Hidradenitis Suppurativa - Treatment - UpToDate PDF

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Hidradenitis suppurativa: Treatment
Author: John R Ingram, MD, PhD

Section Editors: Robert P Dellavalle, MD, PhD, MSPH, Mark V Dahl, MD
Deputy Editor: Abena O Ofori, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Oct 06, 2017.
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
cases 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).
The management and prognosis 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"
and "Surgical management of hidradenitis suppurativa".)
PRINCIPLES The pain, odor, drainage, and disfigurement caused by HS profoundly affects quality of life
[1]. Patients often experience feelings of sadness or depression related to the disease, and feelings of shame
may contribute to self-imposed social isolation [2-4]. Diagnostic delay, which averages seven years,
combined with the significant physical and emotional toll of HS, may lead to patient frustration with medical
care [5].
Treatment goals Untreated, HS can remain active for many years after onset, which is typically in early
adulthood. Interventions for HS target one or more of three major goals:
To reduce the frequency of new lesions, minimizing pain and suppuration
To prevent disease progression by limiting the formation of scarring
To treat existing lesions and scarring, a goal which may require a combination of medical and surgical
intervention
More than 50 interventions exist for treatment of HS, including patient self-management strategies, topical
therapy, oral systemic agents, biologic therapies, surgery, and laser and light interventions. Disease severity,
patient tolerance of specific agents, comorbidities, and treatment cost and availability guide treatment
choices. (See 'Treatment' below.)
Staging systems The Hurley clinical staging system is frequently utilized to describe the severity of HS
[6]. In accordance with this system, HS is divided into three stages:
Stage I Abscess formation (single or multiple) without sinus tracts and cicatrization/scarring (picture 2)
Stage II Recurrent abscesses with sinus tracts and scarring, single or multiple widely separated
lesions (picture 3)
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Stage III Diffuse or almost diffuse involvement, or multiple interconnected tracts and abscesses across
the entire area (picture 1A-B)
Outcome measure instruments The Hurley staging system has insufficient responsiveness to change to
be used as a clinical study outcome measure. The Sartorius scale [7] and modified Sartorius scale [8,9] have
been used in clinical trials, and a newer assessment tool, the Hidradenitis Suppurativa Clinical Response
(HiSCR), has been developed and validated [10]. The HIdradenitis SuppuraTiva cORe outcomes set
International Collaboration (HISTORIC) is developing a core domain set for HS trial outcomes [11].
In a busy clinic setting, other instruments are useful for quickly assessing disease severity. Patients can
complete a quality-of-life instrument, such as the Dermatology Life Quality Index or Skindex, and a pain
visual analogue scale (form 1) [12,13]. They can also be asked to record the number of new or recurrent
lesions occurring in the preceding month.
TREATMENT The multifaceted clinical features of HS and the unpredictable course of the disease make a
uniform approach to treatment challenging. (See 'General approaches' below and 'Hurley stage I (mild
disease)' below and 'Hurley stage II' below and 'Hurley stage III (severe and refractory disease)' below.)
General approaches Regardless of disease severity, attention to patient education and support, patient
self-management, management of comorbidities, and pain management may be beneficial.
Education and support Because HS is a psychologically distressing disorder that can have a major
impact on patient quality of life, patient education and support are essential components of management. The
clinician should inquire about the impact of the disease on the patient's quality of life and assess for
symptoms of depression [14]. (See "Screening for depression in adults".)
Patients should be informed that the disease is neither contagious nor due to poor hygiene. Patients should
also be offered resources for psychologic support [3], such as contact information for local HS patient
societies.
Self-management Patient self-management is an important part of the approach to HS. Patients

should be offered individualized self-management strategies.
Avoidance of skin trauma Factors that promote skin maceration and follicular trauma may contribute
to worsening of HS due to the promotion of inflammation, follicular occlusion, and follicular rupture. We
advise patients to wear loose, light clothing and to actively avoid excessive heat, friction, and shearing
trauma. Washing with loofahs or brushes should be avoided to prevent unnecessary skin trauma and
irritation.
Dressings Whether dressing untreated but actively draining lesions or the postoperative wound,
dressings should be selected 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.
Smoking cessation Smoking is commonly associated with HS. The case for smoking as a causative
factor is strengthening [8,15-18], and documentation of improvement in HS after smoking cessation has
appeared in a few case reports [19]. Despite the fact that the impact of smoking cessation on HS is
untested by clinical trials, this observed association, the observed increase in risk for cardiovascular-
associated death among patients with HS compared with patients without the disease [20], and the
overall negative impact of smoking on health lead us to routinely discourage smoking and other nicotine
use. Ideally, smoking cessation support should be offered as part of the multidisciplinary approach to HS
management. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on
'Associated factors' and "Overview of smoking cessation management in adults" and "Behavioral
approaches to smoking cessation".)
Weight management As with smoking, excess weight has been linked to HS, but a causative
association between weight and HS has not been definitively established [8,15,16]. Factors related to
excess weight, such as skin occlusion, skin friction, shearing forces on skin, hyperinsulinemia and other
hormonal changes that can occur in association with excess weight, and dietary factors appear to be
contributing factors in HS. Thus, we encourage and support weight management in our HS patients. In
addition, we sometimes prescribe metformin, an antidiabetes drug that may be beneficial for HS and
may have a modest effect on weight loss [21,22]. (See "Hidradenitis suppurativa: Pathogenesis, clinical
features, and diagnosis", section on 'Associated factors' and "Obesity in adults: Overview of
management" and 'Metformin' below.)
Data are emerging regarding the effect of substantial weight loss in obese HS patients. In a retrospective
survey of 45 Danish patients who had undergone bariatric surgery, 35 achieved substantial weight loss,
defined as at least a 15 percent reduction in baseline body mass index, and, of these, 17 experienced
resolution of their HS, 7 were improved, and 11 had unchanged or worsened disease [23]. Removal of
excess skin following substantial weight loss may be required to prevent disease exacerbations related
to increased frictional effects.
Antiseptics Topical antiseptic washes such as chlorhexidine 4% may be helpful for HS. Chlorhexidine
can be used for showering, beginning with once per week use and increasing up to once daily as
tolerated. In addition, some patients find emollients containing benzalkonium chloride, an antimicrobial
agent, to be helpful.
Management of comorbidities Patients with HS may be at increased risk for alcohol dependence,
arthropathies, autoimmune conditions, cardiovascular risk, diabetes, drug dependence, dyslipidemia,
follicular syndromes, hypertension, lymphoma, malignancies, metabolic syndrome, nicotine addiction, obesity,
polycystic ovarian syndrome, psychiatric and psychologic disorders, rheumatologic conditions, and thyroid
disease [24,25]. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on
'Associated disorders and syndromes'.)
Multidisciplinary management of comorbidities can improve patient outcomes. 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 been published [26]. 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.
Pain management Pain from HS nodules and abscesses may cause sleep disturbance, limit function,
and induce psychologic distress. Nonsteroidal anti-inflammatories can be used to treat both pain and
inflammation. Additional analgesia, including opioid analgesia, may be needed. (See "Overview of the
treatment of chronic non-cancer pain".)
Hurley stage I (mild disease) Local therapy combined with the general approaches described above is
the preferred treatment of mild HS (picture 2). (See 'General approaches' above.)
Useful local measures include topical clindamycin, intralesional corticosteroid injections, punch debridement,
and topical resorcinol. When these measures are insufficient, oral tetracyclines may be beneficial.
Topical clindamycin Topical clindamycin is often utilized as a first-line therapy for mild HS. A
randomized three-month trial supported its efficacy for mild inflammatory lesions and demonstrated the
relative safety and tolerability of this regimen [27]. Patients with mild HS were treated with twice-daily
applications of clindamycin 1% solution (13 patients) or vehicle (14 patients). Treatment efficacy was
assessed with an unvalidated scoring system that was designed to assess the amount of disease. The trial
found that the cumulative disease burden score improved to a significantly greater degree in patients treated
with topical clindamycin than in patients who were given placebo at all study time points (one, two, and three
months after the start of treatment). Treatment with clindamycin was well tolerated; two patients treated with
clindamycin 1% solution and three patients treated with vehicle solution reported slight burning sensations at
the sites of treatment.
Intralesional corticosteroids Intralesional corticosteroid therapy is often useful as an adjunctive

therapy for reducing symptoms of HS. The intent of treatment is to accelerate the resolution of early, painful
inflammatory lesions. 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 supports this approach [28].
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 day 1 to day 2 after the injection. (See
"Intralesional injection".)
Punch debridement Performance of punch debridement (partial deroofing) to evacuate a new

inflamed nodule that is centered around a single folliculopilosebaceous unit (FPSU) can be effective for
eliminating new lesions. Simple incision and drainage are usually not performed because incised nodules
usually recur. (See "Surgical management of hidradenitis suppurativa", section on 'Punch debridement' and
"Surgical management of hidradenitis suppurativa", section on 'Role for I&D'.)
Topical resorcinol Resorcinol is a topical chemical peeling agent with keratolytic and anti-inflammatory
properties that is used by some clinicians for HS. Topical 15% resorcinol in a proprietary cream base is
applied directly to inflammatory nodules.
In an open study of 12 patients with Hurley stage I or stage 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 [29]. The expected adverse effect of local desquamation occurred in all
patients. Recurrences may follow discontinuation of the medication.
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.
Systemic antibiotics Short courses (eg, seven days) of penicillin-type antibiotics do not appear to alter
the natural history of an acute HS lesion [30]. In addition, multiple short antibiotic courses may promote
bacterial resistance. A strategy endorsed by the European HS guidelines is to give a more prolonged course
of an oral tetracycline such as lymecycline or doxycycline, with the treatment goal to prevent or reduce the
frequency of new lesions [31]. (See 'Oral tetracyclines' below.)
Hurley stage II Hurley stage II HS is characterized by inflammatory nodules, sinus tracts, and scarring
(picture 3).
Antibiotic therapy The mechanism by which antibiotic therapy improves HS has not been definitively
determined. Antibiotics may help to control skin bacterial load, however; the anti-inflammatory effects
associated with some antibiotics may also play a role [32].
First-line antibiotic therapy
Oral tetracyclines Tetracyclines are a key treatment for mild to moderate HS, in part because of
their favorable adverse effect profile. A common regimen for adults is 100 mg of doxycycline given once to
twice daily. Alternative tetracycline regimens include lymecycline (408 mg once or twice daily), tetracycline
(500 mg twice daily), and minocycline (100 mg once or twice daily). Treatment is generally continued for
several months.
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) [33]. 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 in the oral tetracycline
group.
Clindamycin and rifampin Combination therapy with clindamycin and rifampin is an option for
patients who fail to respond to oral tetracyclines. Use of this regimen is based upon uncontrolled studies [34-
37]. In the largest study 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 [34]. 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 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 [35]. 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) [37]. Relapse did not occur in 7 of the 17 responders (41 percent) available for follow-up one year
after treatment.
Combination therapy with clindamycin and rifampin is usually reserved for patients who are unresponsive to
oral tetracyclines due to concern for drug-related adverse effects. Gastrointestinal adverse effects of this
treatment regimen are common [34,35]. While the potential for Clostridium difficile infection exists, this not
been highlighted as a major issue in the HS literature. Patients should also be advised that rifampin causes
orange discoloration of bodily secretions, and the effectiveness of hormonal contraception may be reduced.
Drug interactions due to rifampin should also be reviewed. (See "Clostridium difficile infection in adults:
Clinical manifestations and diagnosis" and "Clostridium difficile in adults: Epidemiology, microbiology, and
pathophysiology", section on 'Antibiotic use' and "Rifamycins (rifampin, rifabutin, rifapentine)", section on
'Adverse effects'.)
Other antibiotics 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 [38,39]. 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) [38]. 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 [39].
As with other medical agents, the disease often recurs after treatment cessation [38,39].
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 [40]. (See "Diagnosis and management of
glucose-6-phosphate dehydrogenase deficiency".)
Combination therapy with rifampin, moxifloxacin, and metronidazole appeared to be beneficial for reducing
disease activity 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) [41]. Patients with stage I
or II HS appeared to benefit most from this intervention.
Erythromycin and cephalosporins have also been used for long-term antibiotic therapy [42].
Oral retinoids Acitretin, isotretinoin, and a newer oral retinoid, alitretinoin, have been used to treat HS.
Acitretin is the primary agent utilized [31]. 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.
Acitretin 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 [43]. Only nine patients
completed the planned nine months of therapy. The primary reasons for withdrawal from the study were
treatment inefficacy and 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 [44]. 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) [45]. 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 [46]. 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) [47]. Alitretinoin is not available in the United States.
Potential adverse effects of systemic retinoids include cheilitis, xerosis, hyperlipidemia, and depression [48].
Retinoids are teratogenic, so use must be avoided in women who are at risk for pregnancy and during
pregnancy. 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. 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 'Isotretinoin
safety'.)
Hormonal therapy Androgens may contribute to the development of HS [32]. Examples of

antiandrogenic therapies that may improve the disease include cyproterone acetate, oral contraceptive pills,
spironolactone, and finasteride.
Cyproterone acetate was compared with norgestrel-containing oral contraceptive pills in a randomized,
double-blind crossover trial of 24 women with moderate to severe HS [49]. 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, and no significant difference in efficacy was detected.
Overall, improvement occurred in 12 patients, including seven patients who achieved complete remissions.
In addition to cyproterone acetate and oral contraceptive agents, spironolactone and finasteride have been
used for HS. A retrospective chart review found that 16 of 29 women (55 percent) treated with various
antiandrogenic drugs (cyproterone acetate containing oral contraceptive, cyproterone acetate, and/or
spironolactone) versus 6 of 23 women (26 percent) treated with oral antibiotics responded to treatment [50].
One 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 [51].
However, interpretation of these results is difficult because five patients were started on concomitant
minocycline 100 mg daily, and seven patients received an oral contraceptive pill. Small case series have
suggested benefit from finasteride [52,53].
Hormonal therapy should not be given to pregnant women because of the risk for adverse effects on the
fetus. Finasteride is also contraindicated in women of childbearing potential.
Surgery Surgery can be used for the treatment of individual nodules and sinus tracts that occur in any
Hurley stage of disease. Punch debridement (limited deroofing [unroofing]) of fresh lesions or deroofing of
single nodules and extensive sinuses is usually sufficient; wide excision is typically reserved for Hurley stage
III disease. (See "Surgical management of hidradenitis suppurativa", section on 'Punch debridement' and
"Surgical management of hidradenitis suppurativa", section on 'Wide excision and reconstruction'.)
Hurley stage III (severe and refractory disease) Both medical and surgical therapies are utilized to
prevent the development of new lesions and to treat existing lesions in patients with refractory Hurley stage II
HS and Hurley stage III HS (picture 1A-B). Although extensive surgical intervention generally offers the
greatest likelihood for the resolution of active inflammation in the treated area [54], 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 'General approaches' above and 'Medical therapy' below
and 'Surgery' below and "Surgical management of hidradenitis suppurativa".)
Medical therapy Patients who do not respond sufficiently to oral antibiotics, oral retinoids, or hormonal
therapies may benefit from biologic treatments, in particular, adalimumab or infliximab. Ustekinumab has
demonstrated benefit in small numbers of patients.
The pharmacologic therapies utilized for severe and refractory disease are reviewed below.
TNF-alpha inhibitors The tumor necrosis factor (TNF)-alpha inhibitors adalimumab and infliximab
have been utilized for the treatment of HS [55-61]. Additional studies are necessary to compare the efficacy
of these biologic therapies with each other and with other therapies used for HS. Adalimumab is the only
agent approved by the US Food and Drug Administration (FDA) for the treatment of HS. Etanercept, another
TNF-alpha inhibitor, does not appear effective for HS [58].
Adalimumab Improvement in HS during weekly treatment with adalimumab has been reported in
randomized trials. 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, then 40 mg once weekly starting on day 29. Every-other-week dosing of
adalimumab does not appear to be effective [58].
The FDA approval of adalimumab for moderate to severe HS was based upon the results of two similar
phase III 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) [59]. 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 antibiotic therapy at stable doses.
At week 12, more patients in the adalimumab groups achieved the Hidradenitis Suppurativa Clinical
Response 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.
Infliximab A beneficial effect of infliximab for HS was demonstrated in a trial of 38 patients with
moderate to severe HS [61]. 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) [58,61].
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.
Maintenance therapy may be required to maintain the effects of TNF-alpha inhibitors [62,63]. In the infliximab
trial, three of five patients who were followed through to 52 weeks relapsed after the discontinuation of
therapy [61]. In one of the adalimumab trials, all patients relapsed after the discontinuation of treatment [64].
The transient benefit attained with treatment with these agents can be useful for reducing disease activity
prior to surgery. Doing so may facilitate definition of the disease margins for the surgeon and may assist with
postsurgical healing [65]. (See "Surgical management of hidradenitis suppurativa", section on 'Perioperative
medication management'.)
Multiple potential adverse effects are associated with anti-TNF therapy, including risks for infection, heart
failure, demyelinating disease, a lupus-like syndrome, and malignancy. Paradoxical HS occurring during
treatment of other disorders with anti-TNF biologic agents also has been reported [66,67]. The adverse
effects of TNF-alpha inhibitors are discussed separately. (See "Tumor necrosis factor-alpha inhibitors: An
overview of adverse effects".)
Conventional immunosuppressants Occasionally, systemic glucocorticoids or cyclosporine are

prescribed for HS; however, evidence on the efficacy of these treatments for HS is limited. In addition,
because these drugs may induce severe adverse effects, they are rarely utilized for long-term therapy [32].
Systemic glucocorticoids 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. (See "Major side effects of systemic glucocorticoids".)
Cyclosporine In a retrospective case note review of 18 HS patients with Hurley stage II or III disease
treated with cyclosporine (2 to 3.5 mg/kg per day for 0.5 to 24 months), only two patients had obvious
reduction of symptoms and inflammation evident to both patients and physicians [68]. Of the remainder,
seven patients had "slight improvement," and nine had "no change." A few case reports describe
moderate to marked improvement in refractory HS with administration of cyclosporine (3 to 5 mg/kg per
day orally in two divided doses) given for several weeks or several months [69-71]. The duration of
cyclosporine treatment is often limited by adverse effects. (See "Pharmacology of cyclosporine and
tacrolimus", section on 'Side effects'.)
Emerging therapies Ustekinumab, anakinra, and canakinumab are biologic therapies that may be
of benefit for patients with severe and refractory HS based upon limited data. A case report also describes a
potential response of HS to oral tacrolimus.
Ustekinumab Positive responses to ustekinumab, an interleukin (IL)-12/23 inhibitor given via

subcutaneous injection, have been reported in patients with moderate to severe refractory HS [72-74].
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 [74]. 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 [75]. 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 [76,77]. 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 [77]. 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 [76].
Failure to respond to anakinra (100 mg per day) has been reported [78-80]. Additional data are needed
to clarify the role of anakinra in HS.
Canakinumab Canakinumab is a human IgG kappa monoclonal antibody that targets the
proinflammatory cytokine interleukin 1 beta. In a case report, two patients with severe HS had
improvement in both Sartorius scores and pain scores during canakinumab therapy [81].
Tacrolimus Clearance of HS after a change in immunosuppression regimen from cyclosporine to oral

tacrolimus is documented in a case report [82]. The patient was a renal transplant recipient who
developed HS two years after renal transplantation.
Surgery Surgical procedures may be performed on individual nodules or sinus tracts and in severe
cases may be used to excise an entire affected area [54]. Surgery should not be used in isolation; combining
surgery with medical therapy provides the best chance for preventing the development of new lesions and
controlling disease progress.
The surgical approach generally becomes more aggressive with higher-stage disease. (See "Surgical
management of hidradenitis suppurativa", section on 'General considerations' and 'Hurley stage I (mild
disease)' above and 'Hurley stage II' above and 'Hurley stage III (severe and refractory disease)' above.)
Surgical procedures for HS are 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'.)
Other nonsurgical therapies Additional therapies that have been reported to be effective in small
numbers of patients are reviewed below. In particular, metformin, oral zinc, and laser or light therapies may
be useful as adjunctive or alternative therapies.
Metformin Early evidence suggests that metformin may be a useful treatment for HS [21,22]. Support
for the efficacy of metformin for HS stems from 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 [22]. Eighteen patients
achieved clinical improvement, including seven who achieved at least a 50 percent reduction in Sartorius
score. Insulin and insulin-like growth factor may contribute to HS, providing a potential underlying mechanism
for a beneficial effect of metformin in HS, along with possible weight loss. Additional studies will be useful for
confirming the efficacy of metformin in HS. The development of nausea can be a limiting factor for treatment
with metformin.
Zinc supplementation Zinc salts have anti-inflammatory and antiandrogenic properties, and there are
limited data for possible benefit in HS [83]. 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 [83]. 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 [84]. 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 [83]; 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.
Laser and light therapy 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 neodymium-doped yttrium aluminum garnet
(Nd:YAG) laser significantly reduced disease severity in inguinal, axillary, and inframammary sites [85]. 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 [86].
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 [87].
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 [88-92]. An intralesional technique for photodynamic
therapy was associated with improvement in case reports and a small retrospective study [93,94].
Intralesional photodynamic therapy is rarely used clinically.
External beam 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 [95]. Although radiation therapy
administered to the affected skin region may be effective [95,96], 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) [15]. (See "Radiation dermatitis" and "Clinical manifestations, prevention, and
treatment of radiation-induced fibrosis".)
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 [97]. Data are insufficient to recommend routine use of this
therapy.
Vitamin D3 Vitamin 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 [98].
Additional study is necessary to confirm efficacy of vitamin D3 supplementation in HS.
Other Treatments that have been reported as beneficial in case reports include botulinum toxin
injections [99,100], cryoinsufflation [101], and the glucagon-like peptide-1 agonist liraglutide [102]. Further
study will be useful for confirming the efficacy of these therapies.
PROGNOSIS Early diagnosis of HS is essential because most cases can be effectively treated when
diagnosed at an early stage [5]. 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 [103], this does not prevent disease progression in
other affected skin regions, and so further medical treatment is required.
Rarely, squamous cell carcinoma develops within sites of HS. Squamous cell carcinoma tends to be seen in
patients who have suffered from HS for 10 years or more and is often advanced at diagnosis [104-107].
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
Hidradenitis suppurativa (HS) is a chronic, painful, inflammatory skin disorder of the

folliculopilosebaceous units characterized by the development of inflammatory nodules, pustules, sinus
tracts, and scars, primarily in intertriginous areas. (See "Hidradenitis suppurativa: Pathogenesis, clinical
features, and diagnosis".)
Physical pain, odor, chronic drainage, and disfigurement are common features of this disorder. The
symptoms of HS often have a profound negative effect on quality of life. (See "Hidradenitis suppurativa:
Pathogenesis, clinical features, and diagnosis".)
Successful treatment of HS requires prevention of new lesions in all stages of the disease to limit
disease progression. Treatment modalities include patient self-management and medical and surgical
interventions. (See 'Treatment' above and "Surgical management of hidradenitis suppurativa".)
Patient self-management strategies are important and include avoidance of skin trauma, smoking
cessation, and weight management where relevant. Patient education and psychologic support are
additional important components of patient management. (See 'General approaches' above.)
The level of disease severity strongly influences the approach to the treatment of HS.
Patients with Hurley stage I HS present with single or multiple nodules and abscesses without
associated sinus tracts or scarring. For these patients, we suggest daily treatment of the involved
areas with topical clindamycin (Grade 2B). A topical antiseptic wash can also be used for
showering.
Acutely inflamed lesions may require analgesia, such as nonsteroidal anti-inflammatories. Punch
debridement (partial deroofing [unroofing]) or intralesional corticosteroid injection may be performed
to reduce inflammation. Topical resorcinol is an alternative patient-administered treatment. (See
'Hurley stage I (mild disease)' above and "Surgical management of hidradenitis suppurativa", section
on 'General considerations' and "Surgical management of hidradenitis suppurativa", section on
'Punch debridement'.)
Patients with Hurley stage II HS exhibit recurrent inflamed nodules and abscesses, some of which
lead to sinus tracts and scarring. Treatment includes continuation of preventive, plus medical and
surgical, therapy.
For the medical treatment of the inflammatory component of Hurley stage II disease, we suggest
oral tetracyclines for first-line therapy (Grade 2C). Treatment with doxycycline (100 mg once daily or
twice daily) is common and should be continued for several months. Combination therapy with
clindamycin and rifampin can be helpful for suppurative disease unresponsive to oral tetracyclines.
Acitretin and antiandrogenic agents may also provide benefit. (See 'Hurley stage II' above.)
The sinus tracts of Hurley stage II HS will not resolve with antibiotic therapy and may require
surgical deroofing (unroofing) if they are recurrently inflamed. (See 'Hurley stage II' above and
"Surgical management of hidradenitis suppurativa", section on 'General considerations' and
"Surgical management of hidradenitis suppurativa", section on 'Unroofing (local or extensive)'.)
Hurley stage III HS is characterized by diffuse or nearly diffuse involvement of the affected area
(intertriginous or not) with fluctuant nodules, interconnecting sinus tracts, and extensive scarring.
For the nonsurgical treatment of Hurley stage III HS that cannot be managed with oral antibiotics,
oral retinoids, or hormonal therapy, we recommend adalimumab as the next-line therapy (Grade
1A).
For patients with severe HS in a localized area that has failed to respond sufficiently to medical
therapy and limited surgical therapy (eg, deroofing), extensive surgical excision offers the best
chance to provide permanent relief. (See 'Hurley stage III (severe and refractory disease)' above
and "Surgical management of hidradenitis suppurativa", section on 'General considerations' and
"Surgical management of hidradenitis suppurativa", section on 'Wide excision and reconstruction'.)
ACKNOWLEDGMENTS
The editorial staff at UpToDate would like to acknowledge Lynette Margesson, MD, FRCPC, FAAD, who
contributed to an earlier version of this topic review.
We are saddened by the death of F. William Danby, MD, FRCPC, FAAD, who passed away in November
2016. UpToDate wishes to acknowledge Dr. Danby's past work as an author for this topic.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Wolkenstein P, Loundou A, Barrau K, et al. Quality of life impairment in hidradenitis suppurativa: a study
of 61 cases. J Am Acad Dermatol 2007; 56:621.
2. Matusiak L, Bieniek A, Szepietowski JC. Psychophysical aspects of hidradenitis suppurativa. Acta Derm
Venereol 2010; 90:264.
3. Esmann S, Jemec GB. Psychosocial impact of hidradenitis suppurativa: a qualitative study. Acta Derm
Venereol 2011; 91:328.
4. Kurek A, Peters EM, Chanwangpong A, et al. Profound disturbances of sexual health in patients with
acne inversa. J Am Acad Dermatol 2012; 67:422.
5. Saunte DM, Boer J, Stratigos A, et al. Diagnostic delay in hidradenitis suppurativa is a global problem.
Br J Dermatol 2015; 173:1546.
6. Hurley HJ. Axillary hyperhidrosis, apocrine bromhidrosis, hidradenitis suppurativa, and familial benign p
emphigus: surgical approach. In: Dermatologic surgery, Roenigk RK, Roenigk HH (Eds), Dekker, New Y
ork 1989. p.729.
7. Sartorius K, Lapins J, Emtestam L, Jemec GB. Suggestions for uniform outcome variables when
reporting treatment effects in hidradenitis suppurativa. Br J Dermatol 2003; 149:211.
8. Sartorius K, Emtestam L, Jemec GB, Lapins J. Objective scoring of hidradenitis suppurativa reflecting
the role of tobacco smoking and obesity. Br J Dermatol 2009; 161:831.
9. Sartorius K, Killasli H, Heilborn J, et al. Interobserver variability of clinical scores in hidradenitis
suppurativa is low. Br J Dermatol 2010; 162:1261.
10. Kimball AB, Jemec GB, Yang M, et al. Assessing the validity, responsiveness and meaningfulness of
the Hidradenitis Suppurativa Clinical Response (HiSCR) as the clinical endpoint for hidradenitis
suppurativa treatment. Br J Dermatol 2014; 171:1434.
11. Thorlacius L, Ingram JR, Garg A, et al. Protocol for the development of a core domain set for
hidradenitis suppurativa trial outcomes. BMJ Open 2017; 7:e014733.
12. Finlay AY, Khan GK. Dermatology Life Quality Index (DLQI)--a simple practical measure for routine
clinical use. Clin Exp Dermatol 1994; 19:210.
13. Chren MM, Lasek RJ, Sahay AP, Sands LP. Measurement properties of Skindex-16: a brief quality-of-
life measure for patients with skin diseases. J Cutan Med Surg 2001; 5:105.
14. Onderdijk AJ, van der Zee HH, Esmann S, et al. Depression in patients with hidradenitis suppurativa. J
Eur Acad Dermatol Venereol 2013; 27:473.
15. Jemec GB. Clinical practice. Hidradenitis suppurativa. N Engl J Med 2012; 366:158.
16. Revuz JE, Canoui-Poitrine F, Wolkenstein P, et al. Prevalence and factors associated with hidradenitis
suppurativa: results from two case-control studies. J Am Acad Dermatol 2008; 59:596.
17. Canoui-Poitrine F, Revuz JE, Wolkenstein P, et al. Clinical characteristics of a series of 302 French
patients with hidradenitis suppurativa, with an analysis of factors associated with disease severity. J Am
Acad Dermatol 2009; 61:51.
18. Knig A, Lehmann C, Rompel R, Happle R. Cigarette smoking as a triggering factor of hidradenitis
suppurativa. Dermatology 1999; 198:261.
19. Simonart T. Hidradenitis suppurativa and smoking. J Am Acad Dermatol 2010; 62:149.
20. Egeberg A, Gislason GH, Hansen PR. Risk of Major Adverse Cardiovascular Events and All-Cause
Mortality in Patients With Hidradenitis Suppurativa. JAMA Dermatol 2016; 152:429.
21. Arun B, Loffeld A. Long-standing hidradenitis suppurativa treated effectively with metformin. Clin Exp
Dermatol 2009; 34:920.
22. Verdolini R, Clayton N, Smith A, et al. Metformin for the treatment of hidradenitis suppurativa: a little
help along the way. J Eur Acad Dermatol Venereol 2013; 27:1101.
23. Kromann CB, Ibler KS, Kristiansen VB, Jemec GB. The influence of body weight on the prevalence and
severity of hidradenitis suppurativa. Acta Derm Venereol 2014; 94:553.
24. Miller IM, McAndrew RJ, Hamzavi I. Prevalence, Risk Factors, and Comorbidities of Hidradenitis
Suppurativa. Dermatol Clin 2016; 34:7.
25. Shlyankevich J, Chen AJ, Kim GE, Kimball AB. Hidradenitis suppurativa is a systemic disease with
substantial comorbidity burden: a chart-verified case-control analysis. J Am Acad Dermatol 2014;
71:1144.
26. Dauden E, Lazaro P, Aguilar MD, et al. Recommendations for the management of comorbidity in
hidradenitis suppurativa. J Eur Acad Dermatol Venereol 2017.
27. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol 1983;
22:325.
28. Riis PT, Boer J, Prens EP, et al. Intralesional triamcinolone for flares of hidradenitis suppurativa (HS): A
case series. J Am Acad Dermatol 2016; 75:1151.
29. Boer J, Jemec GB. Resorcinol peels as a possible self-treatment of painful nodules in hidradenitis
suppurativa. Clin Exp Dermatol 2010; 35:36.
30. von der Werth JM, Williams HC. The natural history of hidradenitis suppurativa. J Eur Acad Dermatol
Venereol 2000; 14:389.
31. Zouboulis CC, Desai N, Emtestam L, et al. European S1 guideline for the treatment of hidradenitis
suppurativa/acne inversa. J Eur Acad Dermatol Venereol 2015; 29:619.
32. Nazary M, van der Zee HH, Prens EP, et al. Pathogenesis and pharmacotherapy of Hidradenitis
suppurativa. Eur J Pharmacol 2011; 672:1.
33. Jemec GB, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of
hidradenitis suppurativa. J Am Acad Dermatol 1998; 39:971.
34. Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin for
hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology 2009; 219:148.
35. van der Zee HH, Boer J, Prens EP, Jemec GB. The effect of combined treatment with oral clindamycin
and oral rifampicin in patients with hidradenitis suppurativa. Dermatology 2009; 219:143.
36. Mendona CO, Griffiths CE. Clindamycin and rifampicin combination therapy for hidradenitis
suppurativa. Br J Dermatol 2006; 154:977.
37. Dessinioti C, Zisimou C, Tzanetakou V, et al. Oral clindamycin and rifampicin combination therapy for
hidradenitis suppurativa: a prospective study and 1-year follow-up. Clin Exp Dermatol 2016; 41:852.
38. Yazdanyar S, Boer J, Ingvarsson G, et al. Dapsone therapy for hidradenitis suppurativa: a series of 24
patients. Dermatology 2011; 222:342.
39. Kaur MR, Lewis HM. Hidradenitis suppurativa treated with dapsone: A case series of five patients. J
Dermatolog Treat 2006; 17:211.
40. Lorenz M, Wozel G, Schmitt J. Hypersensitivity reactions to dapsone: a systematic review. Acta Derm
Venereol 2012; 92:194.
41. Join-Lambert O, Coignard H, Jais JP, et al. Efficacy of rifampin-moxifloxacin-metronidazole combination
therapy in hidradenitis suppurativa. Dermatology 2011; 222:49.
42. Danby FW, Margesson LJ. Hidradenitis suppurativa. Dermatol Clin 2010; 28:779.
43. Matusiak L, Bieniek A, Szepietowski JC. Acitretin treatment for hidradenitis suppurativa: a prospective
series of 17 patients. Br J Dermatol 2014; 171:170.
44. Boer J, Nazary M. Long-term results of acitretin therapy for hidradenitis suppurativa. Is acne inversa
also a misnomer? Br J Dermatol 2011; 164:170.
45. Soria A, Canoui-Poitrine F, Wolkenstein P, et al. Absence of efficacy of oral isotretinoin in hidradenitis
suppurativa: a retrospective study based on patients' outcome assessment. Dermatology 2009;
218:134.
46. Boer J, van Gemert MJ. Long-term results of isotretinoin in the treatment of 68 patients with hidradenitis
suppurativa. J Am Acad Dermatol 1999; 40:73.
47. Verdolini R, Simonacci F, Menon S, et al. Alitretinoin: a useful agent in the treatment of hidradenitis
suppurativa, especially in women of child-bearing age. G Ital Dermatol Venereol 2015; 150:155.
48. Danby FW. Night blindness, vitamin A deficiency, and isotretinoin psychotoxicity. Dermatol Online J
2003; 9:30.
49. Mortimer PS, Dawber RP, Gales MA, Moore RA. A double-blind controlled cross-over trial of
cyproterone acetate in females with hidradenitis suppurativa. Br J Dermatol 1986; 115:263.
50. Kraft JN, Searles GE. Hidradenitis suppurativa in 64 female patients: retrospective study comparing oral
antibiotics and antiandrogen therapy. J Cutan Med Surg 2007; 11:125.
51. Lee A, Fischer G. A case series of 20 women with hidradenitis suppurativa treated with spironolactone.
Australas J Dermatol 2015; 56:192.
52. Joseph MA, Jayaseelan E, Ganapathi B, Stephen J. Hidradenitis suppurativa treated with finasteride. J
Dermatolog Treat 2005; 16:75.
53. Farrell AM, Randall VA, Vafaee T, Dawber RP. Finasteride as a therapy for hidradenitis suppurativa. Br J
Dermatol 1999; 141:1138.
54. Ellis LZ. Hidradenitis suppurativa: surgical and other management techniques. Dermatol Surg 2012;
38:517.
55. Shuja F, Chan CS, Rosen T. Biologic drugs for the treatment of hidradenitis suppurativa: an evidence-
based review. Dermatol Clin 2010; 28:511.
56. Rambhatla PV, Lim HW, Hamzavi I. A systematic review of treatments for hidradenitis suppurativa. Arch
Dermatol 2012; 148:439.
57. Blok JL, van Hattem S, Jonkman MF, Horvth B. Systemic therapy with immunosuppressive agents and
retinoids in hidradenitis suppurativa: a systematic review. Br J Dermatol 2013; 168:243.
58. Ingram JR, Woo PN, Chua SL, et al. Interventions for hidradenitis suppurativa. Cochrane Database
Syst Rev 2015; :CD010081.
59. Kimball AB, Okun MM, Williams DA, et al. Two Phase 3 Trials of Adalimumab for Hidradenitis
Suppurativa. N Engl J Med 2016; 375:422.
60. Kimball AB, Kerdel F, Adams D, et al. Adalimumab for the treatment of moderate to severe Hidradenitis
suppurativa: a parallel randomized trial. Ann Intern Med 2012; 157:846.
61. Grant A, Gonzalez T, Montgomery MO, et al. Infliximab therapy for patients with moderate to severe
hidradenitis suppurativa: a randomized, double-blind, placebo-controlled crossover trial. J Am Acad
Dermatol 2010; 62:205.
62. Mekkes JR, Bos JD. Long-term efficacy of a single course of infliximab in hidradenitis suppurativa. Br J
Dermatol 2008; 158:370.
63. Blanco R, Martnez-Taboada VM, Villa I, et al. Long-term successful adalimumab therapy in severe
hidradenitis suppurativa. Arch Dermatol 2009; 145:580.
64. Miller I, Lynggaard CD, Lophaven S, et al. A double-blind placebo-controlled randomized trial of
adalimumab in the treatment of hidradenitis suppurativa. Br J Dermatol 2011; 165:391.
65. Jacob SE, Kerdel SA. Biologics for hidradenitis suppurativa (Verneuil's disease in the Era of biologics). I
n: Hidradenitis suppurativa, 1st ed, Jemec GBE, Revuz J, Leyden J (Eds), Springer, Berlin 2006. p.145.
66. Harvin G, Kasarala G. Two Cases of Paradoxical Hidradenitis Suppurativa while on Adalimumab. Case
Rep Gastroenterol 2016; 10:88.
67. Faivre C, Villani AP, Aubin F, et al. Hidradenitis suppurativa (HS): An unrecognized paradoxical effect of
biologic agents (BA) used in chronic inflammatory diseases. J Am Acad Dermatol 2016; 74:1153.
68. Anderson MD, Zauli S, Bettoli V, et al. Cyclosporine treatment of severe Hidradenitis suppurativa--A
case series. J Dermatolog Treat 2016; 27:247.
69. Gupta AK, Ellis CN, Nickoloff BJ, et al. Oral cyclosporine in the treatment of inflammatory and
noninflammatory dermatoses. A clinical and immunopathologic analysis. Arch Dermatol 1990; 126:339.
70. Buckley DA, Rogers S. Cyclosporin-responsive hidradenitis suppurativa. J R Soc Med 1995; 88:289P.
71. Rose RF, Goodfield MJ, Clark SM. Treatment of recalcitrant hidradenitis suppurativa with oral
ciclosporin. Clin Exp Dermatol 2006; 31:154.
72. Sharon VR, Garcia MS, Bagheri S, et al. Management of recalcitrant hidradenitis suppurativa with
ustekinumab. Acta Derm Venereol 2012; 92:320.
73. Gulliver WP, Jemec GB, Baker KA. Experience with ustekinumab for the treatment of moderate to
severe hidradenitis suppurativa. J Eur Acad Dermatol Venereol 2012; 26:911.
74. Blok JL, Li K, Brodmerkel C, et al. Ustekinumab in hidradenitis suppurativa: clinical results and a search
for potential biomarkers in serum. Br J Dermatol 2016; 174:839.
75. Tzanetakou V, Kanni T, Giatrakou S, et al. Safety and Efficacy of Anakinra in Severe Hidradenitis
Suppurativa: A Randomized Clinical Trial. JAMA Dermatol 2016; 152:52.
76. Zarchi K, Dufour DN, Jemec GB. Successful treatment of severe hidradenitis suppurativa with anakinra.
JAMA Dermatol 2013; 149:1192.
77. Leslie KS, Tripathi SV, Nguyen TV, et al. An open-label study of anakinra for the treatment of moderate
to severe hidradenitis suppurativa. J Am Acad Dermatol 2014; 70:243.
78. van der Zee HH, Prens EP. Failure of anti-interleukin-1 therapy in severe hidradenitis suppurativa: a
case report. Dermatology 2013; 226:97.
79. Menis D, Maroas-Jimnez L, Delgado-Marquez AM, et al. Two cases of severe hidradenitis
suppurativa with failure of anakinra therapy. Br J Dermatol 2015; 172:810.
80. Russo V, Alikhan A. Failure of Anakinra in a Case of Severe Hidradenitis Suppurativa. J Drugs
Dermatol 2016; 15:772.
81. Houriet C, Seyed Jafari SM, Thomi R, et al. Canakinumab for Severe Hidradenitis Suppurativa:
Preliminary Experience in 2 Cases. JAMA Dermatol 2017.
82. Ducroux E, Ocampo MA, Kanitakis J, et al. Hidradenitis suppurativa after renal transplantation:
complete remission after switching from oral cyclosporine to oral tacrolimus. J Am Acad Dermatol 2014;
71:e210.
83. Brocard A, Knol AC, Khammari A, Drno B. Hidradenitis suppurativa and zinc: a new therapeutic
approach. A pilot study. Dermatology 2007; 214:325.
84. Drno B, Khammari A, Brocard A, et al. Hidradenitis suppurativa: the role of deficient cutaneous innate
immunity. Arch Dermatol 2012; 148:182.
85. Tierney E, Mahmoud BH, Hexsel C, et al. Randomized control trial for the treatment of hidradenitis
suppurativa with a neodymium-doped yttrium aluminium garnet laser. Dermatol Surg 2009; 35:1188.
86. Xu LY, Wright DR, Mahmoud BH, et al. Histopathologic study of hidradenitis suppurativa following long-
pulsed 1064-nm Nd:YAG laser treatment. Arch Dermatol 2011; 147:21.
87. Highton L, Chan WY, Khwaja N, Laitung JK. Treatment of hidradenitis suppurativa with intense pulsed
light: a prospective study. Plast Reconstr Surg 2011; 128:459.
88. Gold M, Bridges TM, Bradshaw VL, Boring M. ALA-PDT and blue light therapy for hidradenitis
suppurativa. J Drugs Dermatol 2004; 3:S32.
89. Strauss RM, Pollock B, Stables GI, et al. Photodynamic therapy using aminolaevulinic acid does not
lead to clinical improvement in hidradenitis suppurativa. Br J Dermatol 2005; 152:803.
90. Guglielmetti A, Bedoya J, Acuna M, et al. Successful aminolevulinic acid photodynamic therapy for
recalcitrant severe hidradenitis suppurativa. Photodermatol Photoimmunol Photomed 2010; 26:110.
91. Schweiger ES, Riddle CC, Aires DJ. Treatment of hidradenitis suppurativa by photodynamic therapy
with aminolevulinic acid: preliminary results. J Drugs Dermatol 2011; 10:381.
92. Fadel MA, Tawfik AA. New topical photodynamic therapy for treatment of hidradenitis suppurativa using
methylene blue niosomal gel: a single-blind, randomized, comparative study. Clin Exp Dermatol 2015;
40:116.
93. Rodrguez-Prieto M, Valladares-Narganes LM, Gonzlez-Sixto B, Noguerol-Cal M. Efficacy of
intralesional photodynamic therapy for the treatment of hidradenitis suppurativa. J Am Acad Dermatol
2013; 68:873.
94. Agut-Busquet E, Roman J, Gilaberte Y, et al. Photodynamic therapy with intralesional methylene blue
and a 635 nm light-emitting diode lamp in hidradenitis suppurativa: a retrospective follow-up study in 7
patients and a review of the literature. Photochem Photobiol Sci 2016; 15:1020.
95. Frhlich D, Baaske D, Glatzel M. [Radiotherapy of hidradenitis suppurativa--still valid today?].
Strahlenther Onkol 2000; 176:286.
96. Trombetta M, Werts ED, Parda D. The role of radiotherapy in the treatment of hidradenitis suppurativa:
case report and review of the literature. Dermatol Online J 2010; 16:16.
97. Deckers IE, van der Zee HH, Balak DM, Prens EP. Fumarates, a new treatment option for therapy-
resistant hidradenitis suppurativa: a prospective open-label pilot study. Br J Dermatol 2015; 172:828.
98. Guillet A, Brocard A, Bach Ngohou K, et al. Verneuil's disease, innate immunity and vitamin D: a pilot
study. J Eur Acad Dermatol Venereol 2015; 29:1347.
99. Feito-Rodrguez M, Sendagorta-Cuds E, Herranz-Pinto P, de Lucas-Laguna R. Prepubertal
hidradenitis suppurativa successfully treated with botulinum toxin A. Dermatol Surg 2009; 35:1300.
100. O'Reilly DJ, Pleat JM, Richards AM. Treatment of hidradenitis suppurativa with botulinum toxin A. Plast
Reconstr Surg 2005; 116:1575.
101. Pagliarello C, Fabrizi G, Feliciani C, Di Nuzzo S. Cryoinsufflation for Hurley stage II hidradenitis
suppurativa: a useful treatment option when systemic therapies should be avoided. JAMA Dermatol
2014; 150:765.
102. Jennings L, Nestor L, Molloy O, et al. The treatment of hidradenitis suppurativa with the glucagon-like
peptide-1 agonist liraglutide. Br J Dermatol 2017; 177:858.
103. Harrison BJ, Mudge M, Hughes LE. Recurrence after surgical treatment of hidradenitis suppurativa. Br
Med J (Clin Res Ed) 1987; 294:487.
104. Williams ST, Busby RC, DeMuth RJ, Nelson H. Perineal hidradenitis suppurativa: presentation of two
unusual complications and a review. Ann Plast Surg 1991; 26:456.
105. Grewal NS, Wan DC, Roostaeian J, Rubayi SR. Marjolin ulcer in hidradenitis suppurativa: case reports.
Ann Plast Surg 2010; 64:315.
106. Lavogiez C, Delaporte E, Darras-Vercambre S, et al. Clinicopathological study of 13 cases of squamous
cell carcinoma complicating hidradenitis suppurativa. Dermatology 2010; 220:147.
107. Makris GM, Poulakaki N, Papanota AM, et al. Vulvar, Perianal and Perineal Cancer After Hidradenitis
Suppurativa: A Systematic Review and Pooled Analysis. Dermatol Surg 2017; 43:107.
Topic 7605 Version 37.0
GRAPHICS
Hidradenitis suppurativa
Hurley stage III disease involving the axilla. Diffuse involvement of the axilla with deep-
seated inflamed nodules, interconnecting sinus tracts, purulent drainage, and rope-like
scars.
Graphic 90465 Version 2.0
Hurley stage I disease. An inflamed nodule (arrow) and an open comedo (arrowhead)
are visible. Sinus tracts and fibrosis are absent.
Hurley stage II disease involving the breast. Inflamed papules and nodules as well as
bridged scars overlying sinus tracts. Comedones are visible in the center of the image.
Severe hidradenitis suppurativa
Reproduced with permission from: F William Danby, MD, FRCPC, FAAD, and Lynne J
Margesson, MD.
Visual analog pain scale
Contributor Disclosures
John R Ingram, MD, PhD Grant/Research/Clinical Trial Support: AbbVie [Hidradenitis suppurativa
(Adalimumab)]. Speaker's Bureau: AbbVie [Hidradenitis suppurativa (Adalimumab)]; UCB Pharm
[Hidradenitis suppurativa]. Other Financial Interest: British Journal of Dermatology [Editorial stipend]. Robert
P Dellavalle, MD, PhD, MSPH Grant/Research/Clinical Trial Support: Pfizer Pharmaceuticals [Independent
research grant to the University of Colorado (Development of patient decision aids)]. Other Financial Interest:
Editorial stipends from the Journal of Investigative Dermatology and the Journal of the American Academy of
Dermatology. Mark V Dahl, MD Consultant/Advisory Boards: Aubio Life Sciences [Lip health (Lip balm)].
Equity Ownership/Stock Options: Paris Therapeutics [Sunscreen]; CTX-Tech [Drug delivery]; Elorac, Inc.
[Acne, scalp psoriasis, inflammatory skin conditions, warts, plaque psoriasis (Oral doxycycline monohydrate
and topical benzoyl peroxide wash; anthralin shampoo; dietary supplements for acne, rosacea, and other
inflammatory skin conditions; salicylic acid wart remover; topical anthralin cream)]. Abena O Ofori,
MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
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Hidradenitis Suppurativa - Treatment - UpToDate PDF

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Hidradenitis suppurativa: Treatment

Author: John R Ingram, MD, PhD

To reduce the frequency of new lesions, minimizing pain and suppuration

To prevent disease progression by limiting the formation of scarring

Self-management Patient self-management is an important part of the approach to HS. Patients

Multidisciplinary management of comorbidities can improve patient outcomes. Recommendations from a

Intralesional corticosteroids Intralesional corticosteroid therapy is often useful as an adjunctive

Punch debridement Performance of punch debridement (partial deroofing) to evacuate a new

First-line antibiotic therapy

Isotretinoin Studies of isotretinoin therapy have demonstrated improvement in relatively low

Hormonal therapy Androgens may contribute to the development of HS [32]. Examples of

Conventional immunosuppressants Occasionally, systemic glucocorticoids or cyclosporine are

potential response of HS to oral tacrolimus.

Ustekinumab Positive responses to ustekinumab, an interleukin (IL)-12/23 inhibitor given via

Tacrolimus Clearance of HS after a change in immunosuppression regimen from cyclosporine to oral

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

SUMMARY AND RECOMMENDATIONS

Hidradenitis suppurativa (HS) is a chronic, painful, inflammatory skin disorder of the

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Topic 7605 Version 37.0

Graphic 90465 Version 2.0

Graphic 90463 Version 3.0

Graphic 90464 Version 1.0

Severe hidradenitis suppurativa

Graphic 65188 Version 4.0

Visual analog pain scale

Graphic 82442 Version 5.0

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