Dermatologic Manifestations of Hidradenitis Suppurativa Medication
- Author: Marina Jovanovic, MD, PhD; Chief Editor: Dirk M Elston, MD more...
Medication Summary
Treatment of hidradenitis suppurativa remains a considerable challenge. Therapeutic options for hidradenitis suppurativa were long restricted to the use of local disinfectants and systemic antibiotics, as well as repeated incision and drainage, which produce only short-term benefits. Medical management is recommended in early stages, whereas surgery should be performed as early as possible after the formation of abscesses, fistulas, scars, and sinus tracts (see Surgical Care).[65]
Treatment should be individualized according to the state and extent of the disease. Absolute cessation of smoking is essential in the treatment of hidradenitis suppurativa. Management with antibiotics or other medications may relieve early symptoms, but radical surgery may be necessary for control and prevention of recurrence.[60]
Alikhan et al suggest a treatment algorithm based upon the Hurley classification or a tiered approach. For patients in Hurley stage I, antibiotics and intralesional injections of corticosteroids represent a good first-line therapy, while flares should be treated with short courses of systemic corticosteroids. If this regimen fails, zinc, or, in females of non-childbearing age, antiandrogen, therapy may be effective. Long-term immunosuppressive therapy or surgical therapy may be required in some patients. For patients in Hurley stage III, wide excision may prove to be the only effective treatment.[28]
Cryotherapy has also been used as adjunctive therapy. In draining sinuses, cryotherapy works by accelerating the resorption of the inflammation. However, patients must be warned about pain, prolonged healing time, and risk of infection after the procedure, and they must be informed that the treatment is unlikely to influence disease progression.[73]
Antibiotics
Class Summary
Acute episodes and relapses of hidradenitis suppurativa should be treated as bacterial infections. Mild topical steroid creams in combination with topical antibiotics in the aminoglycoside group, such as clindamycin 2% solution, gentamicin collagen sponge, and erythromycin 3% gel, have been favored.[66, 74] Some authors advocate long-term treatment with systemic antibiotics (eg, tetracycline, minocycline, clindamycin, erythromycin in combination with metronidazole), but long-term outcomes are often poor.[27, 28]
Tetracycline (Panmycin, Sumycin, Tetracap)
Used to treat gram-positive and gram-negative organisms and mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunits.
Doxycycline (Doryx, Vibramycin, Bio-Tab)
Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Clindamycin (Cleocin)
Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Erythromycin (E.E.S., E-Mycin, Eryc)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half the total daily dose may be taken q12h. For more severe infections, double the dose.
Retinoids
Class Summary
Vitamin A derivatives have many roles. They encourage cellular differentiation, are antiproliferative, and serve as immunomodulators. Although some patients have dramatic responses to isotretinoin 1 mg/kg/d as monotherapy[36] or combined with prednisolone (ie, when isotretinoin was introduced after 8 wk of prednisolone and erythromycin therapy),[18] retinoids may be useful only as an adjunct to reduce inflammation before and after surgery.[33, 64]
Results from a long-term follow-up study indicate that although the response of hidradenitis suppurativa to isotretinoin is only moderate and is related to the severity of the disease, the promising effects of acitretin therapy described in this case series suggests the need for a randomized, controlled trial.[75] The dose of isotretinoin is unlikely to be important in treating hidradenitis suppurativa.
Others propose that long-term treatment with isotretinoin is more successful than the usual 4-month to 6-month regimen.[18] Isotretinoin does not affect the size of the apocrine gland, and etretinate or acitretin (25 mg bid) may be more useful, at least in some cases. The fact that some conditions do not respond to isotretinoin, yet do respond to etretinate and acitretin, suggests that the suppression of hyperkeratinization is more important than glandular shrinkage. In parous women, a prolonged course of isotretinoin is probably a safer initial choice; however, severe complications, such as acute pancreatitis associated with hyperlipidemia, may occur, even in patients without an identifiable risk factor.[76]
Isotretinoin (Accutane)
Affects epidermal differentiation, especially at the follicular infundibulum. Also has immunomodulating effects. Has been used as chemoprophylaxis for skin cancers.
A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.
Sulfones
Class Summary
These agents have anti-inflammatory effects.[77]
Dapsone (Avlosulfon)
Bactericidal and bacteriostatic against mycobacteria; mechanism of action similar to that of sulfonamides, in which competitive antagonism of PABA prevents formation of folic acid, inhibiting bacterial growth.
Corticosteroids
Class Summary
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli. Intralesional injection with either a syringe or an automatic needleless injector usually decreases the size of draining sinuses. The injection of 0.05-0.25 mL of triamcinolone acetonide suspension (2.5-10 mg/mL) into each lesion is recommended for its anti-inflammatory effects. This treatment can be repeated every 2-3 weeks if necessary.[29] The anti-inflammatory effects of systemic corticosteroids may be useful in acute exacerbations. Prednisolone 60 mg/d with lower maintenance doses provides some long-term control.[43]
Triamcinolone (Amcort, Aristospan Intra-Articular)
For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Intramuscular injection may be used for widespread skin disorder. Intralesional injections may be used for localized skin disorder.
Prednisolone (Prelone)
Decreases autoimmune reactions, possibly by suppressing key components of immune system.
Hormones
Class Summary
Combined treatment with the antiandrogen cyproterone acetate and ethinyl oestradiol has been shown to be of benefit to women with long-standing hidradenitis suppurativa. Treatment with the antiandrogen cyproterone acetate in combination with estrogen ethinyl estradiol and ethinyl estradiol in combination with the low-dose progestin norgestrel may significantly improve disease activity, especially in patients with mild forms of hidradenitis suppurativa, but many conditions do not respond to these treatments. Finasteride, a competitive inhibitor of 5-alpha reductase type II isoenzyme, may be beneficial in hidradenitis suppurativa.[78]
Cyproterone acetate (Androcur)
Inhibits androgen binding to target cells.
Ethinyl estradiol (Estinyl)
Reduces secretion of LH and FSH from pituitary gland by decreasing amount of gonadotropin-releasing hormones.
Immunosuppressants
Class Summary
Because of the concurrent presentation of hidradenitis suppurativa and Crohn disease, as well as the morphological and histological similarities, these 2 conditions may share the same pathogenesis, namely excess tumor necrosis factor-alpha (TNF-alpha) production. This was supported by several reports in the literature of patients with hidradenitis suppurativa and Crohn disease who responded to infliximab.[31, 79, 80, 81, 82] Infliximab is an inhibitor of TNF-alpha. Although approved by the US Food and Drug Administration (FDA) for the treatment of Crohn disease and rheumatoid arthritis, infliximab has also been used in hidradenitis suppurativa.[83] The benefits outweigh the risks associated with its use, especially when it is administrated in severe chronic cases resistant to standard therapies.[67]
Patients self-report that pain significantly decreased following infliximab treatment. This correlated with significant physician-observed clinical improvement (P = .0001). Patients reported a rapid response after the first infusion, and some of them noticed decreased pain after 24 hours.[83, 84] Although the efficacy has proven impressive and short-term adverse effects have been few and relatively benign, the long-term adverse effects have not been studied. Further multicenter studies are needed to assess effects of its prolonged use, as well as to determine safety, optimal frequency of dosing, and time to relapse after cessation of therapy.[84, 85]
Moreover, the existing prospective studies have described variable patient responses and significant adverse reactions, including hypersensitive reactions, lupuslike reactions, and abdominal pain secondary to colon cancer, tuberculosis, and motor neuropathy. The studies varied in their outcome assessment, population studied, and dose of infliximab used in patients with hidradenitis suppurativa.[86, 87, 88]
Other inhibitors, including etanercept (a human fusion protein receptor consisting of 2 human TNF-alpha receptors and Fc domain of human immunoglobulin G1) and adalimumab (a fully humanized recombinant anti-TNF-alpha monoclonal antibody) have also produced variable patient responses and significant adverse reactions. Enough information is not yet available to assess the true risks of TNF-alpha inhibitor use as therapy for hidradenitis suppurativa. None of the studies used a control group. Thus, randomized controlled studies are necessary to determine the risk-to-benefit ratio of TNF-alpha inhibitor therapy in the treatment of hidradenitis suppurativa.[89, 90, 91, 92]
Therapeutic experience with nonspecific immunosuppression in hidradenitis suppurativa using methotrexate is unlikely to offer any significant advance. Before finally determining the value (or lack of value) of methotrexate in hidradenitis suppurativa, investigation of different dosage schedules in future patients with hidradenitis suppurativa would be worthwhile.[93]
Infliximab (Remicade)
Inhibits TNF-alpha activity and triggers complement-mediated lysis of TNF-alpha–expressing cells in vitro. Monoclonal chimeric antibody made from human constant and mouse variable regions of IgG, with binding specificity for human TNF-alpha. Binds to inactive TNF-alpha and can bind specifically to both membrane-bound and soluble TNF-alpha. Binds to inactive TNF-alpha monomers, preventing their association into active trimers. Used to treat severe inflammatory diseases that do not respond to systemic corticosteroids or immunosuppressants.
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