Verneuil’s Disease: The Link to Hidradenitis Suppurativa

Verneuil’s disease is the eponymous name for hidradenitis suppurativa (HS), a chronic inflammatory skin condition marked by painful, recurring lumps and abscesses that typically form in areas where skin rubs together, such as the armpits, groin, buttocks, and under the breasts. The condition was first described in detail by the French surgeon Aristide Auguste Stanislas Verneuil in the nineteenth century, and the name persists widely in European medical literature. Despite affecting roughly 1–4 percent of the population in various estimates, HS remains dramatically underdiagnosed, with patients waiting an average of ten years between first symptoms and a correct diagnosis.

What Happens in the Skin

The disease starts in hair follicles, not in sweat glands as was long believed. The earliest change is a buildup of keratin, the tough protein that forms the outer layer of skin, inside the hair follicle. This plugs the follicle opening. In one study examining surgical tissue samples, more than four in five specimens showed follicular plugging, and a similar proportion showed thickening of the follicle lining. Inflammatory immune cells then crowd around the blocked follicle, and eventually the follicle wall ruptures, spilling its contents into the surrounding tissue. That rupture triggers a much larger inflammatory response, leading to the painful nodules and abscesses patients experience.¹

Once the disease becomes chronic, bacterial biofilms can form inside the tunnels and sinus tracts that develop under the skin. These biofilms appear to be a secondary event rather than the root cause. They likely take hold because the damaged tissue creates an ideal environment for bacteria to colonize and form sticky, treatment-resistant colonies.² This is an important distinction: HS is not an infection, even though infected-looking abscesses are one of the main reasons it gets misdiagnosed as ordinary boils.

Underneath all of this sits an overactive immune system. Patients with HS show elevated levels of several inflammatory signaling molecules, including TNF-alpha and various interleukins involved in driving both innate and adaptive immune responses.³ This immune dysregulation helps explain why the disease is systemic rather than just a skin problem, and why it so often travels alongside other inflammatory conditions.

Who Gets It and Why

HS typically begins after puberty, with an average age of onset around eighteen years old.⁴ Women are affected roughly two to three times more often than men, though men tend to develop more severe disease. In a study of nearly 500 patients, about 72 percent were female. Women more commonly had involvement of the armpits, inner thighs, and under the breasts, while men were significantly more likely to have lesions on the posterior neck, perianal region, and ears. The most severe stage of disease was over twice as common in men as in women.⁵

Genetics play a role, though not in a simple one-gene pattern. In some families, HS follows a clear hereditary line tied to mutations in genes that code for the gamma-secretase enzyme complex. These mutations account for a small but distinct subset of patients and tend to produce a recognizable pattern of disease.⁶ For most patients, however, the genetic picture is murkier. A family history of HS is common but not universal, and no single gene explains the majority of cases.

The Smoking and Obesity Connection

Smoking is one of the most consistent and modifiable risk factors for HS severity. Over half of HS patients in large registries are active smokers, and the data strongly suggests a dose-response relationship: the more someone has smoked over their lifetime, the more body areas tend to be affected. There is also a striking correlation between the age a person starts smoking and the age their HS begins.⁷

Current smokers are more than twice as likely to be in the most severe disease stage compared to people who have never smoked, and they report worse quality of life and greater overall disease burden.⁸ Beyond the direct effect on HS, smoking also amplifies the metabolic problems that travel with the disease. HS patients who smoke more heavily are significantly more likely to have high blood pressure, diabetes, and high cholesterol.⁹

Obesity follows a similar pattern. Higher body mass index is positively correlated with more severe disease scores in HS patients.¹⁰ The relationship is probably bidirectional: excess weight increases skin friction and sweat in fold areas, which may worsen flares, while the pain, immobility, and depression associated with severe HS can make weight management harder. Quitting smoking and managing weight are not cures, but dermatologists consistently recommend both as foundational steps before or alongside medical therapy.

Why It Takes So Long to Get a Diagnosis

One of the most frustrating aspects of living with Verneuil’s disease is the extraordinary delay between when symptoms start and when someone finally gets a correct diagnosis. On average, patients wait about ten years. During that decade, they typically see more than three different doctors and receive more than three wrong diagnoses.¹¹

The misdiagnoses are predictable. Because HS lesions look like boils, abscesses, or infected cysts, patients are commonly told they have recurrent skin infections, folliculitis, or ingrown hairs. Some are sent to surgeons for drainage of what are assumed to be isolated abscesses, only to have them recur in the same area. Women with groin involvement may be diagnosed with recurrent Bartholin’s cysts or vulvar abscesses. The pattern of recurring, painful lumps in skin-fold areas that heal with scarring is the diagnostic hallmark, and no lab test or imaging study is required to make the diagnosis. It is entirely clinical. Yet awareness of HS among general practitioners remains poor, which is the primary driver of the delay.

This matters beyond frustration. Untreated HS progresses. Repeated cycles of inflammation create scar tissue, and over time the tunneling sinus tracts that connect lesions under the skin become permanent structural damage that cannot be reversed with medication alone. The earlier treatment begins, the more tissue and function can be preserved.

Conditions That Travel with HS

Verneuil’s disease rarely exists in isolation. Metabolic syndrome, the cluster of high blood pressure, elevated blood sugar, abnormal cholesterol, and excess abdominal fat, appears at higher rates among HS patients even in mild disease.¹² The shared inflammatory pathways between HS and metabolic syndrome probably account for much of this overlap.

Crohn’s disease, an inflammatory bowel condition, has a well-documented association with HS. The two conditions can coexist in the same patient, and when they do, both tend to be more severe and require more intensive medical and surgical therapy.¹³ If you have HS and develop persistent gastrointestinal symptoms, it is worth mentioning the connection to your doctor.

Depression and anxiety are strikingly common in HS patients. One study found that how patients perceived their illness, whether they felt it was controllable, how long they expected it to last, and how much they believed it affected their identity, predicted depression, anxiety, and quality of life far more powerfully than the objective severity of their disease.¹⁴ This finding underscores that psychological support is not an afterthought in HS management. The shame, isolation, and pain from chronic draining wounds in intimate areas of the body exact a mental health toll that deserves direct treatment.

Medical Treatment Options

Treatment for HS is staged based on severity. Mild disease may be managed with topical antiseptics and antibiotics. For moderate cases, the combination of clindamycin and rifampicin, two oral antibiotics given together for several months, is one of the most commonly prescribed regimens. In a European cohort study, this combination produced a meaningful clinical response in about 48 percent of patients, roughly comparable to a tetracycline-based regimen that achieved response in about 40 percent.¹⁵ These response rates are honest but humbling: fewer than half of patients achieve a meaningful improvement with antibiotics alone.

For moderate-to-severe disease, biologic medications have changed the landscape. Adalimumab, a TNF-alpha blocker, was the first biologic approved specifically for HS and remains the most widely used. More recently, secukinumab, which targets the IL-17 pathway, has been approved and is expanding options. Other classes under investigation include IL-1 inhibitors and Janus kinase (JAK) inhibitors.¹⁶ Real-world experience with secukinumab and other IL-17 blockers is still accumulating; early case reports are encouraging but larger-scale data is needed to define how they compare head-to-head with adalimumab.¹⁷

Biologics are not quick fixes. They require regular injections or infusions, often for years, and not everyone responds. But for patients who do respond, the reduction in new nodules, abscesses, and drainage can be life-altering.

When Surgery Becomes Necessary

Surgery enters the picture when HS lesions have progressed to the point where chronic sinus tracts and scarring cannot be addressed with medication. The choice of surgical technique matters for recurrence rates. A meta-analysis found that wide excision, which removes the entire affected area with a margin of healthy tissue, had the lowest average recurrence rate at about 13 percent. Local incision, where individual lesions are cut out more conservatively, recurred about 22 percent of the time. Deroofing, a procedure that removes the roof of sinus tracts while preserving the floor, had a recurrence rate of about 27 percent.¹⁸

Wide excision sounds straightforwardly superior on numbers alone, but the trade-offs are real. It creates larger wounds that may need skin grafts or flaps, involves longer recovery, and can leave significant scars in sensitive areas. Deroofing is faster and heals more easily but is better suited to isolated lesions rather than widespread disease. Most patients with severe HS end up needing some combination of surgery and ongoing medical therapy, since surgery addresses existing damage while medication aims to prevent new flares.

Diet and Lifestyle Adjustments

The evidence on diet is still limited to small studies and surveys, but some consistent patterns have emerged. Reducing dairy and refined carbohydrates has been associated with symptom improvement across several investigations. In one study, clinical improvement was reported in 83 percent of HS patients who followed a dairy-free diet. Patients themselves frequently identify sweets, bread, pasta, and dairy products as foods that seem to trigger or worsen flares.¹⁹

A particularly intriguing finding involves brewer’s yeast. Among patients with a specific immune sensitivity to brewer’s yeast, avoiding it for twelve months led to stabilization and regression of lesions. In a separate study of 37 patients on a yeast exclusion diet, 70 percent reported improvement, and most experienced recurrence within a week of resuming yeast-containing foods like beer. Supplementation with zinc, vitamin D, and vitamin B12 has also shown promise for partial or complete resolution in some patients.²⁰

None of these dietary approaches have been tested in large randomized trials, so they should be viewed as potentially helpful additions to standard treatment, not replacements. That said, the low risk of cutting back on refined carbohydrates and dairy makes these changes worth trying for most HS patients, particularly since the potential benefit is meaningful and the cost is minimal.

HS in Adolescents

Although HS is often thought of as an adult disease, it can begin in adolescence, sometimes shortly after puberty. Early recognition is critical in this age group because the disease tends to progress if untreated, and the psychological impact on adolescents, who may already be struggling with body image and social acceptance, can be severe. A multidisciplinary approach that includes psychotherapy, health education, healthy lifestyle habits, and consistent medical treatment is considered the standard of care. Aggressive surgical interventions are generally reserved for severe cases in adolescents, because extensive surgery can extend hospital stays and worsen psychological distress in young patients.²¹

The problem of diagnostic delay is likely even worse for younger patients, because doctors may not think of HS in someone who does not fit the stereotypical adult patient profile. Any adolescent with recurring painful lumps in skin-fold areas, particularly if there is a family history, should be evaluated with HS in mind.

Emerging Therapies and the JAK Inhibitor Pipeline

The treatment landscape for HS is evolving faster now than at any point in the disease’s history. Among the most promising emerging drug classes are JAK inhibitors, which target the intracellular signaling pathways that drive inflammation. Several are in clinical trials for HS. Phase II randomized trials are testing three different kinase inhibitors, including an IRAK4 inhibitor and two TYK2-pathway inhibitors, while a phase I trial has examined another IRAK4 inhibitor in healthy volunteers to establish safety before moving into patient studies.²²

JAK inhibitors are already approved for other inflammatory conditions such as rheumatoid arthritis and atopic dermatitis, so there is a reasonably well-understood safety profile to build on. Whether they will prove effective enough in HS to earn regulatory approval is still an open question, but the fact that multiple agents targeting different nodes of the inflammatory cascade are being tested simultaneously means the chances of new approved options in the coming years are higher than they have ever been. For patients who do not respond to adalimumab or secukinumab, this pipeline represents genuine cause for cautious optimism.

Why the Name Still Matters

You will see this disease referred to as hidradenitis suppurativa, Verneuil’s disease, and acne inversa, sometimes in the same medical record. The name “hidradenitis suppurativa” literally means “suppurating inflammation of the sweat glands,” which is a misnomer because the disease originates in hair follicles, not sweat glands. “Acne inversa” was proposed as a more accurate alternative, emphasizing the connection to follicular occlusion, the same underlying process as acne vulgaris but occurring in inverse (fold) areas of the body. “Verneuil’s disease” persists largely in French and Southern European clinical usage as a historical eponym.

The naming confusion is more than trivia. When patients search for information online, using one name may return a completely different set of results than another. Support groups and research registries are indexed under “hidradenitis suppurativa” far more often than under the other names, which can leave patients who know their condition only as Verneuil’s disease feeling isolated or unable to find resources. If you have been given the diagnosis under any of these names, know that they all refer to the same condition, and searching under “hidradenitis suppurativa” or the abbreviation “HS” will connect you to the broadest range of patient communities, clinical trial listings, and treatment information available.