Hidradenitis Suppurativa: A Closer Look Stephen W. Gordon, MD IndianaDolis. Indiana

The following is a review of the literature concerning hidradenitis suppurativa with emphasis on aspects of this disease which suggest that it may be a result of altered host-defense mechanisms. Deep fistula formation, anemia, and the development of carcinoma are complications seen only in disease affecting the perianal area. The term perianal is used loosely to describe the buttock, perineum, pubic, and genital areas. A variety of treatment regimens has been used with limited success. Surgery has evolved as the treatment of choice for advanced and chronic disease. Hidradenitis is derived from the Greek words Hidros, sweat, and adenos, gland. The disease appears to primarily affect the apocrine glands, and some authors' use the term "apocrinitis" rather than hidradenitis. Hidradenitis suppurativa (HS) poses a difficult problem fdr both the physician and the patient and little progress has been made in nonsurgical treatment in over 100 years. The etiology and, to a certain extent, the pathogenesis still remain obscure.

History In 1833, Purkinje discovered sweat glands in human skin. In 1839, the first clinical description of HS, as a distinct disease, was made by Velpeau. Robin, in 1845, described the structure and location of the apocrine glands and as a result of Robin's work, Verneuil, in 1854, related hidradenitis to the apocrine glands.2 This relationship was based purely on clinical suspicioh. It was not until 1922 that Schiefferdecker classified, named, and clarified sweat glands as eccrine and apocrine and related HS specifically to the apocrine gland. Lane, in 1933, wrote the first article on HS in the English language.3

From the Department of Surgery, Methodist Hospital, Indianapolis, Indiana. Presented in part to the 82nd annual convention of the National Medical Association, Los Angeles, California, August 1, 1977. Requests for reprints should be addressed to Dr. Stephen W. Gordon, 1925 North Senate Avenue, #28, Indianapolis, IN 46202.

Anatomy The cutaneous glands of man include holocrine or sebaceous glands and merocrine or sweat glands. Merocrine glands are subdivided into eccrine and apocrine glands. Apocrine glands are located deep within the dermis, and usually are associated with the pilosebaceous apparatus. The ducts empty into the hair follicle or onto the skin surface (Figure 1). The apocrine glands develop from hair follicles during the fourth to fifth month of intrauterine life.4'5 Only a small percentage of hair follicles actually give rise to apocrine glands and these are commonly found in the axillar, perineal, anal, buttocks, groin, pubic, sacral, and periumbilical areas, and in the periareolar area of the breast. Irregularly scattered apocrine glands may also be found on parts of the scalp and back, particularly the interscapular area, and the zygomatic and cheek areas of the face.5 Eccrine gland secretions are watery, contain NaCl, fatty acids, and urea and are odorless.6 This is true sweat. However, apocrine gland secretions are thick and milky, more pigmented, and contain cholesterol, iron, and larger lipid droplets.7 8 The secretion from apocrine glands apparently provides a rich milieu for bacterial reproduction and proliferation and odors are produced.2 Eccrine glands begin to function early in life, but apocrine glands do not begin to function until puberty7'9 and HS does not occur before that time. Apocrine glands secrete in response to pain, anger, sexual arousal,

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and sympathetic drugs.10"1' Woolard and others'12"3 have indicated that blacks have more apocrine glands than whites. Armstrong' has stated that women of both races have more apocrine glands than men, and Nance'4 points out that, overall, women are affected with HS up to three times more commonly than men. Axillary HS is more common in women and perianal HS more common in men.15 In a large series by Jackman'16 the axilla was involved either alone or with some other site 72 percent of the time. The duration of HS at the time of presentation for surgical treatment usually averages three to six years and the median age is 33-35 years of age.2"7"8

Pathogenesis HS is regarded as a poral occlusion disease with subsequent bacterial infection. Dermatopathologists recognize the infection as arising in the pilosebaceous follicles and secondarily invading the contiguous apocrine glands. Following apocrine ductal occlusion, microscopically one sees dilation of the apocrine gland, inflammatory cells, and typical signs of acute inflammation. The dilation eventually leads to rupture of the apocrine gland with spread of the infection to adjacent apocrine and eccrine glands. As the suppuration spreads under the skin, a deep cellulitis with a honeycomb of fiIstulous tracts and multiple draining sinuses develops. Pockets of pus and granulomatous inflammatory infiltrates can be found in the subcutaneous and deep cutaneous tissues.'9 Attempts at healing result in fibrosis, induration, and hypertrophic scarring of the overlying skin, which can cause contracture formation and limited range of motion, particularly in the axilla. Symptoms include pruritis, burning, and hyperhidrosis.20 Cultures nearly always demonstrate mixed organisms,'7'2' however, coliforms predominate in the perianal areas and staphylococci predominate in other areas.'3'20 Usually the infection 339

DeGmis

Eccri ne Gland

Apocrine Gland Sebaceous Hair Gland

Follicle Figure 1. Schematic drawing of a cross section of skin showing the relationship of glands to the hair

follicle.

limits itself to spread throughout the subcutaneous and deep cutaneous layers of tissue, however, some authors have described cases in which the infection has spread to involve the fascia leading to a fasciitis and loss of joint mobility and to muscle and regional lymphatics.1422 Fistulas to deeper tissues such as anus, rectum, urinary tract, bladder, testes, and urethra, with subsequent problems, have also been

described.23'24 Lymphatic spread of the infection from areas of cellulitis or lymphadenitis has been reported.6'14'20'25 This has been noted in axillary HS secondary to hand infections, but this route of spread is rare. Chronic HS after years of activity may eventually become quiescent having destroyed most of the apocrine glands of the body.26 A decline in disease activity after the menopause has also been noted.

In those iin'tan'ces of familial disease, inherited malformations of the ducts has been suggested but not proven.28 A personal or family history of diabetes mellitus, abnoi'mal teroid metabolism,14,28 or hypogammoglobulinemia26 has coexisted with HS and may be contributory. Physical or chemical irritation may induce HS but probably would not be Fhsponsible for the chronicity of the problem.28 Chronic bacterial infectiong have spmetimes been found to coexist with dr precede the development of HS, eg, chronic salpingitis, or infected pilonidal sinuses.28

Other follicular occlusion diseases, particularly acne, may coexist with HS. 13,26'29 In a large series reviewed by Conway, 70 percent of patients with HS had active acne or evidence of!severe past acne. Likewise, virilism and Cushing disease tend to acti'Vate or worsen the disease. Many investigators believe the disease activity is hormonally influenced. Exacerbations of HS can be noted in women a day or two before and during their menstrual periods.5'25 In normal women, histologically, one sees increased apocrine gland activity during the menses8'9 and it is probable that this increased activity is associated with the disease flareUp.14 On the other hand, the disease appears to subside during pregnancy and exacerbate shortly after delivery.8'28'30 Despite these observations, no altered hormone levels have consistently been described, in HS victims and none of the available hormone products known to be increased during pregnancy has been of any value when administered to patients with HS.8 Furthermore, systemic and local administration and implanatation of estrogenic and androgenic pellets have failed to of result in the developmenttS.5

Etiologic factors include poor hygiene, tightly fitting garments, the onset of puberty,27 use of dipilatories, shaving or plucking of hairs, and the use of film-producing deodorants or anhidrotic agents.2"l0 In addition, com-

Disease Variations Apocrine glands, in modified forms, appear in other areas of the body, iticluding the malar area of the face, but in most instances these glands are smaller than usual and nonfunctional.5 However, facial HS involving these glands has been described.31 It tends to

binations of metabolic27 and physiologic factors such as obesity contribute to the development of HS.'8'2fi

occur late in the course of the disease after other areas have been involved. Sachs1t described a case of HS of

Etiology

340

the glands of Moll. Again, this involvement came rather late in the course of the disease. The patient had HS involving her perianal area before spreading successively to each breast and finally involving her axilla, retroauricular, and vulvar areas. The glands of Moll open into the hair follicles of the eyelashes, into the ducts of th6e Zeis§ glands (which are sebaceous glands associated with the eyelash follicle), or onto the skin edge of the lid. The ducts of the glands of Moll usually are rather dilated in comparison to apocrine sweat glands, and this fact may help to explain the rarity of disease in these glands. Another eye problem associated with chronic HS is ititerstitial keratitis. Bergeron32 found four cases in a study of 62 patiefits who had HS. Interstitial keratitis is generally thought to be a delayed corneal allergic reaction which usually presents at age 5-12 years as a result of congenital syphilis.33 However, granulomatous diseases such as tuberculosis, leishmaniasis, lepromatous leprosy, and sarcoidosis are also causative factors. HS preceded the keratitis by five, seven, eight, and nine years, respectively. All four patients had moderately severe to very severe disease in multiple sites and all four had a microcytic hypochromic anemia and increased gamma globulin levels. A pattern of HS involving the head and neck is the triad of follicular occlusion.6'34 This generally consists of advanced or chronic HS, acne conglobata, and dissecting cellulitis of the scalp (perifolliculitis capitis). Acne conglobata is a severe form of cystic acne comprised of comedones, papules, and pustules located on the back, shoulder, or chest. Perifolliculitis capitis is a chronic and progressive infection of the hair follicles of the scalp which can coalesce and produce subcutaneous abscesses. Advanced HS can produce an anemia identical to that caused by other chronic diseases or malignant processes.23 In a study of 42 patients, who had HS, ten patients without concomitant systemic disease were found to have marked anemia.35 The hemoglobin levels were 10 gm/100 ml or less. The anemias were hypoferremic and unresponsive to parenteral iron therapy, presumably because of decreased serum transferrin. The disease in these ten anemic patients was severe, present for a minimum of two years, and in-

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Table 1. Lesions Confused With Hidradenitis Early (acute)

Furuncle and carbuncle Dermoid cyst Pilonidal cyst Lymph3denitis Multiple infectei sebaceous cysts Acne Perirectal abscess Ischiorectal abscess Cutaneous blastomycosis Cellulitis

volved the perianal area. It has been stated that the greater the number of organisms in the infected area, the more severe the anemia will be. It is also apparent that the anemia (which can be normochromic-norniocytic or hypochromic-microcytic) tends to be present only in the more severe cases of perianal HS. Surgery is necessary to correct the anemia. With any chronic, irritating process, one must constantly be aware of and look for the development of a malignancy. Cases of squamous cell carcinoma developing in chronic osteomyelitis sinus tracts, figtula-in-ano sinuses, and a chronic dmpyema sinus tract have been docutndnted.36 The first account of squamous cell carcinoma arising in HS came in 1958 when Dockerty and Anderson15 described two patients who had penanal HS for 25 and 32 years before developing malignant changes. One year later Jackman37 published the largest series to date of carcinoma in longstanding HS. In his study of 125 cases of perianal HS, four patients developed squamous cell epitheliomas after a disease duration of 19 to 32 years. The

Late (chronic)

Tuberculosis cutis

Lymphogranuloma venereum Granuloma inguinale Anal fistula Nocardia Actinomycosis Tularemia Cat scratch disease

seventh3 and eighth38 cases of squamous cell carcinoma likewise developed in longstanding perianal HS, and the ninth and most recent case of carcinoma was reported by Gordon39 and involved the postsacral skin in a 28year-old black female after 17 years of chronic HS. The shortest period of time between the development of HS and carcinoma has been eight years. Perianal HS is the most troublesome site of involvement. It is difficult to reduce the infection sufficiently to allow skin grafts or flaps to take and a temporary colostomy may have to be done.2'14'29 The seriousness of perianal HS can be further appreciated in view of the idcreased frequency of severe anemia, the development of fistulas to underlying organs,, and the development of carcinomas particularly in the buttock area. These complications have not been found secondary to HS in other areas. Moschella23 reports the death of a patient, Wecondary to severe anemia and extensive fistula formation to pelvic organs, in a black male. This patient developed fistulas to his rectum, penile urethra, urinary bladder, and peritoneum.

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Differential Diagnosis The differential diagnosis of HS varies depending on where the lesions are, whether the disease is in an acute or chronic phase, and the patiept's history. When the axillas are involved the diagnosis of HS is easier. When the perianal area is the sole site of involvement, the diagnosis is more difficult (Table 1). Clinical behavior, laboratory and skin tests, and lack of response to conservative therapy sets HS apart from other entities even though grossly they may appear to be similar (Table 2). Christensen40 reported eight cases of HS originally believed to be anal fistula. Perineal urinary fistulas41 and "recurrent" pilonidal cysts'6 may occasionally prove to be HS in disguise.

Treatment The treatment of HS continues to be a problem. Early disease is often regarded as a minor skin infection and the patient is treated accordingly. Classi341

Table 2. Aids in the Differential Diagnosis of Hidradenitis Suppurativa

History and physical examination TB skin tests and smears for acid fast Fungal skin tests and cultures Frei test

Proctosigmoidoscopic examination Barium enema Donovan bodies in gram stain Tularemia skin test or agglutination test

cally the patient will respond initially to antibiotics and incision and drainage procedures only to have flare ups, recurrences, or extension of the disease after the antibiotics are discontinued. Mild cases involving a few small lesions can often be adequately treated with antibiotics with no further problems.34 X-ray therapy of early HS has produced encouraging results. In a series of 54 patients Schenck42 found that 100-200 rads three times weekly for a total 1,000 to 1,200 rads was very effective. More recent work by Zeligman43 indicated that 450-500 rads given once would suffice. According to both authors, hair loss occurs and it is Zeligman's contention that this facet of treatment promoted drainage and was at least partially responsible for the beneficial effects. In all of Zeligman's patients, regrowth of hair occurred and no recurrence of disease was evident at one year. Radiodermatitis was avoided by using the smaller dose of radiation. Adrenal corticosteroids have been shown to be of some value for mild disease. In a study by Danto,4 four patients with HS of up to eight years duration were given hydrocortisone systemically. The steroid was administered daily for two months in gradually decreasing doses. No adjunctive treatment was given and at one year no disease recurrence could be appreciated. 342

Surgery currently is the best therapy for severe, chronic, and advanced disease.'3 Many authors urge early surgical intervention in efforts to avoid the numerous incisions and drainages and patient expense incurred by trying to manage this problem more conservatively.45 Exteriorization, curettage, and electrocoagulation is an effective technique for all but the most extensive cases.4647 Electrosurgery is bactericidal, hemostatic, and destroys sinus tract epithelium. Complete healing by secondary intention is possible in four to six weeks time. Excision with the application of sulfonamide-type creams followed by wet to dry dressings recently has been suggested.48 The wound is thus allowed to granulate and epithelialization is said to be complete using this method in approximately four weeks time. The remaining surgical procedures are variations of primary closures, split-thickness skin grafts,2' or flaps49 after the infected tissue and adjacent apocrine glandbearing areas are excised. Failure to remove adjacent hair-bearing tissue enhances chances for recurrence.'8 The location of the problem will tend to dictate which method is most feasible. In general, primary closure with minimal undermining has the least complications and is especially useful in axillary disease.4,17,18

Discussion and Conclusion It appears that perianal HS is the worst area of involvement. Treatment tends to be more difficult and complications are more grave. The axillae contain the highest concentration of apocrine sweat glands and are in fact involved with HS most frequently. Yet, the more serious complications of this disease, ie, carcinoma, anemia, and deep fistula formation have not resulted from axillary involvement. The presence of specific organisms is generally thought to be of no significance in the production of HS even though coliforms and enteric bacteria have been described as being more common in perianal disease. Perhaps some form of bacterial or viral synergism is part of this problem and should be reexamined. More subcutaneous adipose is located in the perianal area and could conceivably promote the extension of infection in the area. A re-evaluation of the histologic and microbiologic differences between axillary and perianal disease would be valuable, particularly in view of the fact that the most recent wound culture data was published 20plus years ago and our methods of obtaining more accurate cultures have improved. Theories strongly implicating hormonal participation in the development

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and extension of the disease are not proven. It is true that the apocrine sweat glands do not begin to function until puberty, and that HS is not found in patients prior to that time,27 however, the incidence is nearly the same in the third and fourth decades of life as it is in the second decade and several authors report the onset of the disease in patients over 50 years of age, all of which suggests an acquired defect in host resistence. The onset of puberty with the attendant hormonal elevations probably plays a minor role. The hormonal alterations commensurate with the menstrual cycle and pregnancy have been fairly well elucidated, and the apocrine glands behave in a predictable manner. During pregnancy the disease generally becomes quiescent, and a day or two before and during the menses the disease exacerbates. It is easy to attribute these changes to hormonal influences, but we need to be mindful of the probability that other significant metabolic changes could be occurring during these times as well. If it were not for the cyclical response of the disease in women, an acquired aberration in immunity might be a more popular thesis. The etiology of HS is unknown, but many references are made to the work of Shelly and Cahn,50 who produced axillary HS experimentally by applying adhesive tape with belladonna to the shaved axillas of 12 volunteers. All 12 had axillary anhidrosis for the entire seven-day test period. Three of the 12 patients developed HS. The authors state that poral occlusion alone would not cause disease, and that the added element of bacterial infection was necessary. It is difficult to believe that these criteria were met in only three of 12 volunteers, and so some difference in the individual patient's immune proficiency is again suggested. It must be recognized that if an immune deficiency does indeed exist in these patients, it is not a major primary defect. Peripheral blood granulocytes from patients with HS have been shown (in vitro) to have normal chemotactic and phagocytic ability and normal intracellular killing of ingested bacteria. Also, patients with HS have elevated or normal levels of immunoglobulins. Dvorak et al,5' in a study of seven patients with HS, indicated that skin tests for delayed hypersensitivity reactions were normal. These factors,

along with the lack of recurrent infections in multiple sites such as the respiratory system, sinuses, and GI tract, suggest that the problem is not a major immune system defect, and that efforts should be focused on local factors which might modulate or inhibit normal host defense mechanisms in the affected skin.

Acknowledgments The author wishes to thank Ms. Valerie Yadon, Ms. Judith Barrett, and the Medical Research and Audio-Visual Departments of Methodist Hospital for their invaluable assistance in the preparation of this manuscript.

Literature Cited 1. Armstrong DP: Axillary hidradenitis suppurativa. Plast Reconstr Surg 36:200-206, 1965 2. Knaysi GA Jr, Cosman B, Crikelair GF: Hidradenitis suppurataiva. JAMA 203(1):19-22, 1968 3. Donsky HJ, Mendelson CG: Squamous cell carcinoma as complication of hidradenitis suppurativa. Arch Dermatol 90:488-491, 1964 4. Tasche C, Angelats J, Jayaram B: Surgical treatment of hidradenitis suppurativa of the axilla. Plast Reconstr Surg 55(5) :559-562, 1975 5. Hurley HJ, Shelly WB: The human apocrine sweat gland in health and disease. Springfield, l1l, Charles C Thomas, 1960, p 120 6. Brunsting HA: Hidradenitis suppurativa: Abscesses of apocrine sweat glands: Study of clinical and pathological features. Arch Dermatol Syph 39:108-120, 1939 7. Arey LB: Human Histology: A textbook in outline form. Philadelphia, WB Saunders, 1974, pp 199-200 8. Cornbleet TL: Pregnancy and apocrine gland diseases-hidradenitis, fox fordyce disease. Arch Dermatol Syph 65:12-19, 1952 9. Bloom F: Textbook of Histology, ed 9. Philadelphia, WB Saunders, 1968, p 501 10. Snyder CC, Farrell JJ: Hidradenitis suppurativa. Plast Reconstr Surg 19:502-508, 1957 11. Sachs DD, Gordon AT: Hidradenitis suppurativa of the glands of Moll. Arch Ophthalmol 77:635-636, 1967 12. Woolard HH: The cutaneous glands of man. J Anat 64:415-421, 1930 13. Conway H, Stark RB, Climo S, et al: The surgical treatment of chronic hidradenitis suppurativa. Surg Gynecol Obstet 95:455-462,1952 14. Nance FC: Hidradenitis suppurativa of perineum: Treated by radical excision. Am Surg 36:331-334, 1970 15. Anderson JJ, Dockerty MB: Perianal hidradenitis supprativa. Dis Colon Rectum 1:23-31, 1958 16. Jackman RJ, McQuarrie HB: Hidradenitis suppurativa: Its confusion with pilonidal disease and anal fistula. Am J Surg 77:349351, 1949 17. Pollock, Virnelli, Ryan: Axillary hidradenitis suppurativa: A simple and effective surgery technique. Plast Reconstr Surg 49:2227, 1972 18. Anderson DK, Perry AW: Axillary hidradenitis. Arch Surg 110(1):69-72, 1975 19. Pinkus H, Mehregan AH: A guide to dermato-histopathology, New York, AppletonCentury-Crofts, 1969, pp 213 20. Paletta FX: Hidradenitis suppurativa: Pathologic study and use of skin flaps. Plast Re-

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constr Surg 31:307-315, 1963 21. Masson JK: Surgical treatment for hidradenitis suppurativa. Surg Clin N Am 49:1043-1052, 1969 22. Cocke WM Jr: Surgery of hidradenitis suppurativa of the perineum. Plast Reconstr Surg 39:178-181, 1967 23. Moschella SL: Hidradenitis suppurativa: Complications resulting in death. JAMA 198:83-86, 1966 24. Ward JN, Washio H, David HS: Hidradenitis suppurativa of scrotum and perineum. Urology 4(4):463-466, 1974 25. Harrison SH: Axillary hidradenitis. Br J Plast Surg 17:95-98, 1964 26. Fitzpatrick TB: Dermatology in general medicine. New York, McGraw-Hill, 1971, p 395 27. Williams PW: Surgical treatment of suppurative hidradenitis. Br J Plast Surg 6:231-237, 1953-1954 28. Steiner K, Grayson LD: Hidradenitis suppurativa of the adult and its management. Arch Dermatol Syph 71:205-211, 1955 29. Ching CC, Stahlgren LH: Clinical review of hidradenitis suppurativa: Management of cases with severe perianal involvement. Dis Colon Rectum 8:349-352, 1965 30. Woods G, Vogel EH, Croak J: Hidradenitis suppurativa and pregnancy: Case report and discussion. Ohio State Med J 68(9):864-866, 1972 31. Greer KE: Facial involvement with hidradenitis suppurativa, letter. Arch Dermatol 109(3):408, 1974 32. Bergeron JR, Stone OJ: Interstitial keratitis associated with hidradenitis suppurativa. Arch Dermatol 95:473-475, 1967 33. Scheie HG, Albert DM: Textbook of Ophthalmology, ed 9. Philadelphia, WB Saunders, 1977, pp 312,363,369 34. Shelley WB: Consultations in Dermatology with Walter B Shelley. Philadelphia, WB Saunders, 1972, pp 74-77 35. Tennant F, Bergeron JR, Stone OJ, et al: Anemia associated with hidradenitis suppurativa. Arch Dermatol 98:138-140, 1968 36. McAnally AK, Dockerty MB: Carcinoma developing in chronic draining cutaneous sinuses and fistulas. Surg Gynecol Obstet 88:87-96, 1949 37. Jackman RJ: Hidradenitis suppurativa: Diagnosis and surgical management- of perianal manifestations. Proc R Soc Med 52 (suppl):110-112, 1959 38. Hymphrey LJ, Playforth H, Leavell UW Jr: Squamous cell carcinoma arising in hidradenitis suppurativa. Arch Dermatol 100:5962, 1969 39. Gordon SW: Squamous cell carcinoma arising in hidradenitis suppurativa. Plast Reconstr Surg 60:800-802, 1977 40. Christensen J: Hidradenitis suppurativa of para-anal region. Am J Surg 79:61-65, 1950 41. Carter AE: Hidradenitis suppurativa masquerading as perineal urinary fistula. Br J Surg 49:686-687, 1962 42. Schenck SG: Hidradenitis suppurativa axillaris-an analysis of 54 cases treated with Roentgen rays. Radiology. 54:74-77, 1950 43. Zeligman I: Temporary x-ray epilation therapy of chronic axillary hidradenitis suppurativa. Arch Dermatol 92:690-694, 1965 44. Danto JL: Preliminary studies of the effect of hydrocortisone on hidradenitis suppurativa. J Invest Dermatol 31:299-300, 1958 45. Shaughnessy DM, Greminger RR, Margolis IB, et al: Hidradenitis suppurativa. A plea for early operative treatment. JAMA 222 (3):320-321, 1972 46. Newell GB, Voelter WW, Mullins JF: Treatment of hidradenitis suppurativa. JAMA 223(5):556-557, 1973 47. Mullins JF, McCash WB, Boudreau RF: Treatment of chronic hidradenitis suppurativa: Surgical modifications. Postgrad Med J 26:805-808, 1959 48. Vickers MA: Operative management of chronic hidradenitis suppurativa of the scrotum and perineum. J Urol 114(3):414-416, 1975 49. Lipshutz H: Closure of axillary hidradenitis defects with local triangular flaps. Plast Reconstr Surg 53(6):677-679, 1974 50. Shelley WB, Cahn MM: The pathogenesis of hidradenitis suppurativa in man. Arch Dermatol Syph 72:562-565, 1955 51. Dvorak VC, Root RK, MacGregor RR: Host defense mechanisms in hidradenitis suppurativa. Arch Dermatol 113:450-453, 1977

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Hidradenitis suppurativa: a closer look.

Hidradenitis Suppurativa: A Closer Look Stephen W. Gordon, MD IndianaDolis. Indiana The following is a review of the literature concerning hidradenit...
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