Updated: Mar 4, 2009
Hidradenitis suppurativa is an annoying chronic condition characterized by swollen, painful, inflamed lesions in the axillae, groin, and other parts of the body that contain apocrine glands. The disease is a chronic acneiform infection of the cutaneous apocrine glands that also can involve adjacent subcutaneous tissue and fascia. The hallmark of the disease is sinus tracts (which can become draining fistulas) in the apocrine gland body areas. Velpeau first described the condition in 1839.
The condition has classically been thought to occur when apocrine gland outlets become blocked by perspiration or are unable to drain normally because of incomplete gland development. Secretions trapped in the glands force perspiration and bacteria into surrounding tissue, causing subcutaneous induration, inflammation, and infection. However, more recent studies have indicated that hidradenitis suppurativa is caused by follicular occlusion first, which, in turn, occludes the apocrine glands and causes perifolliculitis. Therefore, it is actually a disorder of the terminal follicular epithelium located in the apocrine gland-bearing skin areas, which may better be termed as acne inversa.1
Hidradenitis suppurativa is confined to areas of the body that contain apocrine glands. These areas are the axillae, areola of the nipple, groin, perineum, circumanal, and periumbilical regions.
Often, patients with hidradenitis suppurativa also are afflicted with acne, pilonidal cysts, and chronic scalp folliculitis; thus, giving rise to the term follicular occlusion tetrad.
For further information, see Hidradenitis Suppurativa.
The problem is somewhat common, thought to occur in 1-2% of the population, but the precise incidence and prevalence are unknown.
A Danish study noted the prevalence of hidradenitis suppurativa to be in 4% of women.2
Hidradenitis suppurativa is painful and can be disabling but is rarely fatal, except when it progresses to overwhelming systemic infection in an immunocompromised patient. Extensive disease can prevent patients from performing normal work functions and from engaging in normal social activities. In some patients, especially those with severe disease, the condition creates significant psychological problems, particularly regarding sexual relationships.
Ingrown hairs are a predisposing factor, thus an increased incidence of the disease occurs in patients with tightly curled hair.
The incidence of hidradenitis suppurativa is greater in females than in males, thought to be in the range of 4:1 or 5:1. Flare-ups have been associated with menses, with a higher incidence in females with shorter cycles and more days of bleeding during the period.3
Hidradenitis suppurativa does not present prior to puberty because the apocrine glands are inactive until triggered by a surge in sex hormones. The condition may be observed in patients of any age after puberty.
The most common presentation is that of painful, tender, firm, nodular lesions under the arms.
Candidiasis
Cellulitis
Erysipelas
Bacterial folliculitis and furunculosis
Granuloma inguinale
Lymphogranuloma venereum
Pilonidal cysts
Tuberculous inflammation of the skin
Carbuncle
Epidermoid or dermoid cyst
Tetracycline and erythromycin may be helpful on a long-term basis, and cephalosporins often will help in acute cellulitis. On a short-term basis in the emergency department, dicloxacillin is considered a good choice. However, consideration must be given to using a sulfonamide or clindamycin antibiotic because of the growing presence of methicillin-resistant Staphylococcus aureus (MRSA) for both short-term and long-term treatment. Topical products, such as benzoyl peroxide, may be helpful. Topical and intralesional injections of corticosteroids are sometimes helpful.
Topical clindamycin cream has also been used with some success. Retin-A has rarely been found to be helpful in some patients. Systemic retinoids (Accutane) can reduce the severity of attacks in some patients but is not a reliable cure for hidradenitis suppurativa. Accutane cannot be prescribed in the emergency department due to requirements set forth by the pharmaceutical company. Hormonal manipulation (eg, certain oral contraceptives) has been useful for some patients but is unlikely to be prescribed from the emergency department.
Therapy must cover all likely pathogens in the context of the clinical setting. In recurrent disease, antibiotics may be administered for 2 or more months.
Treats susceptible bacterial infections of both gram-positive and gram-negative organisms as well as mycoplasmal, chlamydial, and rickettsial infections.
250 mg PO qid or 500 mg PO tid
Condition not seen in children
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
For the treatment of infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Rickettsia, Chlamydia, and Mycoplasma.
100 mg PO bid
Condition not seen in children
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines; hepatitis or lupuslike syndromes may occur
Binds to one or more penicillin-binding proteins, which, in turn, inhibit synthesis of bacterial cell walls. For treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected.
Resistance to this drug results from alterations in penicillin-binding proteins.
125-500 mg PO qid 1-2 h ac or 2 h pc for 7-10 d
Condition not seen in children
Decreases efficacy of oral contraceptives; may decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients with renal impairment
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
160 mg TMP/800 mg SMZ PO q12h for 10-14 d
Condition not seen in children
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Do not use during last trimester of pregnancy because of potential toxicity to newborn (eg, jaundice, hemolytic anemia, kernicterus)
Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: Recommended IV dose q18h
CrCl 50-10: Recommended IV dose q24h
CrCl <10: Not recommended
HD: 4-5 mg/kg after HD
During peritoneal dialysis: 0.16-0.8 g q48h
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholics, elderly, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in G-6-PD deficient individuals; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
Recommended dosing schedule of erythromycin may result in GI upset, causing one to prescribe an alternative macrolide or change to tid dosing. Covers most potential etiologic agents, including Mycoplasma species.
Erythromycin is less active against H influenzae. Although 10 d seems to be a standard course of treatment, treating until the patient has been afebrile for 3-5 d seems a more rational approach. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
Has the added advantage of being a good anti-inflammatory agent by inhibiting migration of polymorphonuclear leukocytes.
250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) q6h PO 1 h ac, or 500 mg q12h.
Alternatively, 333 mg PO q8h; increase to 4 g/d depending on severity of infection
Condition not seen in children
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin, increases risk of rhabdomyolysis; decreases metabolism of repaglinide, thus increasing serum levels and effects
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI side effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by liver and kidneys.
Used for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci).
150-300 mg/dose PO q6-8h; not to exceed 1.8 g/d; alternatively, 600 mg IV divided q8h, depending on degree of infection; not to exceed 4.8 g/d
Topical: Apply 2% lotion sparingly over affected area
Condition not seen in children
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile
Topical dosage form is for external use only, avoid contact with eyes (in event of accidental contact with eye, rinse with copious amounts of cool tap water)
These agents inhibit sebaceous gland function and keratinization.
Decreases sebaceous gland size and sebum production; may also inhibit sebaceous gland differentiation and abnormal keratinization.
40-60 mg/d PO for 4 mo
Condition not seen in children
Toxicity may occur with vitamin A coadministration; pseudotumor cerebri or papilledema may occur when coadministered with tetracyclines; isotretinoin may reduce plasma levels of carbamazepine
Documented hypersensitivity
X - Contraindicated; benefit does not outweigh risk
May decrease night vision; inflammatory bowel disease may occur; may be associated with development of hepatitis; occasional exaggerated healing response of acne lesions (excessive granulation with crusting) may occur
Diabetes patients may experience problems in controlling their blood sugar level while on isotretinoin; avoid exposure to UV light or sunlight until tolerance achieved; discontinue treatment if rectal bleeding, abdominal pain, or severe diarrhea occur
Mood swings or depression may occur; caution if history of depression
These agents modify the body's immune response to a variety of stimuli. Intralesional injections have been used in addition to the cream.
Treats inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.
Apply a thin film bid/tid until favorable response
Condition not seen in children
None reported
Documented hypersensitivity; fungal infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use in decreased skin circulation; prolonged use, applications over large areas, and use of potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria
Sellheyer K, Krahl D. "Hidradenitis suppurativa" is acne inversa! An appeal to (finally) abandon a misnomer. Int J Dermatol. 2005;44(7):535-40. [Medline].
Jemec GB. The symptomatology of hidradenitis suppurativa in women. Br J Dermatol. Sep 1988;119(3):345-50. [Medline].
Shah N. Hidradenitis suppurativa: a treatment challenge. Am Fam Physician. Oct 15 2005;72(8):1547-52. [Medline]. [Full Text].
Slade DE, Powell BW, Mortimer PS. Hidradenitis suppurativa: pathogenesis and management. Br J Plast Surg. 2003;56(5):451-61. [Medline].
von der Werth JM, Williams HC. The natural history of hidradenitis suppurativa. J Eur Acad Dermatol Venereol. Sep 2000;14(5):389-92. [Medline].
Attanoos RL, Appleton MA, Douglas-Jones AG. The pathogenesis of hidradenitis suppurativa: a closer look at apocrine and apoeccrine glands. Br J Dermatol. Aug 1995;133(2):254-8. [Medline].
Chaikin DC, Volz LR, Broderick G. An unusual presentation of hidradenitis suppurativa: case report and review of the literature. Urology. Oct 1994;44(4):606-8. [Medline].
Deroo H, Aelbrecht M, t'Kindt J, Vermander F, De Bersaques J. Hidradenitis suppurativa. Dermatologica. 1990;180(3):193-4. [Medline].
Edlich RF, Silloway KA, Rodeheaver GT. Epidemiology, pathology, and treatment of axillary hidradenitis suppurativa. J Emerg Med. 1986;4(5):369-78. [Medline].
Gee BC, Dawber RP. Hidradenitis suppurativa. J R Soc Med. Dec 2000;93(12):661. [Medline]. [Full Text].
Hughes LE. Pathogenesis, clinical features and management of hidradenitis suppurativa. Ann R Coll Surg Engl. Jul 1997;79(4):309-10. [Medline].
Jemec GB, Heidenheim M, Nielsen NH. Hidradenitis suppurativa--characteristics and consequences. Clin Exp Dermatol. Nov 1996;21(6):419-23. [Medline].
Jemec GB, Heidenheim M, Nielsen NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. Aug 1996;35(2 Pt 1):191-4. [Medline].
Konig A, Lehmann C, Rompel R. Cigarette smoking as a triggering factor of hidradenitis suppurativa. Dermatology. 1999;198(3):261-4. [Medline].
Leitch DN, Holland CD, Langtry JA. Hidradenitis suppurativa and monoarthritis of the hip [letter]. Clin Exp Dermatol. Jul 1997;22(4):206-7. [Medline].
Paletta C, Jurkiewicz MJ. Hidradenitis suppurativa. Clin Plast Surg. Apr 1987;14(2):383-90. [Medline].
Parks RW, Parks TG. Pathogenesis, clinical features and management of hidradenitis suppurativa. Ann R Coll Surg Engl. Mar 1997;79(2):83-9. [Medline].
Radcliffe KW. Hidradenitis suppurativa. Genitourin Med. Feb 1991;67(1):58. [Medline].
Rayner CR. Pathogenesis, clinical features and management of hidradenitis suppurativa. Ann R Coll Surg Engl. Jul 1997;79(4):309. [Medline].
Rorison P, Ghosh M. Pathogenesis, clinical features and management of hidradenitis suppurativa. Ann R Coll Surg Engl. Sep 1997;79(5):385. [Medline].
Thomas R, Barnhill D, Bibro M. Hidradenitis suppurativa: a case presentation and review of the literature. Obstet Gynecol. Oct 1985;66(4):592-5. [Medline].
Watson JD. Hidradenitis suppurativa--a clinical review. Br J Plast Surg. Oct 1985;38(4):567-9. [Medline].
Williams ST, Busby RC, DeMuth RJ. Perineal hidradenitis suppurativa: presentation of two unusual complications and a review. Ann Plast Surg. May 1991;26(5):456-62. [Medline].
hidradenitis suppurativa, acne inversa, follicular occlusion, acne, pilonidal cysts, chronic scalp folliculitis, spiradenitis, apocrine glands, sweat glands, chronic acneiform infection, nodular lesions, cellulitis, excessive perspiration, Crohn disease, irritablebowel syndrome, Down syndrome, arthritis, Graves disease, Hashimoto thyroiditis, Sjögren syndrome, herpes simplex, Crohn's disease, Sjögren's syndrome
Diana Fite, MD, FACEP, Clinical Assistant Professor, Department of Emergency Medicine, University of Texas Medical School at Houston, Hermann Hospital
Diana Fite, MD, FACEP is a member of the following medical societies: American Association of Women Emergency Physicians, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Texas Medical Association
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Robert M McNamara, MD, FAAEM, Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine
Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine
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Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
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John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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