Aug 6, 1996 - involving the apocrine glandular zones. Affected patients may present with acute abscesses, but the condition often progresses to a chronic ...
Ann R Coll Surg Engl 1997; 79: 83-89
REVIEW
Pathogenesis, clinical features and management of hidradenitis suppurativa R W Parks FRCS Surgical Registrar T G Parks
MCh FRCS Professor of Surgical Science
Department of Surgery, The Queen's University of Belfast
Key words: Hidradenitis suppurativa; Pathogenesis; Surgical management
Hidradenitis suppurativa is a chronic skin condition involving the apocrine glandular zones. Affected patients may present with acute abscesses, but the condition often progresses to a chronic state with persistent pain, sepsis, sinus tract and fistula formation, purulent discharge and dermal scarring. Treatment of patients with severe disease can be difficult and may require complex surgical intervention. This review encompasses the pathogenesis, clinical manifestations and management options for patients with hidradenitis suppurativa.
Hidradenitis suppurativa is a chronic recurrent inflaminvolving apocrine sweat glands and adjacent connective tissue. Velpeau was the first to describe the disease process in 1839 when he reported clinical features of a patient with an inflammatory disorder involving the skin of the axillary, mammary and perianal regions (1). However, it was Verneuil in 1854, reporting a series of patients with superficial suppurative lesions of the axilla and groin, who first suggested that these lesions originated in sweat glands (2), although it was not until 1922 that Schiefferdecker associated this condition with apocrine glands (3). For many years, the condition was described as Verneuil's disease, but subsequently became known as hidradenitis suppurativa. In the 1930s, Lane (4) and Brunsting (5) described in detail the clinical features of the disease and highlighted its frequent association with acne. Shelley and Cahn have described an experimental matory process
Correspondence to: Mr R W Parks FRCS, Department of Surgery, Institute of Clinical Science, Grosvenor Road, Belfast BT12 6BJ, Northem Ireland
model of the disease in which zones of apocrine glands of normal human volunteers were occluded using adhesive tape applied to the skin (6). The condition encompasses a wide spectrum of severity. Some cases involve only one site and remain mild or even sometimes undergo spontaneous remission. However, other cases progress to involve complete apocrine areas and often affect multiple sites. If diagnosed and treated early, hidradenitis suppurativa can be managed initially by medical measures. Nevertheless, as the disease becomes chronic, complete resolution is increasingly difficult to achieve, and in advanced cases may be impossible (7). In more severe established disease, surgical intervention is the only treatment that has any significant effect on the course of the condition.
Pathogenesis While axillary and inguinoperineal regions are the most commonly affected areas, other zones which harbour apocrine glands may occasionally be affected, namely the areola of breast, submammary region, periumbilical region, scalp, face, external auditory meatus, nape of neck and shoulders. Apocrine glands are compound sweat glands which extend down through the dermis into the subcutaneous tissue. Each gland consists of a deep coiled secretory component which drains via a long straight excretory duct, usually into a hair follicle. Secretion from these glands is opalescent and malodorous. Although the precise cause of hidradenitis suppurativa is unclear, it is generally agreed that the initiating event is
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Figure 1. Schematic diagram of the believed development of hidradenitis suppurativa.
occlusion of the apocrine or follicular ducts by keratinous plugging, leading to ductal dilatation and stasis in the glandular component. Bacteria enter the apocrine system via the hair follicles, become trapped beneath the keratinous plugs and subsequently multiply rapidly in the nutrient environment of the apocrine sweat (8). The glands may rupture, leading to extension of infection into adjacent glands and the surroundings area (9). Superadded bacterial infection with Streptococci, Staphylococci and other organisms may result in further local inflammation, tissue destruction and skin damage (10). The chronicity of the healing process results in extensive fibrosis and hypertrophic scarring of the overlying skin (Fig. 1). In hidradenitis involving the perineal region, there is an increased incidence of Streptococcus milleri, the presence of which is significantly associated with disease activity. Other organisms which may be identified when the disease affects this site include Staphylococcus aureus, anaerobic Streptococcus and Bacteroides (9). Previously, it had been propounded that hidradenitis suppurativa was secondary to depilation or mechanical irritation of the axilla or inguinal region. Some authors considered that deodorants may be aggravative (11,12), whereas others have found no correlation between trauma or exposure of the skin to chemicals and the development of hidradenitis suppurativa (13). Morgan (14), in a retrospective study, compared 40 patients suffering from hidradenitis with age-matched controls and found no significant difference in shaving habits, the use of deodorants, or the application of chemical depilatory agents.
As initial presentation of hidradenitis suppurativa is often at the time of puberty, several authors have
investigated the possible role of an endocrine abnormality. Harrison et al. (15) reported a dysfunction of the hypothalamopituitary system in 13 women with premenstrual exacerbation of hidradenitis suppurativa, but could not demonstrate a direct correlation. Mortimer (16) also reported an exacerbation of symptoms during the premenstrual period in two-thirds of a group of 42 women and in these patients found a higher serum concentration of total testosterone than in a control group. Several authors support the concept of the condition being androgen-dependent in adults (17,18). Flare-up of hidradenitis was noted after hormone administration (19) and in cases of increased androgen secretion associated with Cushing's syndrome (20). However, many women with hidradenitis suppurativa have normal androgen levels. Several authors have noted the association of obesity and diabetes mellitus with hidradenitis suppurativa (13,21). Patients with these disorders are more prone to recurrent infections and may have problems in the healing of common inflammatory skin disorders. It has also been suggested that hidradenitis may be related to reduced cutaneous levels of calprotectin, zinc or ascorbate (22). Also reported is a high incidence of atopy, eczema and drug allergies in hidradenitis sufferers (23). There have been numerous reports of arthritis associated with hidradenitis, leading some authors to suspect an immunological aetiology. However, Dvorak (24) reported normal immunological parameters in his group of patients. Wiltz et al. (13) reported an interesting yet unexplained association between cigarette smoking and perianal hidradenitis in 70% of the patients in their series and suggested that the disorder may be caused by the effect of nicotine on the exocrine glands. Initially, nicotine stimulates glandular secretion but eventually inhibits normal function, and hence possibly provides a mechanism that prediposes to plugging of the ducts of the glands, leading to an inflammatory reaction. There appears to be a genetic form of the disease with a single gene transmission (25-27). Jemec (28) found that 18 of 70 patients (26%) with hidradenitis suppurativa had a positive family history, whereas of 96 control subjects chosen from hospital staff, matched for age and sex who themselves did not have hidradenitis suppurativa, only two relatives suffered from the disease. Chronic hidradenitis suppurativa may lead to the development of squamous cell carcinoma (29-35). In those rare instances where malignancy supervenes, the cancer tends to arise in an area which has been affected by the disease for more than 10 years. A series of conditions which bear an aetiological resemblance to each other has become known as the 'follicular occlusion triad' comprising (a) acne conglobata, (b) dissecting cellulitis of the scalp (perifolliculitis capitis), and (c) hidradenitis suppurativa (36). Acne conglobata is a severe manifestation of acne that involves the chest, back and buttocks. Comedones, together with multiple areas of small purulent nodules, are prominent features. Perifolliculitis capitis is a similar process involving the scalp, with
Hidradenitis suppurativa
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inflammation and pustular nodule formation. Discrete zones of fistulous tracts and scarring develop leading to areas of alopecia. Patients manifesting any combination of the follicular occlusion triad may be encountered. After a careful histological examination of axillary skin from patients with hidradenitis suppurativa, Yu and Cook (37) postulated that the condition was a disease of follicular epithelium rather than a disease of apocrine glands. They identified squamous epithelium-lined cysts or sinuses in the dermis of the majority of cases and noted that all these structures contained laminated keratin and half of them contained hair shafts suggesting hair follicle derivation. Inflammation in apocrine glands was noted in only one-third of specimens, and in these cases inflammation was present around eccrine glands, hair follicles and the epithelium-lined structures. Inflammatory infiltrate was more marked where the 'cysts' were disrupted. These workers suggested that the findings probably represented abnormal dilated hair follicles and that these are a more constant diagnostic feature in hidradenitis suppurativa than inflammation of apocrine glands which appears to be a secondary phenomenon.
Epidemiology The apocrine glands do not become active until puberty and thus it is rare to encounter hidradenitis suppurativa before the onset of puberty (17). Most patients present in the second, third or fourth decade of life (8). The disease affects both sexes. Some authors report a higher incidence of axillary disease among women, whereas perineal involvement is more common in males (12,38). In the review by Wiltz et al. (13) of the Lahey Clinic experience of perineal hidradenitis suppurativa, 93% of the patients were male; however, this degree of male preponderance is unusual. The exact prevalence of the disease is unknown, but may be as high as 1 in 300 (27). It is found in all races (13); however, the incidence in blacks is higher than in Caucasians (21). Homma, in 1926, reported that individuals among the black population had three times the number of apocrine glands when compared with counterparts in white races (39).
Clinical manifestations Hidradenitis suppurativa presents initially with deepseated nodules which tend to coalesce and may become infected resulting in acute abscesses. These may temporarily resolve or alternatively may progress, ultimately culminating in chronic sepsis with sinus and fistula formation, multiple abscesses, persistent pain, and dermal scarring (8,21). Infected ruptured apocrine glands coalesce creating subcutaneous abscesses which discharge through multiple openings. Progressive destruction of the normal skin architecture occurs with development of periductal and periglandular inflammation and dermal
Figure 2. Perineal hidradenitis suppurativa in a male patient with multiple sinuses/fistulas and dermal scarring.
and subcutaneous fibrosis (Fig. 2). Malodorous discharge may be thin and serous or frankly purulent in nature. There is a wide variation in the extent and severity of the disorder. Some patients suffer from relatively mild disease involving only one region and spontaneous remission may occur in a proportion of these (40). Other patients have extensive involvement of both axillae, the whole perineum, and additional zones where apocrine glands are sited. Perianal hidradenitis suppurativa may present with pain, swelling, purulent discharge, pruritus or bleeding and can mimic several common problems, such as furunculosis, anal fistula, pilonidal disease, perianal abscess or Crohn's disease (13,41). Fistulas to the anal canal may occur in hidradenitis as pointed out by Culp (42) and Brown et al. (43), but these should extend only into the lower portion of the anal canal, in the skin of which apocrine glands can be found. Church et al. (41) in reviewing the Cleveland Clinic experience of 61 patients with perianal hidradenitis suppurativa, noted that Crohn's disease coexisted in 24 (39%) of the cases. Ostlere et al. (44) also reported three cases of Crohn's disease associated with hidradenitis. Church et al. (41) suggested that the local swelling and inflammation associated with Crohn's disease may precipitate the development of perianal hidradenitis suppurativa in patients already prone to it. However, it
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would not explain the frequent presence of axillary, groin and buttock disease, which may imply a possible constitutional or genetic predisposition to hidradenitis in patients with rectal Crohn's disease. The coexistence of the two conditions may have implications for the treatment of perianal sepsis in such patients. Each condition may mask the other and therefore appropriate treatment may be withheld, or inappropriate treatment may be given. Hidradenitis suppurativa may adversely affect the clinical course of patients with Crohn's disease. The serious nature of combined disease is exemplified by the series of Church et al. (41) in which proctectomy was required in 70% and faecal diversion in 91% of patients suffering from Crohn's disease and perineal hidradenitis. Furthermore, patients in whom both conditions coexist are more prone to persistent skin sepsis after proctocolectomy.
Management Medical treatment Hidradenitis suppurativa of the axillary region in its early stages is frequently managed by the dermatologist. Therapy may consist primarily of antibiotics (usually antistaphylococcal medications for axillary involvement and broad-spectrum agents for perineal disease) and simple measures, such as the frequent application of local antiseptic or warm compresses (21). Although some authors have advocated long-term antibiotics, such as tetracycline or a penicillin derivative, on the premise that patients with acne often obtain benefit from such therapy, there is no evidence that long-term antibiotics alter the natural history of hidradenitis suppurativa (42,45). Topical synthetic retinoids have been tried and variable results have been reported (46-51). Intralesional administration of triamcinolone may produce remission in some instances (7). Immunotherapy using agents such as staphage lysate has yielded limited benefit and does not appear to significantly affect the progression of the disease process (52). Camisa et al. (53) used combination hypothalamic-pituitary-ovarian axis and adrenal suppression and reported some benefit, but this has not gained widespread favour.
Surgical treatment Controversy still exists regarding the optimal surgical approach in the management of hidradenitis suppurativa. Factors influencing the decision include the site affected, the extent of the disease, the acute or chronic nature at the time of presentation and the bias of the surgeon treating the case. Conservative surgery Local incision and drainage. Local incision and drainage of individual purulent lesions is often required in the acute phase and while helpful in the short term in giving relief,
it is almost inevitable that recurrent episodes of inflammation will occur.
Deroofing of sinuses and fistulous tracts. Deroofing of sinus tracts which may be partially epithelialised and laying open and curettage of fistulous tracts which may ramify extensively in the subcutaneous plane, have a distinct role, particularly in the acute phase of perineal disease. These procedures may be preliminary to more definitive intervention. Once the disease becomes extensive and established, surgical excision of the involved tissue is generally indicated. The average duration of the disease before definitive treatment in numerous series is between 3 and 6 years (54). Limited local excision with primary closure. Where the extent of the skin involvement is limited, local excision and direct primary suture may be feasible. Local excision of sinus tracts, when used as an alternative to wide ablative en bloc excision, is associated with a higher recurrence rate but a lower morbidity rate. Recurrence rates of over 50% have been reported after simple local excision alone (8,30). In 1972, Pollock (55) advocated a specific technique of excision and primary closure in the management of axillary disease. In this method minimal undermining of the skin edges was undertaken. Skin closure incorporated the use of subcuticular and interrupted vertical mattress sutures in addition to nylon retention sutures tied over a bolus dressing. Radical surgery When the disease process has become chronic and extensive, most authors agree that removal of the affected area and the adjacent apocrine glandular zone for a distance of 2 cm beyond the diseased portion, is the best option if the likelihood of recurrence is to be minimised. To define the apocrine gland-bearing area, which is particularly applicable to the axillary region, the iodinestarch method is employed. This technique involves first blocking the eccrine secretion using 1.2 mg of atropine intravenously, followed by 2 units of oxytocin intravenously to stimulate the myoepithelial cells that surround the apocrine glands. Iodine (2%) is applied to the area to be tested, followed by the application of a mixture comprising 75 g of fine starch powder in 100 ml of castor oil. The zone of apocrine sweating is identified by the appearance of little black spots, usually in the vicinity of hair follicles where the sweat has made contact with the iodine-starch interface. The block of tissue excised should be not only adequately wide but also sufficient in depth. This means removal of subcutaneous tissue down to the deep fascia, or at least excision of a minimum of 5 mm of subcutaneous fat, to ensure that the deep coils of apocrine glands have been removed. During excisional surgery for inguinoperineal disease, a bridge of skin should be preserved between the anus and the scrotum or vulva. In female patients, the labia minora
Hidradenitis suppurativa and the inner portions of the labia majora should also be conserved. In some patients with perineal disease it may be preferable to undertake staged excision of diseased quadrants, down to normal fascia or fat, in an effort to maintain more normal anatomy. Adequate excision to eradicate the disease often results in a defect that precludes primary closure and hence other techniques have to be adopted to achieve wound healing. Techniques to obtain skin cover include the application of skin grafts (56) or the use of transposed (57) or pedicle (58) flaps. Skin grafting has its limitations and drawbacks. It is generally considered unsuitable in the management of inguinoperineal disease and when attempted it usually fails. Immediate skin grafting can be carried out in the axilla if the wound is clean, but often this is not a practical option because of poor vascularity and bacterial contamination of the subcutaneous fat. Even with delayed skin grafting, it is unusual to achieve 100% take. Furthermore, simultaneous bilateral grafting of axillae is inappropriate for the majority of patients because of the degree of immobilisation engendered. It is difficult to undertake an accurate comparative assessment of the various surgical approaches because of the incomplete reporting of long-term results and the limited number of controlled clinical trials. Wiltz et al. (13), Masson (58) and Thomton and Abcarian (59) have recommended excision of skin and subcutaneous fat of the affected area down to fascia and allowing the wound to heal by subsequent granulation. Morgan et al. (60) have suggested the use of Silastic® foam dressing as a useful adjunct to this type of treatment. Those who advocate excision and healing by secondary intention claim this technique permits adequate disease clearance and results in a cosmetically acceptable scar, superior to that obtained by skin grafting and with little limitation of movement. Morgan et al. (61) compared split-thickness skin grafting with healing by secondary intention in 10 consecutive patients with bilateral axillary disease. Each patient had excision of the affected areas; a splitthickness skin graft was performed on one side and a Silastic foam dressing was applied on the other, allowing the wound to heal by secondary intention. Although wound healing occurred somewhat more rapidly after skin grafting, these authors and their patients preferred the method whereby the wound was allowed to heal by secondary intention. Furthermore, a painful split-skin donor site was avoided when the latter method was adopted.
Adjunctive surgery. Ching and Stahlgren (62) advocated the use of diverting colostomies for patients with severe perianal hidradenitis affecting the entire perineal area. However, most patients with inguinoperineal disease are managed satisfactorily without the necessity for faecal diversion, particularly if a staged wide local excision technique is adopted. There is one group of patients in whom the necessity for a stoma is a likely requirement eventually, namely those patients who suffer from
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coexistent hidradenitis suppurativa and Crohn's disease of the anorectum. Among the surgical relics of the past, orchidectomy was occasionally used as an adjunct in the management of perineoscrotal involvement (63). This unappealing and unrewarding procedure has been abandoned.
Outcome The extent of the skin excision may influence recurrence rates more than a particular method of wound management. Recurrence after surgery is likely if excision is inadequate or if there is an unusually wide distribution of apocrine glands. Watson (8) reported that 54% of patients with axillary hidradenitis suppurativa treated by local excision and primary suture required a second operation, whereas only 19% required reoperation after local flap repair and only 13% after split-skin grafting. This implies that in those cases where primary skin closure was being contemplated there was a degree of compromise in the extent of the excision margin leading to an increased incidence of recurrence (40). Broadwater et al. (11) found that wide excision and split-skin grafting (either immediate or delayed) resulted in the lowest incidence of recurrence in their series of patients in whom hidradenitis suppurativa affected multiple sites. As apocrine glands are more diffuse in the inguinoperineal and inframammary regions, complete excision in these areas is more difficult to achieve and hence recurrence at these sites is more common than in the axilla. In a series of 82 patients treated by radical surgery for intractable hidradenitis, the recurrence rate varied considerably depending on the site affected and ranged form zero for perianal, 3% for axillary, 37% for inguinoperineal to 50% for submammary involvement (45). Recurrence developed from 3 to 72 months (median 24 months) after initial excision. Two distinct patterns of recurrence emerged in relationship to the original anatomical site: (a) in the immediate vicinity of the scar, especially in the groin or posterior-inferior margins after inguinoperineal excision-usually a solitary lesion, and (b) in the skin adjacent to the previous excision or even a few centimetres away-often multiple lesions. These workers emphasised that on long-term follow-up almost one-quarter of their patients who had recurrence of hidradenitis suppurativa developed the problem at a previously unaffected anatomical site. In most instances, recurrent disease is managed adequately by wide local excision of the affected area, allowing the wound to heal by secondary intention (40).
References 1 Velpeau A. In: Z Bechet Jeune, ed. Dictionnaire de Medicine, un Repertoire General des Sciences Medicales sons le Rapport. Theorique et Pratique. 2nd Edition Volume 2. Paris, 1839: 91. 2 Verneuil A. Etudes sur les tumeurs de la peau et quelques maladies des glandes sudoripores. Arch Gen Med 1854; 94:
693-705.
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3 Schiefferdecker B. In: Schweizerbart E, ed. Die Hautdrusen des Menschen und der Saugetiere, ihre Histologishe und rassena natomische Bednutung Sowie die Muscularis Sexualis. Stuttgart, 1922. 4 Lane JE. Hidrosadenitis axillaris of Verneuil. Arch Derm Syph (Berl) 1933; 28: 609-14. 5 Brunsting HA. Hidradenitis suppurativa: abscess of the apocrine sweat glands. Arch Derm Syph (Berl) 1939; 39: 108-20. 6 Shelley WB, Cahn MM. Pathogenesis of hidradenitis suppurativa in man: experimental and histologic observations. Arch Dermatol 1955; 72: 562-5. 7 Newell GB. Treatment of hidradenitis suppurativa. JAMA 1973; 223: 556-7. 8 Watson JD. Hidradenitis suppurativa-a clinical review. BrJ Plast Surg 1985; 38: 567-9. 9 Highet AS, Warren RE, Weekes AJ. Bacteriology and antibiotic treatment of perineal suppurative hidradenitis. Arch Dermatol 1988; 124: 1047-51. 10 Ebling FJ. Apocrine glands in health and disorder. Int J Dermatol 1989; 28: 508-11. 11 Broadwater JR, Bryant RL, Petrino RA, Mabry CD, Westbrook KC, Casali RE. Advanced hidradenitis suppurativa: review of surgical treatment in 23 patients. Am J Surg 1982; 144: 668-70. 12 Rogers IW, Ryan RF. Surgical treatment of hidradenitis suppurativa. J La State Med Soc 1983; 10: 21-4 13 Wiltz 0, Schoetz DJ, Murray JJ, Roberts PL, Coller JA, Veidenheimer MC. Perianal hidradenitis suppurativa: the Lahey Clinic experience. Dis Colon Rectum 1990; 33: 731-4 14 Morgan WP. The role of depilation and deodorants in hidradenitis suppurativa. Arch Dermatol 1982; 118: 101-2. 15 Harrison BJ, Kumar S, Read GF, Edwards CA, Scanlon MF, Hughes LE. Hidradenitis suppurativa: evidence for an endocrine abnormality. Br J Surg 1985; 72: 1002-4. 16 Mortimer PS. Mediation of hidradenitis suppurativa by androgens. Br Med J 1986; 292: 245-8. 17 Ebling FJG. Hidradenitis suppurativa: an androgen-dependent disorder. Br J Dermatol 1986; 115: 259-62. 18 Lewis F, Messenger AG, Wales JKH. Hidradenitis suppurativa as a presenting feature of premature adrenarche. Br J Dermatol 1993; 129: 447-8. 19 Sulberger MB in discussion in Ludy JB, Drant P. Hidradenitis suppurativa, papulonecrotic tuberculoid and bromoderma. AMA Arch Dermatol Syph 1941; 44: 494. 20 Wile UJ, Curtis AC. Cushings syndrome with hidradenitis suppurativa. AMA Arch Dermatol Syph 1948; 58: 746-7. 21 Paletta C, Jurkiewicz MJ. Hidradenitis suppurativa. Clin Plast Surg 1987; 14: 383-90. 22 Anonymous. Calprotectin, zinc and abscesses. Lancet 1991; 338: 855-6. 23 Anderson DK, Perry AW. Axillary hidradenitis. Arch Surg 1975; 110: 69-72. 24 Dvorak VC. Host-defence mechanisms in hidradenitis suppurativa. Arch Dermatol 1977; 113: 450-3. 25 Fitzsimmons JS, Fitzsimmons EM, Gilbert G. Familial hidradenitis suppurativa: evidence in favour of single gene transmissions. J Med Genet 1984; 21: 281-5. 26 Fitzsimmons JS, Gilbert G. A family study of hidradenitis suppurativa. J Med Genet 1985; 22: 367-73. 27 Fitzsimmons JS, Guilbert PR, Fitzsinmmons EM. Evidence of genetic factors in hidradenitis suppurativa. Br J Dermatol 1985; 113: 1-8.
28 Jemec GBE. The symptomatology of hidradenitis suppurativa in women. Br J Dermatol 1988; 119: 345-50. 29 McAnally AK, Dockerty MB. Carcinoma developing in chronic cutaneous sinuses and fistulas. Surg Gynecol Obstet 1949; 88: 87-96. 30 Anderson MJ Jr, Dockerty MB. Perineal hidradenitis suppurativa. Dis Colon Rectum 1958; 1: 23-31. 31 Jackman RJ. Hidradenitis suppurativa: diagnosis and surgical management of perianal manifestations. Proc R Soc Med 1959; 52: 110-12. 32 Donsky HJ, Mendelson CG. Squamous cell carcinoma as a complication of hidradenitis suppurativa. Arch Dermatol 1964; 90: 488-91. 33 Humphrey LJ, Playforth H, Leavell UW. Squamous cell carcinoma arising in hidradenitis suppurativa. Arch Dermatol 1969; 100: 59-62. 34 Gordon SW. Squamous cell carcinoma arising in hidradenitis suppurativa. Plast Reconstr Surg 1977; 60: 800-2. 35 Zachary LS, Robson MC, Rachmaninoff N. Squamous cell carcinoma occurring in hidradenitis suppurativa. Ann Plast Surg 1987; 18: 71-3. 36 Self SJ, Montes LFL. Follicular occlusion triad. South Med J 1979; 63: 156-60. 37 Yu CCW, Cook MG. Hidradenitis suppurativa: a disease of follicular epithelium, rather than apocrine glands. Br J Dermatol 1990; 122: 763-9. 38 Cornbleet T. Pregnancy and apocrine gland diseases: hidradenitis and Fox Fordyce disease. AMA Arch Dermatol Syph 1952; 65: 12-19. 39 Homma H. On apocrine sweat glands in white and Negro men and women. Bull Johns Hopkins Hosp 1926; 38: 365-71. 40 Banerjee AK. Surgical treatment of hidradenitis suppurativa. Br J Surg 1992; 79: 863-6. 41 Church JM, Fazio VW, Lavery IC, Oakley JR, Milson JW. The differential diagnosis and comorbidity of hidradenitis suppurativa and perianal Crohn's disease. IntJ Colorectal Dis 1993; 8: 117-19. 42 Culp CE. Chronic hidradenitis suppurativa of the anal canal: a surgical skin disease. Dis Colon Rectum 1983; 26: 669-76. 43 Brown SCW, Kazzazi N, Lord PH. Surgical treatment of perineal hidradenitis suppurativa with special reference to recognition of the perianal form. BrJ Surg 1986; 73: 978-80. 44 Ostlere LS, Langtry JA, Mortimer PS, Staughton RC. Hidradenitis suppurativa in Crohn's disease. Br J Dermatol 1991; 125: 384-6. 45 Harrison BJ, Mudge M, Hughes LE. Recurrence after surgical treatment of hidradenitis suppurativa. Br Med J 1987; 294: 487-9. 46 Jones DH, Cunliffe W, King K. Hidrandenitis suppurativalack of success with 13-cis-retinoic acid. Br Jf Dermatol 1982; 107: 252. 47 Shalita AR, Cunningham W, Leyden J et al. Isotretinoin treatment of acne and related disorders: an update. J Am Acad Dermatol 1983; 9: 629-38. 48 Dicken CH, Powell ST, Spear KL. Evaluation of isotretinoin treatment of hidradenitis suppurativa. J Am Acad Dermatol 1984; 11: 500-2. 49 Norris JF, Cunliffe WJ. Failure of treatment of familial widespread hidradenitis suppurativa with isotretinoin. Clin Exp Dermatol 1986; 11: 579-83. SO Brown CF, Gallup DG, Brown VM. Hidradenitis suppurativa of the anogenital region: response to isotretinoin. Am J Obstet Gynecol 1988; 158: 12-15. Si Hogan DJ, Light MJ. Successful treatment of hidradenitis
Hidradenitis suppurativa suppurativa with acitretin. J Am Acad Dermatol 1988; 19: 355-6. 52 Kress DW. A preliminary report on the use of Staphage Lysate for treatment of hidradenitis suppurativa. Ann Plast Surg 1981; 6: 393-5. 53 Camisa C, Sexton C, Friedman C. Treatment of hidradenitis suppurativa with combination hypothalamic-pituitary-ovarian and adrenal suppression. J Reprod Med 1989; 34: 543-6. 54 Hurley HJ, Shelly WB. The Human Apocrine Sweat Gland in Health and Disease. Springfield, Ill: Thomas, 1969: 120. 55 Pollock WJ. Axillary hidradenitis suppurativa: a simple and effective surgical technique. Plast Reconstr Surg 1972; 49: 22-7. 56 Knaysi GA, Cosman B, Crikelair GF. Hidradenitis suppurativa. JAMA 1968; 203: 73-6. 57 Harrison SH. Axillary hidradenitis. BrJ Plast Surg 1964; 17: 95-8. 58 Masson JK. Surgical treatment for hidradenitis suppurativa. Surg Clin North Am 1969; 49: 1043-52.
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59 Thornton JP, Abcarian H. Surgical treatment of perianal and perineal hidradenitis suppurativa. Dis Colon Rectum 1978; 21: 573-7. 60 Morgan WP, Harding KG, Richardson G, Hughes LE. The use of Silastic foam dressing in the treatment of advanced hidradenitis suppurativa. Br J Surg 1980; 67: 277-80. 61 Morgan WP, Harding KG, Hughes LE. A comparison of skin grafting and healing by granulation following axillary excision for hidradenitis suppurativa. Ann R Coll Surg Engl 1983; 65: 235-6. 62 Ching CC, Stahlgren LH. Clinical review of hidradenitis suppurativa: management of cases with severe perianal involvement. Dis Colon Rectum 1965; 8: 349-52. 63 Vickers MA. Operative management of chronic hidradenitis suppurativa of the scrotum and perineum. J Urol 1975; 114: 414-16. Received 6 August 1996
