension occurs (Crohn’s coexists in up to 39% of perianal HS cases in some series). Bilateral groin involvement, as with axillary disease, strongly suggests HS over isolated infectious processes.

The inframammary fold (under the breasts) is less commonly affected early in the disease and almost exclusively involves women. The American Academy of Dermatology notes that HS “tends to begin in an area with thick, coarse hair like the armpits and groin” and that breast involvement typically develops as the disease progresses. Inframammary HS presents as inflammatory nodules and abscesses in the breast crease, sometimes extending to periareolar areas, and is associated with the “axillary-mammary phenotype” — the classic HS pattern in women. This location poses a distinct diagnostic hazard: inframammary and periareolar HS can be misdiagnosed as granulomatous mastitis, breast abscess, or even inflammatory breast cancer, sometimes triggering unnecessary oncologic workup.

Telling HS Apart from the Conditions It Mimics

The conditions most frequently confused with early HS share superficial similarities but differ in critical, identifiable ways. A side-by-side breakdown of hidradenitis suppurativa vs. acne vulgaris addresses one of the most common mix-ups in detail.

Ordinary boils (furuncles) are caused by Staphylococcus aureus infection and form around a visible hair follicle, develop a central pustular head, and respond definitively to antibiotics or incision and drainage. HS nodules are deeper, lack central necrosis, yield sterile or mixed-flora cultures rather than staph monocultures, and provide only temporary relief from antibiotics. The most decisive difference is recurrence pattern: boils are typically isolated events, while HS lesions return to the same anatomic zone repeatedly over months to years.

Folliculitis produces small, superficial red bumps or pustules (usually under 0.5 cm) centered on individual hair follicles. It can occur anywhere on the body, resolves within one to two weeks with topical treatment, and rarely scars. HS nodules are substantially larger (0.5–2 cm), much deeper, restricted to intertriginous areas, persist for weeks, and progressively scar. Folliculitis does not produce the comedones, sinus tracts, or hypertrophic scarring characteristic of HS.

Ingrown hairs produce superficial papules with a visible trapped hair, directly related to shaving or hair removal, that resolve once the hair is freed. HS occurs independently of hair removal practices and does not resolve when shaving is stopped — a simple but powerful differentiator.

Epidermoid cysts are benign, keratin-filled sacs that can appear anywhere on the body. They are typically solitary, discharge thick white material, and can be curatively excised. HS lesions are multiple, bilateral, specifically located in skin folds, discharge serosanguinous or malodorous material, and form interconnecting tracts — features cysts never exhibit.

Fungal infections (tinea) in the groin or skin folds produce flat, scaly, ring-shaped patches with central clearing. They itch rather than cause deep pain, are superficial, and resolve completely with antifungal treatment. The deep, painful, nodular morphology of HS is fundamentally different from the flat scaling of dermatophyte infection.

A 7-to-10-Year Diagnostic Delay That Has Not Improved

The most sobering statistic in HS research is the diagnostic delay of 7 to 10 years, consistently documented across multiple countries and study designs, with no measurable improvement over recent decades. The PIRANHA study (Germany, n=394) found a mean delay of 10.0 ± 9.6 years, during which patients consulted more than three different physicians and received more than three misdiagnoses. A 2024 Portuguese study confirmed a mean delay of 10.1 years with no trend toward improvement. A Greek systematic review published in 2024 found a mean delay of 6.5 years and 3.2 physician consultations before diagnosis. Only 28% of patients receive a correct diagnosis at their first consultation.

Each additional year of diagnostic delay increases the risk of progression to Hurley Stage II or III by approximately 6%, according to UNITE registry data. This progression involves the development of sinus tracts (subcutaneous tunnels), chronic draining wounds, and disabling fibrotic scarring — damage that is irreversible even with optimal treatment. The most common misdiagnoses preceding correct HS identification are recurrent skin abscesses (53% of cases), folliculitis, infected cysts, and in the groin, sexually transmitted infections. Clinician unfamiliarity with HS, patient embarrassment about lesions in intimate areas, and treatment approaches that focus on draining individual abscesses without recognizing the recurrent pattern all contribute to the delay.

A 2024 machine learning study found that among patients coded in medical records as having cellulitis, up to 50% in some metropolitan areas may have underdiagnosed HS, and up to 13% among those coded as having abscesses.

Hurley Stage I Represents a Critical Treatment Window

The Hurley staging system classifies HS severity per anatomic region. Hurley Stage I — defined as abscess formation without sinus tracts and without scarring — describes roughly 55 to 70% of all HS patients, and most of these patients never progress beyond it. Stage I HS consists of isolated or small numbers of painful nodules and abscesses that recur in typical locations but have not yet produced the subcutaneous tunnels or rope-like fibrotic scars of more advanced disease.

This early stage represents what researchers increasingly call a “window of opportunity.” A 2025 publication in Dermatologic Therapy described a paradigm shift toward early biologic intervention before irreversible tissue damage occurs. Three biologic therapies are now approved — adalimumab (2015), secukinumab (2023), and bimekizumab (2024) — and Stage I disease responds most favorably to medical treatment. Ultrasound imaging studies have shown, however, that even clinically apparent Stage I disease may harbor subclinical tunnels and dermal inflammation invisible to the naked eye, meaning true disease burden can be underestimated by surface examination alone.

The 2024–2025 European S2k guidelines introduced a new dual classification system that separates HS into an active inflammatory form (scored by the IHS4 scale) and a predominantly non-inflammatory form (staged by Hurley). This framework recognizes that HS has distinct phases requiring different therapeutic strategies and supports earlier intervention during the inflammatory phase before structural damage accumulates.

Ten Warning Signs That “Recurring Boils” May Be HS

Clinical guidelines and expert consensus identify a clear pattern of red flags. These are the features that, taken together, should prompt evaluation by a dermatologist. If you are preparing for that appointment, our list of 15 questions to ask your dermatologist can help you make the most of the visit.

• Recurrence in the same anatomic zone — the single most important red flag. HS lesions return to the same intertriginous areas repeatedly over months and years; ordinary boils do not.
• Location in skin folds — axillae, groin, inner thighs, under the breasts, buttocks, and perineum. This distribution is characteristic of HS.
• Bilateral or symmetric involvement — HS often affects both armpits or both sides of the groin simultaneously.
• Failure to resolve permanently with antibiotics — temporary improvement followed by relapse strongly suggests HS.
• Double-headed comedones (paired blackheads) — a pathognomonic finding unique to HS.

Additional warning signs include involvement of multiple intertriginous areas simultaneously, onset after puberty (typically ages 18–30), prodromal burning or tingling before lesions appear, foul-smelling discharge, and progressive scarring between flares. A family history of similar lesions is present in approximately 33% of patients and increases clinical suspicion. The modified Dessau diagnostic criteria — typical lesions, in typical locations, recurring at least twice in six months — achieve 97% diagnostic accuracy in identifying HS, per the German S2k guideline.

Dermatologist Vivian Shi of the University of Arkansas has proposed a practical three-question screening tool for primary care:

1. Do you have painful nodules, abscesses, or draining sores?
2. Are they in the armpits, groin, under the breasts, or buttocks?
3. Have they been recurring?

If the answer to all three is yes, HS should be strongly suspected and dermatology referral initiated.

What Recent Guidelines Say About Getting Diagnosed Sooner

The period from 2023 to 2025 has produced a substantial body of new HS guidelines and evidence. The European S2k guidelines (Zouboulis et al., JEADV 2025) represent the most comprehensive update, introducing the dual inflammatory/non-inflammatory classification and an updated treatment algorithm incorporating all three approved biologics. The 2025 North American guidelines (JAAD) extended HS management guidance to seven special populations including pregnancy, pediatrics, and patients with concurrent malignancy. An updated practical management algorithm provides a stepwise framework building on the foundational 2019 North American guidelines.

The Lancet Seminar on HS (Sabat et al., 2025) synthesized current understanding of pathogenesis, confirming that HS originates in the terminal hair follicle through infundibular hyperkeratosis causing follicular occlusion, which triggers perifollicular inflammation, follicular rupture, and amplified immune response through IL-17, TNF-α, and IL-23 pathways. Understanding HS as a primarily inflammatory follicular disease — not a primarily infectious one — is essential to the diagnostic paradigm shift: the goal must move from treating individual “abscesses” to recognizing a chronic immune-mediated condition that benefits from early systemic therapy.

An international consensus on ultrasound in HS (EADV, November 2025) has standardized imaging protocols that can detect subclinical disease invisible to the eye, offering a tool for earlier and more accurate staging. Machine learning models using insurance claims data are being developed to flag patients likely to have underdiagnosed HS among those repeatedly coded for abscesses or cellulitis — a promising approach to closing the diagnostic gap at a population level.

Conclusion

The central clinical challenge in HS is not treatment but timing. The disease announces itself with a recognizable signature — deep, painful nodules recurring in skin folds, bilateral involvement, failure to respond to antibiotics, prodromal symptoms, and distinctive double-headed comedones — yet this signature goes unread for an average of seven to ten years. The cost of that delay is measured in irreversible sinus tracts, disabling scars, and substantially diminished quality of life. With three approved biologics and growing evidence for a “window of opportunity” in early disease, the gap between what medicine can now offer HS patients and when patients actually receive it represents one of the most consequential failures of pattern recognition in clinical dermatology. Any patient experiencing two or more painful, deep lumps in the armpits, groin, or under the breasts within a six-month period should seek dermatologic evaluation — not after years of repeated emergency department visits, but at the point when the pattern first becomes apparent.