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Hidradenitis suppurativa: Management

Hidradenitis suppurativa: Management
Author:
John R Ingram, MD, PhD
Section Editors:
Robert P Dellavalle, MD, PhD, MSPH
Cindy Owen, MD
Deputy Editor:
Abena O Ofori, MD
Literature review current through: Jul 2022. | This topic last updated: Jun 30, 2022.

INTRODUCTION — Hidradenitis suppurativa (HS) is a chronic, painful, follicular, occlusive disease that affects the folliculopilosebaceous unit mainly, but not exclusively, in intertriginous axillary, groin, perianal, perineal, genital, and inframammary skin. The clinical course is highly variable, ranging from relatively mild disease characterized by the recurrent appearance of papules, pustules, and a few inflammatory nodules to severe cases demonstrating deep, fluctuant abscesses; draining sinuses; and severe, rope-like scars (picture 1A).

Numerous interventions exist for treatment of HS, including topical therapies, oral therapies, biologic therapies, surgery, and laser and light interventions. Disease severity, patient tolerance of specific agents, comorbidities, and treatment cost and availability guide treatment selection.

The management of HS will be reviewed here. Information on the pathogenesis, clinical features, and diagnosis of HS and a detailed discussion of the surgical techniques used in the treatment of HS are provided separately.

(See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)

(See "Surgical management of hidradenitis suppurativa".)

GOALS OF TREATMENT — Treatment of HS is generally recommended. HS can remain active for many years after onset, and the pain, odor, drainage, and disfigurement caused by HS profoundly affect quality of life, even when the disease is relatively mild [1-3]. Patients often experience feelings of anxiety or depression related to the disease, and feelings of shame may contribute to self-imposed social isolation [4-6].

Interventions for HS target one or more of three major goals:

To reduce formation of new inflammatory lesions, skin tunnels, and scarring

To treat existing lesions and reduce associated symptoms (eg, pain, suppuration)

To minimize associated psychologic morbidity

ASSESSMENT OF DISEASE SEVERITY AND RESPONSE — The severity of HS influences the approach to treatment. Key features used to determine disease severity include the extent of skin involvement and the presence of secondary lesions, including skin tunnels and scarring. Responses to treatment are indicated by reduced frequency and severity of inflammatory lesions, improvement in symptoms, and improvement in quality of life:

Clinical setting – In addition to describing the features present, common methods of defining disease severity in the clinical setting include the three-stage Hurley clinical staging system and use of the terms "mild," "moderate," and "severe" [7]. Hurley stage I HS is generally considered to correlate with mild disease, and stages II and III may be considered to represent the continuum of moderate to severe disease.

The Hurley staging system stratifies HS severity as follows [7]:

Stage I – Abscess formation (single or multiple) without skin tunnels and cicatrization/scarring (picture 2)

Stage II – Recurrent abscesses with skin tunnels and scarring, single or multiple widely separated lesions (picture 3)

Stage III – Diffuse or almost diffuse involvement, or multiple interconnected skin tunnels and abscesses across the entire area (picture 1A-B)

The term "abscess" is typically considered to include both inflammatory nodules and true abscesses when staging HS.

Assessment of the impact of treatment both on skin disease and patient quality of life is useful for determining treatment benefit. In addition to the clinician's physical examination at follow-up visits, patients can be asked to record the number of new or recurrent, painful lesions occurring in the preceding month. Asking patients to complete a quality-of-life instrument, such as the Dermatology Life Quality Index or Skindex, or a pain visual analogue or numeric scale may also be helpful (form 1 and figure 1) [8,9].

Clinical trials – The Hurley staging system is often used in the clinical setting due to its simplicity. However, it has insufficient responsiveness to change to be used as a clinical trial outcome measure. The Sartorius scale and modified Sartorius scale have been used in clinical trials, and newer assessment tools, such as the Hidradenitis Suppurativa Clinical Response (HiSCR) and Severity Assessment of Hidradenitis Suppurativa Score, have been developed and validated [10-14]. In addition, the Hidradenitis Suppurativa Core outcomes set International Collaboration (HISTORIC) has identified six core domains to measure in all future HS trials: pain, physical signs, HS-specific quality of life, global assessment, progression of course, and symptoms [15,16].

INTERVENTIONS FOR ALL PATIENTS — The multifaceted clinical features of HS and the unpredictable course of the disease make a uniform approach to treatment challenging. Regardless of disease severity, attention to patient education; patient support; and appropriate management of wounds, pain, and comorbidities can be beneficial [17,18]. (See 'Education and support' below and 'Wound and skin care' below and 'Pain management' below and 'Assessment and management of comorbidities' below.)

Education and support — HS is a psychologically distressing disorder that can have a major impact on quality of life and is often associated with several years or more of diagnostic delay, making patient education and support essential components of management [19]. We suggest the following interventions:

Patients should be educated about the diagnosis of HS. We typically communicate the following:

HS is a chronic, inflammatory condition that is neither contagious nor due to poor hygiene.

Although HS has been associated with smoking and obesity, HS can also occur in the absence of these characteristics. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated factors'.)

A family history of HS is common among individuals with HS. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated factors'.)

The course of HS varies from person to person; reliable predictors of progression to more severe disease have not been identified.

The clinician should inquire about the impact of the disease on the patient's life and assess the patient's specific concerns and needs regarding the condition [20]. An assessment for signs or symptoms of depression should be included [21]. (See "Screening for depression in adults".)

Patients should be offered resources for psychologic support [5], such as contact information for local HS patient societies. Patients may find the Hidradenitis Suppurativa Foundation and other resources helpful.

Wound and skin care — Providing patients with guidance regarding care techniques for draining lesions and wounds can be helpful. In general, patients should utilize wound dressings that minimize skin trauma. To prevent absorbent dressings from sticking to the wound, simple white petrolatum can be applied. Adhesive tape should be avoided, and instead, elastic fishnet dressings can be customized to hold absorbent material in place.

Some experts suggest use of topical antiseptic washes, such as chlorhexidine 4%, benzoyl peroxide, or zinc pyrithione, to cleanse skin in the affected areas [22]. However, evidence to confirm benefit of these interventions for improving HS are lacking.

Pain management — Pain from HS nodules and abscesses may cause sleep disturbance, limit function, and induce psychologic distress. Nonsteroidal anti-inflammatory drugs can be used to treat both pain and inflammation. Additional analgesia, including opioid analgesia, may be needed in some cases [23].

Conscientious selection of pain medication, particularly opioids, is indicated. A multidisciplinary approach may be helpful for identifying an appropriate pain management plan for patients experiencing chronic pain. The approach to the management of chronic pain is reviewed in detail separately. (See "Approach to the management of chronic non-cancer pain in adults".)

Assessment and management of comorbidities — Patients with HS may be at increased risk for multiple health disorders, including alcohol dependence, autoimmune conditions, cardiovascular disease, diabetes, drug dependence, dyslipidemia, follicular occlusion syndromes, hypertension, inflammatory arthropathies, cutaneous squamous cell carcinoma, metabolic syndrome, nicotine addiction, obesity, polycystic ovary syndrome (PCOS), and psychiatric and psychologic disorders (table 1) [24,25]. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated disorders and syndromes'.)

Patient evaluation — We agree with recommendations from the United States and Canadian Hidradenitis Suppurativa Foundations and guidelines from the British Association of Dermatologists that support routine screening of patients with HS for comorbidities [18,22]. Our approach, which is loosely based upon these sources, is as follows:

Perform a review of systems and physical examination to screen for tobacco use, obesity, hypertension, PCOS, inflammatory bowel disease, autoinflammatory syndromes, and inflammatory arthropathy.

Obtain laboratory testing to screen for diabetes mellitus, hyperlipidemia, and anemia [26]. (See "Screening for type 2 diabetes mellitus" and "Screening for lipid disorders in adults".)

Screen for depression and anxiety using a recognized screening tool for these conditions. (See "Screening for depression in adults" and "Generalized anxiety disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis", section on 'Assessment and Diagnosis'.)

Recommendations from a multispecialty working group for the management of comorbidities, including cardiovascular risk factors, excess weight, inflammatory bowel disease, inflammatory joint disorders, psychologic disorders, alcohol use, and tobacco use, in patients with HS have also been published [27]. The document provides guidance for dermatologists for patient assessment and referral and reviews the implications of treatments for HS on comorbidities. We agree with the importance of assessing for comorbidities on a yearly basis and support multidisciplinary involvement in the management of comorbidities.

Smoking cessation and weight loss — Smoking and obesity are common among patients with HS. Pathogenic roles for these conditions in the development and persistence of HS have been proposed but not definitively proven [11,28-31]. In the case of obesity, conditions related to excess weight, such as skin occlusion, skin friction, shearing forces on skin, hyperinsulinemia, and other hormonal changes that occur in association with obesity, are proposed to contribute. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated factors'.)

Although benefits of smoking cessation and weight loss on HS severity are postulated, data conflict and benefit of these interventions has not been confirmed. We routinely advise smoking cessation or weight loss to our HS patients who smoke or are obese based upon the potential for benefit in HS, the other recognized health benefits of these interventions, and observations that support increased risk for morbidity or mortality from related conditions among patients with HS, such as cardiovascular diseases [32]. Metformin, one of the medications used to treat HS, may have a modest beneficial effect on weight loss. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated factors' and "Overview of smoking cessation management in adults" and "Obesity in adults: Overview of management" and 'Metformin' below.)

Additional study to clarify whether smoking cessation and weight loss improve HS is warranted. A retrospective survey of 45 Danish patients who underwent bariatric surgery suggests benefit; of the 35 patients who achieved substantial weight loss, defined as at least a 15 percent reduction in baseline body mass index, 17 (49 percent) experienced resolution of their HS, 7 (20 percent) improved, 7 (20 percent) had unchanged disease, and 4 (11 percent) had worsened disease [33]. In addition, improvement in HS after smoking cessation has been documented in case reports [34].

INFLAMMATORY LESIONS WITHOUT SKIN TUNNELS OR SCARRING (HURLEY STAGE I OR MILD DISEASE) — The initial management of patients in whom HS manifests as inflammatory lesions without skin tunnels or scarring (Hurley stage I or mild HS) consists of therapies to reduce disease burden (ie, reduce lesion development and inhibit disease progression) and interventions to improve acute, symptomatic lesions (picture 2). (See 'Reducing burden of disease' below and 'Acute symptomatic lesions' below.)

Reducing burden of disease — Common therapies for reducing disease burden in mild HS include topical clindamycin, oral tetracyclines, antiandrogenic agents, and metformin.

Initial therapy — Topical clindamycin is often tried prior to proceeding to oral agents.

Topical clindamycin — Topical clindamycin is a well-tolerated therapy that may improve HS through reducing inflammatory lesions. The drug is typically applied two times per day in skin areas subject to recurrent flares.

Although frequently prescribed, data to support efficacy of topical clindamycin are limited. In a three-month trial in which 30 patients with HS of the axillae and/or groin were randomly assigned to treatment with either clindamycin 1% solution or vehicle, an analysis of the effect on an unvalidated cumulative disease burden score for the 13 patients in the clindamycin group and 14 patients in the vehicle group that completed treatment demonstrated greater improvement in the clindamycin group than in the vehicle group after one, two, and three months of treatment [35]. Topical clindamycin was well tolerated; slight burning pain after application occurred in two patients in the clindamycin group and three in the vehicle group.

Failure of initial therapy — Patients who do not achieve disease control with topical clindamycin are candidates for oral therapy. Oral tetracyclines are frequently prescribed in this scenario. (See 'Oral tetracyclines' below.)

Antiandrogenic drugs and metformin are additional treatment options that may be used alone or in conjunction with antibiotic therapy. Some authors have suggested that female patients who experience flares of HS in association with menses or have features of polycystic ovarian syndrome may be more likely to benefit from antiandrogenic drugs [22]. We tend to use metformin in obese patients because the drug also promotes modest weight loss and helps improve metabolic profile. (See 'Antiandrogenic agents' below and 'Metformin' below and "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Weight loss'.)

Oral tetracyclines — The mechanism by which antibiotic therapy improves HS is not definitively known. Antibiotics may help to control skin bacterial load, which may be an exacerbating factor for HS. However, the anti-inflammatory effects associated with some antibiotics may also play a role [36].

A common regimen for adults is 100 mg of doxycycline given once to twice daily. Examples of alternative tetracycline regimens include lymecycline (408 mg once or twice daily) and tetracycline (500 mg twice daily). Minocycline (100 mg twice daily) is an additional option but has the disadvantage of a broader side effect profile. Lymecycline is not available in the United States.

Data are insufficient to confirm the best approach to tetracycline therapy. Tetracyclines are typically given for a few months, though longer treatment courses may be appropriate in select cases [22,37]. In our practices, we typically treat with tetracyclines for three months prior to assessing the response. Patients who fail to improve are transitioned to other therapies. (See 'Refractory disease' below.)

Patients who achieve satisfactory disease control with a course of tetracycline therapy may stop treatment. Upon stopping treatment, we often prescribe daily application of topical clindamycin for maintenance therapy. Patients who experience rapid recurrence after cessation of oral antibiotic treatment may benefit from use of other therapies.

Randomized trial evidence for oral tetracyclines is sparse. In a trial, 46 patients with stage I or II HS were randomly assigned to treatment with oral tetracycline (500 mg twice daily) or topical 1% clindamycin solution (applied twice daily) [38]. Patients were treated for 16 weeks, and while there was no difference between the groups in terms of pain, number of lesions, or physician global assessment, there was a greater improvement in patient global assessment of disease in the oral tetracycline group.

Treatment with tetracyclines is generally well tolerated. Common adverse effects include gastrointestinal distress and photosensitivity. Minocycline may also cause vertigo, skin discoloration, and a lupus-like syndrome.

Antiandrogenic agents — Antiandrogenic therapy for HS is based upon the theory that androgens may contribute to the development of HS [36]. Examples of antiandrogenic therapies that may improve the disease include combined oral contraceptives, spironolactone, and finasteride [39-45]. High-quality efficacy data for these therapies are limited, and relative efficacy is unclear [17]. Antiandrogenic therapy should not be given to pregnant women because of the risk for adverse effects on the fetus.

Selection of an antiandrogenic agent is based upon consideration of patient preference, contraceptive needs, and comorbidities. We typically treat female patients with oral contraceptives or spironolactone; efficacy data for finasteride are more limited (see "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated factors'):

Oral contraceptives – Oral contraceptives are taken daily, identical to the regimen advised for contraception. Use is limited to female patients.

An oral contraceptive regimen containing cyproterone acetate and ethinyl estradiol was compared with norgestrel-containing oral contraceptive pills in a randomized, double-blind, crossover trial of 24 women with moderate to severe HS [39]. Patients were treated with 50 mcg of ethinyl estradiol (cycle days 5 to 25) and 50 mg of cyproterone acetate (cycle days 5 to 14) for six months and ethinyl estradiol 50 mcg/norgestrel 500 mcg (cycle days 5 to 25) for six months. Although six patients dropped out of the trial prior to completion due to drug intolerance or worsening of disease, both treatment regimens were associated with clinical improvement in disease activity, and no significant difference in efficacy was detected. Overall, improvement occurred in 12 patients, including 7 patients who achieved complete remissions.

Oral contraceptive therapy is usually well tolerated but is associated with a variety of risks and adverse effects. Clinicians should assess for contraindications to oral contraceptive drugs prior to initiating therapy. (See "Combined estrogen-progestin oral contraceptives: Patient selection, counseling, and use".)

SpironolactoneSpironolactone is taken daily. Use is limited to female patients.

A typical dose of spironolactone is 100 mg per day, though doses utilized range from 25 to 200 mg per day. Starting at a lower dose (eg, 50 mg per day) and subsequently increasing to 100 mg per day after a few weeks may help to optimize patient tolerance of the drug. Responses to spironolactone are usually evident within three months.

Retrospective studies of spironolactone for HS suggest benefit [41,45,46]. A retrospective study of 67 women with Hurley stage I to III HS (74 percent with Hurley stage II HS) associated spironolactone therapy with improvement in pain, inflammatory lesion count, and physician-assessed disease severity [45]. Patients received 25 to 200 mg of spironolactone per day (average dose 75 mg per day) and were followed for an average of 7 months (range 0.75 to 28 months). Treatment with spironolactone was well tolerated; only two patients discontinued the drug because of side effects. Some patients also received antibiotics, hormonal contraceptives, or other HS therapies.

In addition, a retrospective case series of 20 women given spironolactone, most at a dose of 100 mg daily, reported remission in 11 patients (55 percent) and clinical response in 17 patients (85 percent) after three months [41]. Five patients were given concomitant minocycline 100 mg daily, and seven patients received an oral contraceptive pill.

Potential side effects of spironolactone include menstrual irregularities, breast tenderness, hypotension, central nervous system symptoms (headaches, dizziness, fatigue), and hyperkalemia. Although an increase in mammary tumors has been reported in rats treated with spironolactone, a relationship between spironolactone and human cancers has not been proven. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults", section on 'Spironolactone'.)

Small case series have suggested benefit from finasteride in female and male patients [42,43,47]. Doses of finasteride for HS range from 1.25 to 5 mg per day. Finasteride is contraindicated in individuals of childbearing potential. We do not typically utilize finasteride for HS.

Metformin — Insulin and insulin-like growth factor may contribute to HS, providing a potential mechanism for benefit of metformin in HS. The drug can also promote modest weight loss, which may also be beneficial for HS. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Associated disorders and syndromes'.)

Metformin is given daily with food. An initial dose of 500 mg is often prescribed and titrated upward by 500 mg every few weeks as tolerated. Our typical maximum dose is 1500 mg per day given in two or three divided doses (eg, 500 mg three times per day). Extended-release metformin may allow for less frequent dosing. Metformin is contraindicated in patients with severe renal dysfunction. Responses to treatment may be evident within the first three months [48]. (See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Suggested approach to the use of metformin'.)

Support for the efficacy of metformin for HS stems from uncontrolled studies [48,49]. In a 24-week, prospective study of 25 nondiabetic patients with HS who were treated with metformin (initial dose 500 mg per day, maximum dose 500 mg three times per day), almost all of whom had failed to achieve sufficient responses to other therapies [48], 18 patients achieved clinical improvement, including 7 who achieved at least a 50 percent reduction in Sartorius score. In addition, in a retrospective case series of 53 patients treated with metformin as monotherapy (mean daily dose 1500 mg per day) for at least one month, the examining dermatologist recorded subjective improvement in 36 (68 percent), including complete response (no active lesions) in 7 of the 36 patients (19 percent) demonstrating improvement [49]. The mean duration of treatment was 11 months.

Gastrointestinal adverse effects are the most common side effects of metformin therapy and can limit use of the drug in some patients. Adverse effects of metformin are reviewed in greater detail separately. (See "Metformin: Drug information".)

Refractory disease — Patients with mild HS that fails to improve with the treatments above may benefit from some of the therapies used for more severe disease. In general, clindamycin and rifampin combination therapy, acitretin, and dapsone are viewed as appropriate systemic options for this population [22]. Neodymium-doped yttrium aluminum garnet (Nd:YAG) laser therapy has also been used in this setting (see 'Nd:YAG laser' below). Treatment with biologic agents, intravenous antibiotics, and immunosuppressive therapies are generally reserved for patients presenting with greater disease severity. (See 'Clindamycin and rifampin' below and 'Oral retinoids' below and 'Oral dapsone' below and 'Inflammatory lesions with skin tunnels or scarring (Hurley stage II or III, moderate to severe HS)' below.)

Acute symptomatic lesions — Intermittent application of warm compresses is a simple measure that may help to improve symptomatic lesions. Additional interventions for symptomatic, inflamed nodules include intralesional corticosteroid injections, punch debridement (partial unroofing), and topical resorcinol. The efficacy of these interventions has not been compared; treatment selection is often based upon treatment availability and patient preference.

Routine incision and drainage of HS lesions is not recommended. (See 'Incision and drainage' below.)

Intralesional corticosteroids — Intralesional corticosteroid injection involves the injection of a corticosteroid, such as triamcinolone acetonide, directly into an inflammatory nodule. We typically use triamcinolone acetonide at a concentration of 10 mg/mL and inject between 0.2 and 1 mL into individual nodules, with the amount injected dependent upon the size of the nodule. Noticeable improvement in symptoms often occurs within one to two days. (See "Intralesional corticosteroid injection".)

A prospective series of 36 HS patients designed to assess the effect of triamcinolone 10 mg/mL (volume range 0.2 to 2 mL) injected into an acute nodule or abscess had findings in support of a beneficial effect [50]. Mean pain, measured on a visual analogue scale (VAS) from 0 to 10, where 10 represents greatest pain, decreased from 5.5 pretreatment to 1.1 at follow-up after a mean of seven days. Significant differences in pain VAS were found between days 0 and 1 and also from days 1 to 2 after the injection.

Cutaneous atrophy and other adverse effects of intralesional corticosteroid therapy are reviewed in detail separately. (See "Intralesional corticosteroid injection", section on 'Side effects, complications, and pitfalls'.)

Punch debridement — Surgical unroofing is a procedure in which the skin overlying an inflamed nodule or skin tunnel is removed, and the resulting wound is allowed to heal via secondary intention. Punch debridement (partial unroofing) is a minor subtype of surgical unroofing that consists of utilization of a punch biopsy tool to evacuate acute, inflamed nodules that are centered around a single folliculopilosebaceous unit. Use of this technique is based upon clinical experience. The technique of punch debridement is reviewed separately. (See "Surgical management of hidradenitis suppurativa", section on 'Punch debridement'.)

Topical resorcinol — Resorcinol is a topical chemical peeling agent with keratolytic and anti-inflammatory properties that is used by some clinicians for HS, where available.

Patients can be instructed to apply a thin film of resorcinol 15% cream directly to a new inflamed nodule twice daily. Resorcinol is not applied to the entire region. As improvement occurs, the frequency of application may be tapered to once daily, and application to the site of the inflamed nodule can be discontinued upon resolution.

Data on resorcinol in HS are limited. In an open study of 12 patients with Hurley stage I or II HS who applied topical 15% resorcinol once to twice daily primarily during disease flares, all patients experienced a reduction in pain and a reduction in duration of painful abscesses [51]. The expected adverse effect of local desquamation occurred in all patients. Recurrences may follow discontinuation of the medication.

Incision and drainage — Incision and drainage may promote lesion recurrence and is not advised for the routine treatment of acute lesions of HS. The procedure should be limited to situations in which immediate relief of severe pain from an inflamed, fluctuant nodule is necessary and treatment with other techniques is not feasible. (See "Surgical management of hidradenitis suppurativa", section on 'Role of I&D'.)

INFLAMMATORY LESIONS WITH SKIN TUNNELS OR SCARRING (HURLEY STAGE II OR III, MODERATE TO SEVERE HS) — Similar to milder disease, management of HS with inflammatory nodules plus skin tunnel formation or scarring (Hurley stage II or III, moderate to severe HS) consists of medical and surgical interventions to reduce disease burden and improve acute, symptomatic lesions. Surgery is particularly useful for findings that tend to have insufficient responses to medical therapy, such as skin tunnels, recurring nodules, and severe, extensive disease. (See 'Reducing burden of disease' below and 'Acute symptomatic lesions' below and 'Skin tunnels and recurrent nodules' below.)

Reducing burden of disease — Patients with moderate to severe presentations of HS are often treated with combination therapy.

Initial therapy — The initial approach often consists of oral antibiotic therapy, usually tetracyclines or combination of clindamycin and rifampin. Antiandrogens (for female patients) or metformin are commonly added as adjunctive therapies.

Tetracyclines are our initial choice for antibiotic therapy for patients who present towards the moderate degree of the spectrum, with findings consistent with Hurley stage II disease. When treatment fails, we often proceed to clindamycin and rifampin. We tend to reserve initial therapy with clindamycin and rifampin for patients with extensive, inflammatory disease.

Patients who fail to achieve adequate disease control with these antibiotics may benefit from other interventions, such as adalimumab, infliximab, oral retinoids, dapsone, or alternative antibiotic therapy. Wide local excision can be beneficial for severe disease that cannot be controlled with medical therapy. (See 'Failure of initial therapy' below.)

Oral tetracyclines — Tetracycline therapy for moderate to severe disease is administered similarly to milder disease. (See 'Oral tetracyclines' above.)

Clindamycin and rifampin — Combination therapy with clindamycin and rifampin is an option for patients who fail to respond to oral tetracyclines or as initial treatment for patients presenting with a substantial inflammatory burden. A typical course is clindamycin (300 mg twice daily) and rifampin (300 mg twice daily) for 10 to 12 weeks. Responses are usually evident within this period. Use of clindamycin alone has also been proposed based upon a retrospective study of 60 patients with HS that found similar responses in patients treated with clindamycin and rifampin and patients treated with clindamycin alone [52]. However, additional study is necessary to confirm the relative efficacy and safety of this treatment strategy.

The best approach to maintaining improvement in patients who respond to a course of clindamycin and rifampin is unclear. Long-term treatment with clindamycin and rifampin has traditionally been avoided because of concern for adverse effects, leading to use of other therapies to maintain improvement. However, some authors have challenged avoidance of long-term treatment with clindamycin and rifampin based upon data that suggest the greatest risk for adverse effects occurs during the initial weeks of treatment [53].

Use of clindamycin and rifampin for HS is based upon uncontrolled studies [54-57]. In one of the largest studies that evaluated this regimen, 116 patients with primarily Hurley stage I and II HS were treated with clindamycin (300 mg twice daily) and rifampin (600 mg once daily) for 10 weeks [54]. Significant decreases in the Sartorius score were observed, from a median of 28 points at baseline to 19 points at the end of treatment, and 8 of the 70 patients (11 percent) who were available for the week 10 assessments achieved complete remissions (Sartorius score of 0).

In a separate retrospective study of 34 patients with stage I, II, or III HS who had failed various other treatments, 16 (47 percent) achieved a complete response (defined as >75 percent improvement) to clindamycin and rifampin administered via various treatment regimens [55]. However, the long-term benefit of treatment after treatment cessation was variable. In the study, 8 of 13 patients (62 percent) who responded completely to a regimen of clindamycin 300 mg twice daily and rifampin 300 mg twice daily (including nine patients treated for ≥10 weeks) relapsed after an average of five months. In a separate prospective case series of 26 patients with HS, treatment with clindamycin (300 mg twice daily) and rifampin (600 mg per day) for 12 weeks was associated with a clinical response (defined as at least 50 percent clinical improvement) in 19 patients (73 percent) [57]. Relapse did not occur in 7 of the 17 responders (41 percent) available for follow-up one year after treatment.

Gastrointestinal adverse effects of this treatment regimen are common [54,55]. While the potential for Clostridioides difficile infection related to clindamycin therapy exists, in practice, it seems to be rare in patients with HS. Enzyme induction by rifampin may reduce circulating concentrations of clindamycin, reducing risk for C. difficile infection [53]. (See "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis" and "Clostridioides difficile infection in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use' and "Rifamycins (rifampin, rifabutin, rifapentine)", section on 'Adverse effects'.)

Patients should also be advised that rifampin causes orange discoloration of bodily secretions, and the effectiveness of hormonal contraception may be reduced. Acute renal failure (usually with a favorable prognosis) and liver injury are additional potential adverse effects. Drug interactions due to rifampin should be carefully reviewed. (See "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis" and "Clostridioides difficile infection in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use' and "Rifamycins (rifampin, rifabutin, rifapentine)", section on 'Adverse effects'.)

Metformin, oral contraceptives, and spironolactone — Metformin, oral contraceptives, and spironolactone are typically used as adjunctive therapies in patients with moderate to severe HS. Some authors have suggested that female patients who experience flares of HS in association with menses or have features of polycystic ovarian syndrome may be more likely to benefit from antiandrogenic drugs [22]. We tend to use metformin in obese patients because the drug also promotes modest weight loss. Treatment regimens are similar to patients with less severe manifestations. (See 'Metformin' above and 'Antiandrogenic agents' above.)

Failure of initial therapy — Reasonable, subsequent medical treatment options for patients with HS presenting with inflammatory lesions, skin tunnels, and scarring who do not achieve satisfactory, sustained disease control with antibiotic therapy, metformin, or antiandrogenic therapy include oral retinoids (in men and nonfertile women), dapsone, and the biologic tumor necrosis factor (TNF) inhibitors adalimumab and infliximab. Etanercept, another TNF-alpha inhibitor, does not appear effective for HS [58].

Selection among these therapies is based upon consideration of efficacy data, risk for adverse effects, patient preference, and drug availability. We often utilize acitretin or dapsone prior to proceeding to biologic therapy, as these agents are generally well tolerated, less immunosuppressive, and lower in cost compared with biologic agents. However, other approaches are reasonable.

Adalimumab is our preferred biologic agent based upon high-quality data to support efficacy in HS. Adalimumab is the only agent approved by the US Food and Drug Administration (FDA) and European Medicines Agency (EMA) for the treatment of HS.

Oral retinoids — Acitretin, isotretinoin, and a newer oral retinoid, alitretinoin, have been used to treat HS. Acitretin is the primary agent utilized [37]. Isotretinoin remains the gold standard treatment for severe acne vulgaris and is often used to treat concomitant acne in HS patients. However, it appears to provide only limited benefit for HS and may worsen the condition, so we avoid it in HS without acne. Combining oral retinoid therapy and treatment with tetracyclines is not recommended due to risk for idiopathic intracranial hypertension (pseudotumor cerebri). Oral retinoid therapy is contraindicated during and for certain periods following pregnancy:

Acitretin – Optimal dosing for acitretin for HS is not established. We typically initiate treatment with a dose of 25 mg per day and increase to 50 mg per day if improvement does not occur and the patient is tolerating therapy. Initial signs of improvement are expected within the first two months of treatment [59,60].

A prospective, uncontrolled study of 17 patients with HS treated with acitretin (mean dose of 0.56 mg/kg/day) found a clinical response (at least 50 percent decrease in the HS Severity Index score after six months of treatment) in 8 of the 14 patients who attended for follow-up [59]. Only nine patients completed the planned nine months of therapy. The primary reasons for withdrawal from the study were treatment inefficacy and nonserious side effects.

A retrospective study of 12 patients with recalcitrant Hurley stage II or III HS treated with acitretin (mean dose 0.6 mg/kg daily) for 9 to 12 months with or without topical therapy found that all patients improved and that nine patients achieved marked or complete remissions [60]. The first initial signs of improvement were noted within approximately two months. Improvement often persisted after treatment, with nine patients maintaining responses for 6 to 45 months after the cessation of therapy.

Isotretinoin – Studies of isotretinoin therapy have demonstrated improvement in relatively low proportions of patients with HS. In a series of 88 patients treated with isotretinoin for an average of eight months (mean daily dose 44 mg/day, range = 20 to 140 mg per day), improvement was reported in only 14 patients (16 percent) [61]. In a retrospective study of 68 patients with various stages of HS who were treated for four to six months with isotretinoin (mean daily doses of 0.5 to 0.8 mg/kg), 16 (24 percent) achieved clearing of disease, and 25 showed lesser improvement [62]. All patients who cleared had disease that was mild or moderate in severity.

Alitretinoin – In a series of 14 patients with HS, treatment with alitretinoin (10 mg per day) for 24 weeks produced improvement in 11 patients (79 percent), including 6 who achieved significant improvement (at least 50 percent reduction in Sartorius score) [63]. Alitretinoin is not available in the United States.

Examples of common adverse effects of systemic retinoids include cheilitis, xerosis, and hyperlipidemia [64]. For additional information, refer to the Lexicomp drug information monographs included within UpToDate.

Retinoids are teratogenic and must be avoided in individuals who are at risk for pregnancy or pregnant. Pregnancy should also be avoided for five weeks following isotretinoin and alitretinoin treatment and for three years after acitretin. Thus, the use of acitretin is typically avoided in women of childbearing potential, which limits its use for HS in the context that the highest prevalence of HS is in young adult women. In the United States, isotretinoin can only be prescribed through the iPLEDGE program, an internet-based risk management program. (See "Oral isotretinoin therapy for acne vulgaris", section on 'iPLEDGE program'.)

Oral dapsone — Dapsone, a sulfone drug with immunomodulatory and antibacterial properties that is utilized for the treatment of multiple neutrophil-predominant skin diseases, may be effective in mild to moderate HS, particularly in the early neutrophil-mediated phase of new lesions [65,66]. We typically treat adults with 50 mg per day and increase to 100 mg per day, if insufficient response. Responses may be evident within the first one to three months of treatment [66].

In a retrospective study of 24 patients with Hurley stage I to III HS who were treated with 50 to 200 mg daily of dapsone, six patients (25 percent) achieved clinically significant improvement and three patients improved slightly (13 percent) [65]. None of the four patients with stage III disease improved with therapy. In addition, dapsone (25 to 150 mg per day) was associated with reductions in disease severity in a case series of five patients [66]. As with other medical agents, the disease often recurs after treatment cessation [65,66].

Hemolysis is a common and expected adverse effect of dapsone therapy, and careful laboratory monitoring for hematologic toxicity is necessary during treatment. It is prudent to test for glucose-6-phosphate dehydrogenase (G6PD) deficiency prior to treatment to avoid severe hemolysis in the G6PD-deficient population. Examples of additional adverse effects of dapsone include methemoglobinemia (which manifests with headaches), agranulocytosis, and a hypersensitivity reaction [67]. (See "Diagnosis and management of glucose-6-phosphate dehydrogenase (G6PD) deficiency".)

Adalimumab — The recommended dosing schedule for adults with HS is an initial 160 mg subcutaneous dose (given at one time or split into two 80 mg doses given over two consecutive days), then 80 mg on day 15, and then 40 mg once weekly starting on day 29 [68]. In 2020, FDA labeling for adalimumab was updated to include 80 mg every other week as an alternative to 40 mg weekly [68]. Given the larger body of evidence to support the 40 mg once-weekly regimen, we typically prescribe 40 mg once weekly [69].

The recommended dosing regimen for adolescents 12 years of age and older who weigh less than 60 kg differs from adult dosing. Adolescents weighing 30 to 60 kg are treated with 80 mg on day 1 and 40 mg on day 8, followed by 40 mg every other week. Adolescents weighing at least 60 kg are treated with the same regimen as adults.

The FDA approval of adalimumab for moderate to severe HS was based upon the results of two similar phase 3, randomized trials (PIONEER I [n = 307] and PIONEER II [n = 326]). Patients with moderate to severe HS were randomly assigned either to adalimumab (40 mg once weekly) or placebo for the initial 12 weeks (period 1) [69]. This was followed by a 24-week phase (period 2) in which patients who received adalimumab in period 1 were randomly assigned to adalimumab weekly, adalimumab every other week, or placebo. Patients who received placebo in period 1 were reassigned to adalimumab weekly in PIONEER I and to placebo in PIONEER II. Patients in PIONEER II were allowed to continue oral tetracycline therapy at stable doses.

At week 12, more patients in the adalimumab groups achieved the Hidradenitis Suppurativa Clinical Response (HiSCR) primary efficacy endpoint (≥50 percent reduction in the total abscess and inflammatory nodule count with no increase in the abscess or draining sinus count) than in the placebo groups (42 versus 26 percent in PIONEER I and 59 versus 28 percent in PIONEER II). In addition, in PIONEER II but not PIONEER I, adalimumab treatment was associated with improvement in the secondary outcomes of lesion count, pain score, and the modified Sartorius score for disease severity at week 12.

The response to adalimumab declined in period 2; among patients who responded to adalimumab in period 1, no significant difference in clinical response rates was detected between patients who received adalimumab versus placebo in period 2. The protocol-mandated cessation of treatment for patients who lost 50 percent or more of the improvement gained during period 1 (even if due to a temporary disease fluctuation) may have contributed to this result. A three-year, open-label, extension study that followed the PIONEER trials suggests long-term efficacy and safety of adalimumab [70]. The study found a sustained rate of response (achievement of HiSCR) over time among patients who received 40 mg of adalimumab once weekly for at least 60 weeks.

Examples of common adverse effects of adalimumab include injection site reactions and increased risk for infection. Adverse effects of adalimumab and other TNF-inhibitors are reviewed in detail separately. (See "Tumor necrosis factor-alpha inhibitors: An overview of adverse effects".)

Infliximab — The optimal regimen for infliximab for HS is unclear. We typically treat with a dosing regimen similar to the standard regimen for psoriasis (5 mg/kg at weeks 0, 2, 6, and then every eight weeks). However, there are clinical observations that suggest that more frequent dosing than used for psoriasis may be beneficial for HS (5 mg/kg at weeks 0, 2, 6 and then every four weeks rather than every eight weeks) [71]. Dosing of 10 mg/kg every four to eight weeks has been suggested by some experts [22].

A beneficial effect of infliximab for HS was demonstrated in a trial of 38 patients with moderate to severe HS [72]. During the initial randomized, double-blind phase of the trial, patients were treated with either infliximab infusions (5 mg/kg on weeks 0, 2, and 6) or placebo infusions. This phase was followed by an open-label phase in which patients in the infliximab group received maintenance doses of infliximab at weeks 14 and 22, and patients in the placebo group were given the opportunity to receive infliximab according to the same treatment regimen. By week 8, there was not a significant difference between the treatment and placebo groups for the primary study outcome (≥50 percent decrease in an unvalidated disease severity score) [58,72]. However, infliximab therapy was associated with statistically significant improvements in patient quality of life, pain, and physician global assessment scores. On physician global assessment, 47 percent of patients in the infliximab group attained 75 to 99 percent improvement compared with none of the placebo-treated patients.

Examples of adverse effects of infliximab include infusion reactions and increased risk for infection. Adverse effects are reviewed in detail separately. (See "Tumor necrosis factor-alpha inhibitors: An overview of adverse effects".)

Severe refractory disease — For patients with refractory, severe (Hurley stage III) disease, wide excision can be beneficial.

Wide excision — Extensive surgical intervention is considered to offer the greatest likelihood for the resolution of active inflammation in the treated area [73]. Of note, the procedure can be disfiguring and involve a prolonged recovery time. In addition, extensive excision is not usually feasible in patients with multiple affected skin regions. (See "Surgical management of hidradenitis suppurativa", section on 'General considerations'.)

Data to support wide excision are limited and primarily consist of data from uncontrolled studies [74]. For example, in one retrospective study in which 31 patients were treated with drainage procedures, limited regional excisions, and wide excision and followed for a mean of 72 months, only 3 of 11 patients treated with wide excision experienced disease recurrence, with a median recurrence interval of 20 months [75]. A study in which 499 patients who underwent surgical intervention for HS, including 88 treated with excisional procedures, were surveyed about their satisfaction with surgery, most patients (85 percent) were satisfied with the outcome of their surgical procedure [76].

The surgical approach to wide excision is discussed in detail separately. (See "Surgical management of hidradenitis suppurativa", section on 'Local procedures' and "Surgical management of hidradenitis suppurativa", section on 'Wide excision and reconstruction'.)

Medical therapies — Patients with moderate to severe HS may respond to other systemic therapies generally reserved for disease refractory to standard approaches. Data from small, randomized trials or uncontrolled studies suggest benefit of ustekinumab, anakinra, interleukin (IL) 17 inhibitors (eg, secukinumab), and intravenous ertapenem:

Ustekinumab – Positive responses to ustekinumab, an IL-12/23 inhibitor given via subcutaneous injection, have been reported in patients with moderate to severe, refractory HS [77-79]. An uncontrolled study in which 17 patients with Hurley stage II or III HS received 45 or 90 mg of ustekinumab at weeks 0, 4, 16, and 28 found at least a 50 percent reduction in the modified Sartorius score in six patients (35 percent) at week 40 and a 25 to 49 percent reduction in the modified Sartorius score in eight patients (47 percent) at week 40 [79]. Less improvement occurred in one patient, and two patients had no improvement. Limitations of this study include the small number of patients and a high premature dropout rate due to lack of response (three patients), withdrawal of informed consent (one patient), and an adverse event of urticaria (one patient).

Anakinra Anakinra, an antagonist of the IL-1 receptor, may be a treatment option for HS. A 24-week, randomized trial in which 20 adults with Hurley stage II or III HS were randomly assigned to subcutaneous injections of anakinra (100 mg) or placebo once daily for 12 weeks found reductions in the disease activity score in six of nine patients (67 percent) in the anakinra group compared with only 2 of 10 patients (20 percent) in the placebo group at the end of treatment [80]. One patient in the anakinra group was lost to follow-up. In addition, anakinra therapy was associated with prolongation of the time to which patients noticed a new exacerbation of HS. Changes in the Sartorius score, patient-reported disease severity, and quality of life did not differ between the anakinra and placebo groups. No serious adverse events occurred.

Other reports of the effects of anakinra on HS include a case series and a case report [81,82]. In the case series of six patients treated with eight weeks of anakinra (100 mg per day via subcutaneous injection) for moderate to severe HS, the five patients who completed the treatment course demonstrated reductions in the modified Sartorius score, physician and patient global assessment scores, and improvement in quality of life [82]. However, the effects of anakinra diminished upon treatment cessation, and rebound of disease was evident eight weeks after the end of treatment. In the case report, a woman with refractory HS treated with anakinra (200 mg per day) achieved disease remission within one year with continued treatment [81].

Failure to respond to anakinra (100 mg per day) has been reported [83-85].

IL-17 inhibitorsSecukinumab is a human monoclonal antibody that inhibits IL-17A. Data from small, open-label studies suggest secukinumab may be a beneficial therapy [86,87]. In an open-label study in which 20 patients with moderate to severe HS received secukinumab (weekly 300 mg doses followed by repeat does either every four weeks or every two weeks), 14 patients achieved the HiSCR endpoint (at least 50 percent reduction in the number of abscesses and inflammatory nodules and no increase in draining fistula or abscess count relative to baseline) after 24 weeks. Another open-label study that included nine patients with moderate to severe HS given subcutaneous secukinumab 300 mg weekly for 5 weeks and then every 4 weeks for a total of 24 weeks found six of the nine patients achieved the HiSCR endpoint [86]. There were no serious adverse events in either study.

Data from a phase 2, randomized trial suggest benefit of the investigational drug bimekizumab, which inhibits both IL-17A and IL-17F. In the trial, 90 adults with moderate to severe HS were randomly assigned in a 2:1:1 ratio to receive bimekizumab (320 mg every two weeks after a 640 mg loading dose at baseline), placebo, or adalimumab (40 mg per week after a 160 mg loading dose at baseline and 80 mg dose at week 2) over a 10-week period [88]. At week 12, more patients in the bimekizumab group achieved HiSCR than patients in the placebo group (57 versus 26 percent; posterior probability of superiority of 0.998 calculated using Bayesian analysis).

Intravenous ertapenem – Patients with severe suppurative disease unresponsive to the oral combination of clindamycin and rifampin may require rescue therapy with intravenous antibiotics. Intravenous ertapenem at a dose of 1 g daily for six weeks was associated with a reduction in disease severity in a retrospective study of 30 patients given ertapenem for severe HS [89]. Local antibiotic stewardship policies should be reviewed prior to use of this regimen.

Additional agents for which benefit is suggested in case series or case reports include guselkumab [90], canakinumab [91], cyclosporine [92-95], and oral tacrolimus [96]. Data from a small, randomized trial and uncontrolled study suggest that bermekimab, an investigational drug, may also be an effective therapy [97,98].

Acute symptomatic lesions — Individual acute, inflammatory nodules may be managed similarly as lesions in the setting of less severe disease. (See 'Acute symptomatic lesions' above.)

Systemic glucocorticoids are an additional option for treating highly symptomatic, acute flares. Based upon clinical experience, a three- to four-day course of prednisone 40 to 60 mg per day, tapered over the subsequent 7 to 10 days, is often sufficient for acutely managing inflammation. We reserve systemic glucocorticoids for rescue therapy to treat severe flares resistant to antibiotic therapy as a bridge to other therapies. (See "Major side effects of systemic glucocorticoids".)

Skin tunnels and recurrent nodules — Skin tunnels are persistent, often draining, malodorous tunnels that tend to form in the setting of multiple recurrent nodules within a localized region. Skin tunnels require surgical intervention for resolution.

Surgical unroofing (also known as deroofing) involves removal of skin overlying skin tunnels or nodules followed by healing by secondary intention. Uncontrolled studies and reports of clinical experience suggest efficacy of surgical deroofing procedures for skin tunnels and recurrent nodules [99-103]. In one study of 88 deroofed lesions in 44 patients with HS, 73 lesions (83 percent) did not recur after a median follow up of 34 months [99]. (See "Surgical management of hidradenitis suppurativa", section on 'Unroofing (local or extensive)'.)

Wide excision is an alternative approach for skin tunnels and nodules in the setting of severe, extensive HS. (See 'Wide excision' above.)

SPECIAL POPULATIONS

Pregnant patients — Although some patients with HS experience improvement in symptoms during pregnancy, others experience persistence or worsening disease [104]. There are safety concerns with most of the systemic therapies utilized for HS. The risks and benefits of therapy should be carefully considered on an individual basis. Oral retinoids are contraindicated in pregnancy.

Children — Children and adolescents with HS are treated with many of the therapies commonly used for adult disease [105,106]. Antimicrobial cleansers (eg, benzoyl peroxide), topical clindamycin, and oral antibiotics (eg, tetracyclines, oral clindamycin alone or in combination with rifampin) are common initial therapies. Of note, tetracyclines are not recommended for children under the age of nine due to the potential drug-induced discoloration of permanent teeth.

Other agents that have been used for pediatric HS include dapsone, short courses of oral glucocorticoids, finasteride (females), biologic tumor necrosis factor (TNF) inhibitors (adalimumab, infliximab), and surgery [105,106].

OTHER THERAPIES — Other therapies may be beneficial in HS. Examples include neodymium-doped yttrium aluminum garnet (Nd:YAG) laser therapy, apremilast, and zinc supplementation.

Nd:YAG laser — In a randomized, within-participant trial of 22 patients with Hurley stage II or III disease, treatment of the affected skin region with a 1064 nm Nd:YAG laser reduced disease severity in inguinal, axillary, and inframammary sites [107]. The mechanism of action of the Nd:YAG laser in HS may involve follicular destruction or dermal heating leading to the disruption of the inflammatory infiltrate [108].

Rifampin, moxifloxacin, and metronidazole — Combination therapy with rifampin, moxifloxacin, and metronidazole has appeared beneficial in uncontrolled studies. In a retrospective study of 28 patients with longstanding HS that was refractory to other treatments (short-course antimicrobials, surgical drainage, and/or surgical excision), treatment with these drugs was associated with reduced disease activity [109]. Patients with stage I or II HS appeared to benefit most from this intervention.

In addition, in a prospective, uncontrolled study, 28 patients with Hurley stage I HS were given a six-week course of rifampin (10 mg/kg once daily), moxifloxacin (400 mg once daily [or 1 g of pristinamycin three times daily if concern for poor tolerance of moxifloxacin]), and metronidazole (250 or 500 mg three times daily), followed by rifampin and moxifloxacin for four weeks and, if remission was obtained, given long-term prophylaxis with either cotrimoxazole (most patients) or doxycycline [110]. At 12 weeks, 75 percent achieved clinical remission, and at the one year follow-up, flare rates had fallen from a median of 21 flares per year to 1 per year.

Some of the potential adverse effects of concern include risk for tendonitis or tendon rupture from moxifloxacin, orange body secretions and drug interactions from rifampin, and alcohol-associated, disulfiram-like reactions and adverse neurologic effects from metronidazole. For additional information, refer to the Lexicomp drug information monograph included within UpToDate.

Apremilast — Limited data suggest benefit of apremilast, a phosphodiesterase 4 inhibitor, for HS [111,112]. A trial in which 20 patients with moderate HS were randomly assigned to receive either 30 mg of apremilast twice daily (15 patients) or placebo (5 patients) found apremilast superior for achieving the Hidradenitis Suppurativa Clinical Response (HiSCR) primary efficacy endpoint (≥50 percent reduction in the total abscess and inflammatory nodule count with no increase in the abscess or draining sinus count) at week 16 [111]. In the apremilast group, 8 out of 15 patients (53 percent) achieved HiSCR compared with none of the patients in the placebo group. Apremilast was generally well tolerated. The most common adverse events among participants who received apremilast were headache, diarrhea, nausea, and the common cold. Additional study is necessary to confirm efficacy and safety of apremilast in the treatment of HS.

Zinc supplementation — Zinc salts have anti-inflammatory and antiandrogenic properties, and there are limited data for possible benefit in HS [113]. The efficacy of zinc gluconate (90 mg per day) was investigated in a pilot study of 22 patients who had failed to achieve satisfactory improvement with systemic antibiotic therapy, antiandrogens, isotretinoin, or surgery [113]. All but one patient had Hurley stage I or II disease. Among the patients, eight (36 percent) achieved complete responses (disappearance of lesions or no new lesions for ≥6 months), and the remainder achieved partial remissions (≥50 percent reduction in the number of nodules and/or a shorter duration of inflammatory lesions). However, relapses occurred upon tapering of the dose to ≤60 mg per day.

Additional support for a beneficial effect of zinc gluconate in HS stems from a prospective study of 12 patients with Hurley stage I or II HS [114]. Deficiencies in innate immune markers detected in lesional and nonlesional skin from patients with HS were improved following three months of treatment with zinc gluconate (90 mg per day).

Gastrointestinal upset may occur as a consequence of zinc sulfate therapy [113]; zinc gluconate (30 mg twice or three times per day in adults) may be better tolerated. Of note, zinc may displace copper, reducing copper absorption.

Other — A number of other treatments have been proposed for HS. However, unclear efficacy or concern for adverse effects preclude recommendations for routine use of these interventions:

Fumarates – Fumarates are anti-inflammatory and immunomodulatory agents used in the treatment of psoriasis. In an uncontrolled, pilot study in which seven patients with treatment-refractory, moderate to severe HS were treated with oral fumarates, three patients seemed to improve during therapy and four patients discontinued treatment because of lack of efficacy [115]. Data are insufficient to recommend routine use of this therapy.

Vitamin D3Vitamin D3 supplementation has been proposed as a treatment for HS based upon hypotheses that a deficiency in innate immunity may contribute to HS and that vitamin D3 may play an important role in innate immunity. In an uncontrolled study in which 14 patients with HS and vitamin D3 deficiency (defined as 25-hydroxyvitamin D3 level <30 ng/mL) received vitamin D3 supplementation (100,000 to 600,000 international units given at baseline and/or after three months depending on the serum vitamin D level), 11 (79 percent) had at least a 20 percent reduction in the number of nodules after six months [116]. Additional study is necessary to confirm efficacy of vitamin D3 supplementation in HS.

Ionizing radiation – A retrospective study of 231 patients with refractory HS treated with radiotherapy found that 38 percent had complete resolution of symptoms, and an additional 40 percent had some degree of improvement in symptoms following radiation treatment [117]. Although radiation therapy administered to the affected skin region may be effective [117,118], this modality is rarely used for HS due to concern for the occurrence of long-term adverse effects (eg, chronic radiation dermatitis, ulceration, cutaneous malignancy) [28]. (See "Radiation dermatitis" and "Clinical manifestations, prevention, and treatment of radiation-induced fibrosis".)

Intense pulsed light – Treatment with intense pulsed light of affected skin regions (axilla, groin, or inframammary area) was also associated with improvement in disease severity in a randomized, within-participant trial of 18 patients with Hurley stage II or III HS [119].

Photodynamic therapy – Photodynamic therapy combines use of a photosensitizer and a light source to induce cellular destruction through porphyrin activation. Treatment of areas of involvement of HS with photodynamic therapy using a topical photosensitizer has yielded variable results [120-124]. An intralesional technique for photodynamic therapy was associated with improvement in case reports and a small, retrospective study [125,126]. Intralesional photodynamic therapy is rarely used clinically.

Other – Examples of treatments that have been reported as beneficial in case reports and small clinical studies include botulinum toxin injections [127,128], cryoinsufflation [129], golimumab [130], risankizumab [131,132], Janus kinase inhibitors [133,134], and the glucagon-like peptide-1 agonist liraglutide [135]. Further study will be useful for confirming the efficacy of these therapies.

Microwave ablation, a noninvasive procedure that destroys sweat glands and hair follicles through thermolysis, is not recommended for HS. A randomized trial in which outcomes of a single treatment in one axilla were compared with findings in the untreated contralateral axilla was discontinued after interim analysis of nine patients suggested no benefit and potential harm of this intervention [136]. Of the eight patients who completed treatment, five experienced worsening of disease after treatment.

PROGNOSIS — Early diagnosis of HS is essential because most cases can be effectively treated when diagnosed at an early stage [19]. Hurley stage III disease is very difficult to manage and requires a multidisciplinary treatment approach, with coordination between dermatologists, dermatology specialist nurses, surgeons who have axillary and inguinal expertise, wound healing experts, and input from clinical psychologists. Although cure is possible in a skin region after extensive surgery [137], this does not prevent disease progression in other affected skin regions and so further medical treatment is required.

RISK FOR SQUAMOUS CELL CARCINOMA — Rarely, squamous cell carcinoma develops within sites of HS. Squamous cell carcinoma tends to be seen in patients who have suffered from HS for many years, particularly in the perianal region, and is often advanced at diagnosis [138-141]. Clinical signs suggestive of squamous cell carcinoma may include a new or rapidly growing, exophytic lesion or ulcer.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hidradenitis suppurativa".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Hidradenitis suppurativa (The Basics)")

SUMMARY AND RECOMMENDATIONS

Overview – Hidradenitis suppurativa (HS) is a chronic, follicular, occlusive disease characterized by the development of inflammatory nodules, skin tunnels, and scars, primarily in intertriginous areas. Pain, odor, chronic drainage, and disfigurement are common features of this disorder. HS can have a profound negative effect on quality of life. (See 'Introduction' above and 'Goals of treatment' above.)

Goals of treatment – Treatment of HS is generally indicated. The major goals of treatment are to reduce the formation of new lesions, skin tunnels, and scarring; to treat existing lesions and reduce associated symptoms; and to minimize associated psychologic morbidity. (See 'Goals of treatment' above.)

Approach to treatment – The severity of HS influences the approach to treatment. Features such as the extent of skin involvement and the presence of skin tunnels or scarring influence disease severity. The Hurley staging system is also used to define disease severity. (See 'Assessment of disease severity and response' above.)

The management of HS involves multiple interventions. In addition to medical or surgical therapy to reduce disease burden and treat acute lesions, patient education, psychologic support resources, wound care guidance, and pain management are important components of treatment. (See 'Interventions for all patients' above.)

Management of acute, painful lesions – Patients with acute, painful, inflammatory nodules may benefit from interventions to accelerate improvement in symptoms in addition to interventions to improve the overall disease burden. Intralesional corticosteroid injections, punch debridement, or topical resorcinol may be used for this purpose.

Incision and drainage is not advised for the routine treatment of acute lesions of HS. Incision and drainage should be restricted to situations in which immediate pain relief is necessary and other interventions for acute lesions are not feasible.

Reducing disease activity – A variety of medical interventions have been used to reduce disease burden in HS. The approach to treatment selection is dependent upon the clinical presentation:

Patients with inflammatory lesions without skin tunnels or scarring – For patients who present with inflammatory lesions without skin tunnels or scarring (Hurley stage I disease):

-Initial therapy – We suggest topical clindamycin as the initial medical treatment (Grade 2C). (See 'Initial therapy' above.)

-Failure of initial therapy – If HS does not improve sufficiently with topical clindamycin, we suggest treatment with an oral tetracycline class antibiotic (Grade 2C). Antiandrogenic drugs and metformin are additional treatment options that may be used alone or in conjunction with antibiotics. (See 'Failure of initial therapy' above.)

-Refractory disease – Treatment options for refractory disease include clindamycin and rifampin combination therapy, acitretin, and oral dapsone. (See 'Refractory disease' above.)

Patients with inflammatory lesions with skin tunnels or scarring – For patients who present with inflammatory lesions with skin tunnels or scarring (Hurley stage II or III disease):

-Initial therapy – We suggest oral antibiotic therapy as the initial medical treatment (Grade 2C). Our first choice for antibiotic therapy for patients with a moderate, inflammatory burden (eg, Hurley stage II disease) is typically an oral tetracycline (eg, doxycycline).

For patients with extensive, inflammatory disease (eg, Hurley stage III HS) we typically begin with combination therapy with clindamycin and rifampin. Antiandrogenic drugs and metformin may be helpful adjunctive therapies. (See 'Initial therapy' above.)

-Failure of initial therapy – Next-line therapies for patients who do not improve sufficiently with oral antibiotics and hormonal therapy include oral retinoids, dapsone, adalimumab, and infliximab. We typically treat with acitretin or dapsone prior to proceeding to biologic therapy, although other approaches are reasonable.

For patients who do not improve sufficiently with oral antibiotics, retinoids, dapsone, and hormonal therapy, we suggest treatment with adalimumab (Grade 2A). Infliximab is a second-line biologic option. (See 'Failure of initial therapy' above.)

-Skin tunnels and recurrent nodules – Medical therapy can be insufficient for improving skin tunnels and some recurrent nodules. Surgical intervention may help to improve these features. (See 'Skin tunnels and recurrent nodules' above and "Surgical management of hidradenitis suppurativa".)

-Severe, refractory disease – Patients with severe HS refractory to medical treatment are candidates for wide excision of skin in the affected areas. A variety of medical therapies have also been utilized for severe, refractory disease. (See 'Severe refractory disease' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Lynette Margesson, MD, FRCPC, FAAD, who contributed to an earlier version of this topic review.

The UpToDate editorial staff acknowledges F. William Danby, MD, FRCPC, FAAD, now deceased, who contributed to an earlier version of this topic review.

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Topic 7605 Version 63.0

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