eMedicine Specialties > Dermatology > Diseases of the Adnexa

Hidradenitis Suppurativa: Differential Diagnoses & Workup

Author: Marina Jovanovic, MD, PhD, Chief of Dermatology Ward and Contact Dermatitis Investigative Unit, Clinic of Dermatoveneroleogic Diseases, Clinical Center, Novi Sad, Serbia and Montenegro; Associate Professor in Dermatology, Medical Faculty, University of Novi Sad, Vojvodina, Serbia and Montenegro
Coauthor(s): George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital; Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Contributor Information and Disclosures

Updated: Aug 17, 2009

Differential Diagnoses

Actinomycosis
Granuloma Inguinale (Donovanosis)
Catscratch Disease
Lymphogranuloma Venereum
Cutaneous blastomycosis
Nocardia infection
Erysipelas
Noduloulcerative syphilis

Other Problems to Be Considered

Abscesses
Apocrine nevus
Infection in a Bartholin cyst
Carbuncle
Crohn disease
Infection in an epidermoid cyst
Lymphadenitis
Multiple trichoepitheliomas
Tuberculosis
Tularemia
Ulcerative colitis

Workup

Laboratory Studies

  • The following laboratory tests may be helpful in the evaluation of hidradenitis suppurativa (HS):
    • CBC count with differential and platelet counts
    • Assessment of erythrocyte sedimentation rate
    • C-reactive protein assay
    • Urinalysis
    • Serum multiphasic analysis with determination of the serum iron level and serum protein electrophoresis
  • Patients with acute lesions may have an elevated erythrocyte sedimentation rate, elevated white blood cell count (occasionally), a low serum iron level, and serum protein abnormalities on electrophoresis.

Imaging Studies

  • Ultrasonography of the hair follicles and dermal thickness in hidradenitis suppurativa patients may reveal abnormalities in the deep part of the follicle.
    • In the genitofemoral region, perilesional clinically normal hair follicles have an abnormal shape and are significantly wider in the deep part of the dermis, compared with control samples.
    • Mean axillary and genitofemoral skin is significantly thicker in patients with hidradenitis suppurativa than in healthy control subjects.
    • Thickened skin may play a role in the pathogenesis of hidradenitis suppurativa.

Other Tests

  • Bacteriologic analysis should include bacteriologic sampling and cultivation.
    • Bacteriologic sampling should be performed at different depths in hidradenitis suppurativa lesions.
    • A carbon dioxide laser can be used to evaporate the diseased tissue, level by level, from the surface downward. Samples can be concurrently obtained from each level, and contamination with bacteria from the level above can be minimized.
    • Almost every microorganism known to bacteriologists can be isolated from hidradenitis suppurativa lesions; these microorganisms include streptococci, gram-positive and gram-negative rods, and the full range of fecal bacteria.62 Among the most frequently found species are Staphylococcus aureus and coagulase-negative staphylococci, anaerobic streptococci (eg, microaerophilic Streptococcus milleri), and Bacteroides species.43,53,54
  • The microbiologic florae are not consistent and change unpredictably.62
  • Immunohistochemical data obtained for various cytokeratins (CKs) and the 6 desmosomal cadherins (ie, desmogleins [Dsgs] 1-3, desmecollins [Dscs] 1-3) showed 3 phenotypes of stratified squamous epithelia covering the sinus tracts in hidradenitis suppurativa: type I cornifying, type II noncornifying and moderately inflamed, and type III noncornifying and strongly inflamed.63
    • The noncornifying types II and III epithelia are characterized by the absence of the terminal differentiation markers CK10 and Dsc1 and by the strong expression of Dsg2 in the basal layer. Compared with the normal epidermis and type I epithelium, types II and III epithelia have Dsc2 and Dsg3 in all layers, whereas Dsc3 is restricted to the basal and parabasal layers. The inflammatory character of type III epithelium, as opposed to that of types I and II, is marked by the presence of CK7 and CK19 and the absence of Dsg1.63
    • All 3 types of epithelia are clearly distinct from the interfollicular epidermis because of the absence of CK2e and the presence of CKs 6, 13, 15, and 16; the presence of these proteins reflects the fact that the sinus tract epithelia have undergone the pathologically altered process of growth, differentiation, and inflammation.
    • CK19 is commonly found in the basal cells of noncornifying stratified squamous epithelia, such as in the outer root sheath (ORS) of the hair follicle. The strongly inflamed CK19-positive parts of the sinus epithelium show no signs of terminal squamous differentiation (ie, nuclei were present in the highest suprabasal layers, and keratohyalin granules were absent). Instead, the inflamed CK–positive parts resembled epidermal keratinocytes grown in organotypic culture, which can be induced to build a noncornifying epithelium and to express CK19 with the addition of retinoic acid to the culture medium.
    • In all specimens in one study, type I epithelium near the opening of the sinus showed strong similarities to the upper pilosebaceous duct from which the inflammation process seemed to emerge.
    • In both normal pilosebaceous duct epithelium and cornifying type I sinus epithelium, CK5 and CK14 are restricted to the basal layer, CK10 and Dsc1 antibodies label the suprabasal cells, Dsg1 and Dsg3 are present in an epidermislike pattern, and CK2e is absent.
    • The relationship of the sinus epithelium to the hair follicles and the apocrine glands has long been debated.45 The sinus epithelium is clearly distinct from the normal epithelium of the subinfundibular ORS of the hair follicle. Thus, CKs 5 and 14 and Dsg2 always remain restricted to the basal cell layer of the sinus epithelium, whereas in the subinfundibular ORS, they are also expressed in the suprabasal layer. The relationship of the sinus epithelium to hair follicles and apocrine glands is in agreement with the theory that hidradenitis suppurativa lesions are caused by follicular plugging and subsequent rupture of the follicular epithelia. The exact role of inflammation in such patterns of differentiation has yet to be elucidated.
    • Thus, in another study of the hidradenitis suppurativa cytokeratin expression reported by Kurokawa et al, the draining sinus tract epithelium of hidradenitis suppurativa lesions were divided into 3 components: infundibularlike keratinized epithelium (type-A), noninfundibular keratinized epithelium (type B), and nonkeratinized epithelium (type C).64
      • Types A and B were similar to the types I and II reported by Kurzen et al,63 although  CK17 was not detected in type A, suggesting fragility of this epithelial type. CK17, which is normally present in the suprabasal layers of healthy skin, represents a useful marker for differentiation of epithelial cells. It is a spacial keratin and has a function related to the maintenance of the 3-dimensional cytoskeleton structure of human adnexal glands. Thus, the absence of CK17 may reflect a fragile follicular structure, resulting in rupture of the follicle, which subsequently forms a subcutaneous abscess.65
      • CK expression in pilonidal sinus is comparable with that in hidradenitis suppurativa, as previously reported. Moreover, in infundibularlike epithelium, CK17 is also absent.65
      • The overlying epidermis in hidradenitis suppurativa lesions has a more undifferentiated hyperproliferative state than that found in healthy epidermis.64 In some cases, CK19 is present in the basal layer of the epidermis, and CK19 is thought to be associated with premalignant change.66

Histologic Findings

Histologically, the fundamental change in hidradenitis suppurativa is the same as in acne vulgaris, namely, hyperkeratosis of the infundibulum that results in comedolike horny impactions.62 Some evidence suggests that the occlusion of abnormal hair follicles may play an important part in the initiation of the lesions.8,67 Follicular occlusion was found in all specimens compared with controls and regardless of disease duration.52 Folliculitis and perifollicular inflammation are common and occur in about two thirds of cases, with or without follicular occlusion.

The earliest inflammatory event is a segmental rupture of the follicular epithelium, followed by spilling of foreign body material. The apocrine glands are not involved in the earliest stage of follicular hyperkeratosis and infundibulofolliculitis.60

The inflammatory infiltrate is composed of neutrophils; lymphocytes, plasma cells, and, occasionally, eosinophils. Active inflammation around the sweat glands is less common than inflammation around the hair follicles. The histologic features reveal inflammation of the apocrine glands in only 33% of cases. Apocrinitis only evolves by extension of the inflammatory process.55 Apocrine gland destruction by neutrophils is occasionally observed. Abscess formation occurs, leading to destruction of the pilosebaceous unit and, eventually, the other adnexal structures. Apoeccrine glands (present in axillae), which drain directly on the epidermal surface, appear intact and not inflammed.68

Chronic lesions have a dermis with an inflammatory cell infiltrate and foreign body–type granulomas around the hair follicles and the sinus tracts. The presence of epithelioid granulomas in so-called granulomatous hidradenitis suppurativa should alert to the possibility of coexisting granulomatous disease, such as Crohn disease or sarcoidosis.30
 
The draining sinus tracts extend predominantly into the dermis and are lined by a variably thickened stratified epithelium; they extend in the form of dissecting tracts, which burrow through the necrotic tissue. The epithelium is constantly breaking down; therefore, the sinus tract is not completely lined with epithelium.29 As previously mentioned, the 3 phenotypes (see Other Tests) of stratified squamous epithelia reflect the dynamic processes of inflammation, proliferation, and stratification that occur in hidradenitis suppurativa.63

Lipid rafts (membrane microdomains composed of cholesterol and gangliosides) have been described and appear to have potentially relevant functions in the formation of sinus tracts. The lipid rafts provide anchor points for growth factor receptors and are expressed on migrating cells such as keratinocytes involved in wound healing. Thus, sinus tract formation may represent an aberrant epidermal repair response executed by the lipid raft-enriched stem cell–like keratinocytes in the epidermis and hair follicles, as well as in sinus tracts in hidradenitis suppurativa, that emerge due to the influence of local inflammatory cytokines and are capable of nonmalignant infiltrative growth in the dermis and subcutis.69

With regard to the expression of CK19 in type II epithelium and overlying epidermis in hidradenitis suppurativa lesions (which can also be induced in epidermal keratinocytes grown in organotypic culture medium with the addition of retinoic acid), study of the expression of retinoic acid and retinoid X receptors in the different epithelial phenotypes of the draining sinus would be interesting.

Retinoids are known to induce a differentiation shift in keratinocytes, which thereby acquire certain features of simple glandular epithelia. Type III epithelium expresses some markers of such epithelia. This finding may be interpreted as a kind of metaplasia toward glandular differentiation.63 Free hair shafts can be found in the sinus and surrounding dermis, without apparent connection to the epithelium.

Difficulty may arise in distinguishing well-differentiated squamous cell carcinoma (SCC) and florid pseudoepitheliomatous hyperplasia. Pseudoepitheliomatous hyperplasia is usually associated with chronic irritation, unlike SCC. Tissue destruction, necrosis, and, often, keratin pearls, are associated with SCCs. Vascular and lymphatic invasion may be present in SCC. Mitotic activity is seen in both conditions, although abnormal mitoses are only seen in SCCs.

High-frequency ultrasonography  shows changes in the clinically uninvolved axillary and genitofemoral hair follicles. The follicles appear to be larger diameter and a distorted shape with a wider deep follicular diameter, in agreement with the clinical impression that the primary event in hidradenitis suppurativa is deep seated rather than superficial.19

Staging

Clinical staging of hidradenitis suppurativa has diagnostic value.70

  • The first stage is characterized by solitary or multiple, isolated abscess formation without scarring or sinus tracts.
  • The second stage is characterized by recurrent abscesses, single or multiple widely separated lesions, with sinus tract formation and cicatrization.
  • The third stage is characterized by diffuse or broad involvement, with multiple interconnected sinus tracts and abscesses.
Dynamic staging system have been used for assessing differences in treatment effects.71 Uniform outcome variables should take into account the known characteristics of hidradenitis suppurativa, including the following71 :
  • Anatomical region involved (axilla, groin, genital, gluteal, or other inflammatory region left and/or right) - Three points per region involved
  • Number and scores of lesions (abscesses, nodules, fistulas, scars)  -  Two points for each nodule, 4 points for each fistulas, 1 point for each scar, 1 point for each "other"
  • The longest distance between 2 relevant lesions, ie, nodules and fistulas, in each region, or size if only 1 lesion - Less than 5 cm, 2 points; less than 10 cm, 4 points; more than 10 cm, 8 points
  • Lesions are clearly separated by normal skin in each region - If yes, 0 points; if no, 6 points.

More on Hidradenitis Suppurativa

Overview: Hidradenitis Suppurativa
Differential Diagnoses & Workup: Hidradenitis Suppurativa
Treatment & Medication: Hidradenitis Suppurativa
Follow-up: Hidradenitis Suppurativa
Multimedia: Hidradenitis Suppurativa
References
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References

  1. Velpeau A. Dictionnaire de Medicine, un Repertoire des Sciences Medicales sons le Rapport, Theorique et Pratique. 2nd ed Paris. 1839:91.

  2. Verneuil A. Etudes sur les tumeurs de la peau et quelques maladies des glandes sudoripores. Arch Gen Med. 1854;4:693-705.

  3. Schiefferdecker B. Die Hautdrusen des Menschen und der Saugetierre ihre Histologishe und rassenanatomische Bedeutung Sowie die Muscularis Sexualis. Stuttgart. 1922.

  4. Brunsting HA. Hidradenitis suppurativa: abscess of the apocrine sweat glands. Arch fur Dermatol und Syph (Berlin). 1939;39:108-20.

  5. Pillsbury DM, Shelley WB, Kligman AM. Bacterial infections of the skin. In: Dermatology. Philadelphia: WB Saunders Co; 1956:482-9.

  6. Plewig G, Kligman AM. Acne: Morphogenesis and Treatment. Berlin: Springer-Verlag; 1975.

  7. Plewig G, Steger M. Acne inversa (alias acne triad, acne tetrad, or hydradenitis suppurativa). In: Marks R, Plewig G, eds. Acne and Related Disorders. London: Martin Dunitz Ltd; 1989:343-57.

  8. Yu CC, Cook MG. Hidradenitis suppurativa: a disease of follicular epithelium, rather than apocrine glands. Br J Dermatol. Jun 1990;122(6):763-9. [Medline].

  9. 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].

  10. 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].

  11. Sellheyer K, Krahl D. "Hidradenitis suppurativa" is acne inversa! An appeal to (finally) abandon a misnomer. Int J Dermatol. Jul 2005;44(7):535-40. [Medline].

  12. Jemec GB. What's new in hidradenitis suppurativa?. J Eur Acad Dermatol Venereol. Sep 2000;14(5):340-1. [Medline].

  13. 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. Oct 2008;59(4):596-601. [Medline].

  14. Jemec GB, Heidenheim M, Nielsen NH. Hidradenitis suppurativa--characteristics and consequences. Clin Exp Dermatol. Nov 1996;21(6):419-23. [Medline].

  15. von der Werth JM, Williams HC. The natural history of hidradenitis suppurativa. J Eur Acad Dermatol Venereol. Sep 2000;14(5):389-92. [Medline].

  16. Parks RW, Parks TG. Pathogenesis, clinical features and management of hidradenitis suppurativa. Ann R Coll Surg Engl. Mar 1997;79(2):83-9. [Medline].

  17. Manolitsas T, Biankin S, Jaworski R, Wain G. Vulval squamous cell carcinoma arising in chronic hidradenitis suppurativa. Gynecol Oncol. Nov 1999;75(2):285-8. [Medline].

  18. Fearfield LA, Staughton RC. Severe vulval apocrine acne successfully treated with prednisolone and isotretinoin. Clin Exp Dermatol. May 1999;24(3):189-92. [Medline].

  19. Jemec GB. Hidradenitis suppurativa. J Cutan Med Surg. Jan-Feb 2003;7(1):47-56. [Medline].

  20. Brown TJ, Rosen T, Orengo IF. Hidradenitis suppurativa. South Med J. Dec 1998;91(12):1107-14. [Medline].

  21. Palmer RA, Keefe M. Early-onset hidradenitis suppurativa. Clin Exp Dermatol. Sep 2001;26(6):501-3. [Medline].

  22. Mengesha YM, Holcombe TC, Hansen RC. Prepubertal hidradenitis suppurativa: two case reports and review of the literature. Pediatr Dermatol. Jul-Aug 1999;16(4):292-6. [Medline].

  23. Weber-LaShore A, Huppert JS. Hidradenitis suppurativa in a pre-pubertal female. J Pediatr Adolesc Gynecol. 2009;22:e53.

  24. Barth JH, Layton AM, Cunliffe WJ. Endocrine factors in pre- and postmenopausal women with hidradenitis suppurativa. Br J Dermatol. Jun 1996;134(6):1057-9. [Medline].

  25. Misery I, Faure M, Claidy A. Pityriasis rubra pilaris and human immunodeficiency virus infection--type 6 pityriasis rubra pilaris?. Br J Dermatol. Dec 1996;135(6):1008-9. [Medline].

  26. Leybishkis B, Fasseas P, Ryan KF, Roy R. Hidradenitis suppurativa and acne conglobata associated with spondyloarthropathy. Am J Med Sci. Mar 2001;321(3):195-7. [Medline].

  27. von der Werth JM, Jemec GB. Morbidity in patients with hidradenitis suppurativa. Br J Dermatol. Apr 2001;144(4):809-13. [Medline].

  28. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol. Apr 2009;60(4):539-61; quiz 562-3. [Medline].

  29. Jansen T, Romiti R, Plewig G, Altmeyer P. Disfiguring draining sinus tracts in a female acne patient. Pediatr Dermatol. Mar-Apr 2000;17(2):123-5. [Medline].

  30. Roy MK, Appleton MA, Delicata RJ, Sharma AK, Williams GT, Carey PD. Probable association between hidradenitis suppurativa and Crohn's disease: significance of epithelioid granuloma. Br J Surg. Mar 1997;84(3):375-6. [Medline].

  31. Martínez F, Nos P, Benlloch S, Ponce J. Hidradenitis suppurativa and Crohn's disease: response to treatment with infliximab. Inflamm Bowel Dis. Nov 2001;7(4):323-6. [Medline].

  32. Church JM, Fazio VW, Lavery IC, Oakley JR, Milsom JW. The differential diagnosis and comorbidity of hidradenitis suppurativa and perianal Crohn's disease. Int J Colorectal Dis. Sep 1993;8(3):117-9. [Medline].

  33. Jansen T, Plewig G. What's new in acne inversa (alias hidradenitis suppurativa)?. J Eur Acad Dermatol Venereol. Sep 2000;14(5):342-3. [Medline].

  34. Gonzalez-Lopez A, Velasco E, Pozo T, Del Villar A. HIV-associated pityriasis rubra pilaris responsive to triple antiretroviral therapy. Br J Dermatol. May 1999;140(5):931-4. [Medline].

  35. Kleeman D, Trueb RM, Schmid-Grendelmeier P. [Reticular pigmented anomaly of the flexures. Dowling-Degos disease of the intertrigo type in association with acne inversa]. Hautarzt. Jul 2001;52(7):642-5. [Medline].

  36. Libow LF, Friar DA. Arthropathy associated with cystic acne, hidradenitis suppurativa, and perifolliculitis capitis abscedens et suffodiens: treatment with isotretinoin. Cutis. Aug 1999;64(2):87-90. [Medline].

  37. Thein M, Hogarth MB, Acland K. Seronegative arthritis associated with the follicular occlusion triad. Clin Exp Dermatol. 2004;29:545-62.

  38. Bhosale P, Barron B, Lamki L. The "SAPHO" syndrome: a case report of a patient with unusual bone scan findings. Clin Nucl Med. Jul 2001;26(7):619-21. [Medline].

  39. Cosman BC, Al-Refaie WB. Mammillary fistula as a manifestation of acne inversa (hidradenitis suppurativa): report of two cases. J Am Coll Surg. Jun 2002;194(6):829-33. [Medline].

  40. Ah-Weng A, Langtry JA, Velangi S, Evans CD, Douglas WS. Pyoderma gangrenosum associated with hidradenitis suppurativa. Clin Exp Dermatol. Nov 2005;30(6):669-71. [Medline].

  41. Pavlovic M. Oboljenja apokrinih znojnih zlezda. In: Karadaglic D, ed. Dermatologija Beograd: Vojnoizdavacki Zavod. 2000:754-61.

  42. Shelley WB, Cahn MM. The pathogenesis of hidradenitis suppurativa in man; experimental and histologic observations. AMA Arch Derm. Dec 1955;72(6):562-5. [Medline].

  43. Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Dermatol. Jan 1999;140(1):90-5. [Medline].

  44. Mowad CM, McGinley KJ, Foglia A, Leyden JJ. The role of extracellular polysaccharide substance produced by Staphylococcus epidermidis in miliaria. J Am Acad Dermatol. Nov 1995;33(5 Pt 1):729-33. [Medline].

  45. Kurzen H, Kurokawa I, Jemec GB, et al. What causes hidradenitis suppurativa?. Exp Dermatol. May 2008;17(5):455-6; discussion 457-72. [Medline].

  46. Fitzsimmons JS, Guilbert PR, Fitzsimmons EM. Evidence of genetic factors in hidradenitis suppurativa. Br J Dermatol. Jul 1985;113(1):1-8. [Medline].

  47. Montgomery JR, White TW, Martin BL, Turner ML, Holland SM. A novel connexin 26 gene mutation associated with features of the keratitis-ichthyosis-deafness syndrome and the follicular occlusion triad. J Am Acad Dermatol. Sep 2004;51(3):377-82. [Medline].

  48. Gao M, Wang PG, Cui Y, et al. Inversa acne (hidradenitis suppurativa): a case report and identification of the locus at chromosome 1p21.1-1q25.3. J Invest Dermatol. Jun 2006;126(6):1302-6. [Medline].

  49. Lapins J, Olerup O, Emtestam L. No human leukocyte antigen-A, -B or -DR association in Swedish patients with hidradenitis suppurativa. Acta Derm Venereol. Jan-Feb 2001;81(1):28-30. [Medline].

  50. Lapins J, Asman B, Gustafsson A, Bergstrom K, Emtestam L. Neutrophil-related host response in hidradenitis suppurativa: a pilot study in patients with inactive disease. Acta Derm Venereol. May 2001;81(2):96-9. [Medline].

  51. Giamarellos-Bourboulis EJ, Antonopoulou A, Petropoulou C, et al. Altered innate and adaptive immune responses in patients with hidradenitis suppurativa. Br J Dermatol. Jan 2007;156(1):51-6. [Medline].

  52. Hunger RE, Surovy AM, Hassan AS, Braathen LR, Yawalkar N. Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor. Br J Dermatol. Apr 2008;158(4):691-7. [Medline].

  53. Champion RH:. Disorder of sweat glands. In: Rook A, Wilkinson DS, Ebling FJ, eds. Textbook of Dermatology. 6th ed. Oxford: Blackwell Science; 1998:1985-2002.

  54. Edlich RF, Winters KL, Britt LD, Long WB 3rd, Gubler KD, Drake DB. Difficult wounds: an update. J Long Term Eff Med Implants. 2005;15(3):289-302. [Medline].

  55. Wiseman MC. Hidradenitis suppurativa: a review. Dermatol Ther. 2004;17(1):50-4. [Medline].

  56. Lewis F, Messenger AG, Wales JK. Hidradenitis suppurativa as a presenting feature of premature adrenarche. Br J Dermatol. Oct 1993;129(4):447-8. [Medline].

  57. Farrell AM, Randall VA, Vafaee T, Dawber RP. Finasteride as a therapy for hidradenitis suppurativa. Br J Dermatol. Dec 1999;141(6):1138-9. [Medline].

  58. Barth JH. Cutaneous Virilism, Apocrine Glands and Hidradenitis Suppurativa [thesis]. London: University of London; 1992.

  59. Jemec GB, Gniadecka M. Sebum excretion in hidradenitis suppurativa. Dermatology. 1997;194(4):325-8. [Medline].

  60. Jansen I, Altmeyer P, Piewig G. Acne inversa (alias hidradenitis suppurativa). J Eur Acad Dermatol Venereol. Nov 2001;15(6):532-40. [Medline].

  61. Wasik F, Barancewicz-Losek M. Hryncewicz-Gwozdz A, Jelen M: Hidradenitis suppurativa complicated by hidradenocarcinoma. Dermatol Klin (Wroclaw). 2001;3 (Suppl 1):64.

  62. Jansen T, Plewig G. Acne inversa. Int J Dermatol. Feb 1998;37(2):96-100. [Medline].

  63. Kurzen H, Jung EG, Hartschuh W, Moll I, Franke WW, Moll R. Forms of epithelial differentiation of draining sinus in acne inversa (hidradenitis suppurativa). Br J Dermatol. Aug 1999;141(2):231-9. [Medline].

  64. Kurokawa I, Nishijima S, Kusumoto K, Senzaki H, Shikata N, Tsubura A. Immunohistochemical study of cytokeratins in hidradenitis suppurativa (acne inversa). J Int Med Res. Mar-Apr 2002;30(2):131-6. [Medline].

  65. Kurokawa I, Nishijima S, Suzuki K, et al. Cytokeratin expression in pilonidal sinus. Br J Dermatol. Mar 2002;146(3):409-13. [Medline].

  66. Kurokawa I, Nishimura K, Yamanaka K, Mizutani H, Tsubura A, Revuz J. Cytokeratin expression in squamous cell carcinoma arising from hidradenitis suppurativa (acne inversa). J Cutan Pathol. Sep 2007;34(9):675-8. [Medline].

  67. Jemec GB, Gniadecka M. Ultrasound examination of hair follicles in hidradenitis suppurativa. Arch Dermatol. Aug 1997;133(8):967-70. [Medline].

  68. Slade DE, Powell BW, Mortimer PS. Hidradenitis suppurativa: pathogenesis and management. Br J Plast Surg. Jul 2003;56(5):451-61. [Medline].

  69. Gniadecki R, Jemec GB. Lipid raft-enriched stem cell-like keratinocytes in the epidermis, hair follicles and sinus tracts in hidradenitis suppurativa. Exp Dermatol. Jun 2004;13(6):361-3. [Medline].

  70. Hurley HJ:. Axillary hyperhidrosis, apocrine bromhidrosis, hidradenitis suppurativa and familial benign pemphigus: Surgical approach. In: Roenigk RA, Roenigk HH Jr, eds. Dermatologic Surgery, Principles and Practice. NY: Marcel Dekker; 1989:717-45.

  71. Sartorius K, Lapins J, Emtestam L, Jemec GB. Suggestions form uniform outcome variables when reporting treatment effects in hidradenitis suppurativa. Br J Dermatol. 2003;149:211-3.

  72. Frohlich D, Baaske D, Glatzel M. [Radiotherapy of hidradenitis suppurativa--still valid today?]. Strahlenther Onkol. Jun 2000;176(6):286-9. [Medline].

  73. Iwasaki J, Marra DE, Fincher EF, Moy RL. Treatment of hidradenitis suppurativa with a nonablative radiofrequency device. Dermatol Surg. Jan 2008;34(1):114-7. [Medline].

  74. Bordier-Lamy F, Palot JP, Vitry F, Bernard P, Grange F. [Surgical treatment of hidradenitis suppurativa: a retrospective study of 93 cases]. Ann Dermatol Venereol. May 2008;135(5):373-9. [Medline].

  75. Buimer MG, Wobbes T, Klinkenbijl JH. Hidradenitis suppurativa. Br J Surg. Apr 2009;96(4):350-60. [Medline].

  76. Rompel R, Petres J. Long-term results of wide surgical excision in 106 patients with hidradenitis suppurativa. Dermatol Surg. Jul 2000;26(7):638-43. [Medline].

  77. Bohn J, Svensson H. Surgical treatment of hidradenitis suppurativa. Scand J Plast Reconstr Surg Hand Surg. Sep 2001;35(3):305-9. [Medline].

  78. Aksakal AB, Adisen E. Hidradenitis suppurativa: importance of early treatment; efficient treatment with electrosurgery. Dermatol Surg. Feb 2008;34(2):228-31. [Medline].

  79. Boer J, van Gemert MJ. Long-term results of isotretinoin in the treatment of 68 patients with hidradenitis suppurativa. J Am Acad Dermatol. Jan 1999;40(1):73-6. [Medline].

  80. Tanaka A, Hatoko M, Tada H, Kuwahara M, Mashiba K, Yurugi S. Experience with surgical treatment of hidradenitis suppurativa. Ann Plast Surg. Dec 2001;47(6):636-42. [Medline].

  81. Golcman R, Golcman B, Tamura BM, Nogueira MA, Zoo CM, Germano JA. Subcutaneous fistulectomy in bridging hidradenitis suppurativa. Dermatol Surg. Oct 1999;25(10):795-8. [Medline].

  82. Bodzin JH. Laser ablation of complex perianal fistulas preserves continence and is a rectum-sparing alternative in Crohn's disease patients. Am Surg. Jul 1998;64(7):627-31; discussion 632. [Medline].

  83. Lapins J, Sartorius K, Emtestam L. Scanner-assisted carbon dioxide laser surgery: a retrospective follow-up study of patients with hidradenitis suppurativa. J Am Acad Dermatol. Aug 2002;47(2):280-5. [Medline].

  84. Madan V, Hindle E, Hussain W, August PJ. Outcomes of treatment of nine cases of recalcitrant severe hidradenitis suppurativa with carbon dioxide laser. Br J Dermatol. Dec 2008;159(6):1309-14. [Medline].

  85. Hynes PJ, Earley MJ, Lawlor D. Split-thickness skin grafts and negative-pressure dressings in the treatment of axillary hidradenitis suppurativa. Br J Plast Surg. Sep 2002;55(6):507-9. [Medline].

  86. Rehman N, Kannan RY, Hassan S, Hart NB. Thoracodorsal artery perforator (TAP) type I V-Y advancement flap in axillary hidradenitis suppurativa. Br J Plast Surg. Jun 2005;58(4):441-4. [Medline].

  87. Rhode JM, Burke WM, Cederna PS, Haefner HK. Outcomes of surgical management of stage III vulvar hidradenitis suppurativa. J Reprod Med. Jun 2008;53(6):420-8. [Medline].

  88. Bong JL, Shalders K, Saihan E. Treatment of persistent painful nodules of hidradenitis suppurativa with cryotherapy. Clin Exp Dermatol. May 2003;28(3):241-4. [Medline].

  89. Buimer MG, Ankersmit MF, Wobbes T, Klinkenbijl JH. Surgical treatment of hidradenitis suppurativa with gentamicin sulfate: a prospective randomized study. Dermatol Surg. Feb 2008;34(2):224-7. [Medline].

  90. Jamshidi M, Obermeyer RJ, Govindaraj S, Garcia A, Ghani A. Acute pancreatitis secondary to isotretinoin-induced hyperlipidemia. J Okla State Med Assoc. Feb 2002;95(2):79-80. [Medline].

  91. Hofer T, Itin PH. [Acne inversa: a dapsone-sensitive dermatosis]. Hautarzt. Oct 2001;52(10 Pt 2):989-92. [Medline].

  92. Katsanos KH, Christodoulou DK, Tsianos EV. Axillary hidradenitis suppurativa successfully treated with infliximab in a Crohn's disease patient. Am J Gastroenterol. Aug 2002;97(8):2155-6. [Medline].

  93. Lebwohl B, Sapadin AN. Infliximab for the treatment of hidradenitis suppurativa. J Am Acad Dermatol. Nov 2003;49(5 Suppl):S275-6. [Medline].

  94. Rosi YL, Lowe L, Kang S. Treatment of hidradenitis suppurativa with infliximab in a patient with Crohn's disease. J Dermatolog Treat. Feb 2005;16(1):58-61. [Medline].

  95. Trent JT, Kerdel FA. Tumor necrosis factor alpha inhibitors for the treatment of dermatologic diseases. Dermatol Nurs. Apr 2005;17(2):97-107. [Medline].

  96. Sullivan TP, Welsh E, Kerdel FA, Burdick AE, Kirsner RS. Infliximab for hidradenitis suppurativa. Br J Dermatol. Nov 2003;149(5):1046-9. [Medline].

  97. Gupta AK, Skinner AR. A review of the use of infliximab to manage cutaneous dermatoses. J Cutan Med Surg. Mar-Apr 2004;8(2):77-89. [Medline].

  98. Winterfield LS, Menter A. Infliximab. Dermatol Ther. 2004;17(5):409-26. [Medline].

  99. Mekkes JR, Bos JD. Long-term efficacy of a single course of infliximab in hidradenitis suppurativa. Br J Dermatol. Feb 2008;158(2):370-4. [Medline].

  100. Fardet L, Dupuy A, Kerob D, et al. Infliximab for severe hidradenitis suppurativa: transient clinical efficacy in 7 consecutive patients. J Am Acad Dermatol. Apr 2007;56(4):624-8. [Medline].

  101. Usmani N, Clayton TH, Everett S, Goodfield MD. Variable response of hidradenitis suppurativa to infliximab in four patients. Clin Exp Dermatol. Mar 2007;32(2):204-5. [Medline].

  102. Lee RA, Dommasch E, Treat J, et al. A prospective clinical trial of open-label etanercept for the treatment of hidradenitis suppurativa. J Am Acad Dermatol. Apr 2009;60(4):565-73. [Medline].

  103. Giamarellos-Bourboulis EJ, Pelekanou E, Antonopoulou A, et al. An open-label phase II study of the safety and efficacy of etanercept for the therapy of hidradenitis suppurativa. Br J Dermatol. Mar 2008;158(3):567-72. [Medline].

  104. Zangrilli A, Esposito M, Mio G, Mazzotta A, Chimenti S. Long-term efficacy of etanercept in hidradenitis suppurativa. J Eur Acad Dermatol Venereol. Nov 2008;22(10):1260-2. [Medline].

  105. Yamauchi PS, Mau N. Hidradenitis suppurativa managed with adalimumab. J Drugs Dermatol. Feb 2009;8(2):181-3. [Medline].

  106. Jemec GB. Methotrexate is of limited value in the treatment of hidradenitis suppurativa. Clin Exp Dermatol. Sep 2002;27(6):528-9. [Medline].

  107. Russ E, Castillo M. Lumbosacral epidural abscess due to hidradenitis suppurativa. AJR Am J Roentgenol. Mar 2002;178(3):770-1. [Medline].

  108. Endo Y, Tamura A, Ishikawa O, Miyachi Y. Perianal hidradenitis suppurativa: early surgical treatment gives good results in chronic or recurrent cases. Br J Dermatol. Nov 1998;139(5):906-10. [Medline].

  109. Gupta S, Kumar B. Dorsal perforation of prepuce: a common end point of severe ulcerative genital diseases?. Sex Transm Infect. Jun 2000;76(3):210-2. [Medline].

  110. Lapins J, Ye W, Nyren O, Emtestam L. Incidence of cancer among patients with hidradenitis suppurativa. Arch Dermatol. Jun 2001;137(6):730-4. [Medline].

  111. Malaguarnera M, Pontillo T, Pistone G, Succi L. Squamous-cell cancer in Verneuil's disease (hidradenitis suppurativa). Lancet. Nov 23 1996;348(9039):1449. [Medline].

  112. Maclean GM, Coleman DJ. Three fatal cases of squamous cell carcinoma arising in chronic perineal hidradenitis suppurativa. Ann R Coll Surg Engl. Oct 2007;89(7):709-12. [Medline].

  113. Crain VA, Gulati S, Bhat S, Milner SM. Marjolin's ulcer in chronic hidradenitis suppurativa. Am Fam Physician. May 1 2005;71(9):1652, 1657. [Medline].

  114. Mandal A, Watson J. Experience with different treatment modules in hidradenitis suppuritiva: a study of 106 cases. Surgeon. Feb 2005;3(1):23-6. [Medline].

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Further Reading

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Keywords

hidradenitis suppurativa, HS, acne inversa, acne triad, acne tetrad, hidradenitis axillaris, apocrinitis, intertriginous acne, pyoderma fistulans sinifica, Verneuil's disease, Verneuil disease, dissecting cellulitis of scalp and neck, acne conglobata, follicular occlusion triad, follicular occlusion tetrad, pilonidal sinus, acneiform disorder, apocrine occlusion

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Contributor Information and Disclosures

Author

Marina Jovanovic, MD, PhD, Chief of Dermatology Ward and Contact Dermatitis Investigative Unit, Clinic of Dermatoveneroleogic Diseases, Clinical Center, Novi Sad, Serbia and Montenegro; Associate Professor in Dermatology, Medical Faculty, University of Novi Sad, Vojvodina, Serbia and Montenegro
Disclosure: Nothing to disclose.

Coauthor(s)

George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital
George Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Medical Society of New Jersey
Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Daniel Mark Siegel, MD, MS, Director, Procedural Dermatology Fellowship Program, Clinical Professor of Dermatology, Department of Dermatology, State University of New York Downstate
Daniel Mark Siegel, MD, MS is a member of the following medical societies: American Academy of Dermatology, American Academy of Facial Plastic and Reconstructive Surgery, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American College of Physician Executives, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, American Society for MOHS Surgery, and International Society for Dermatologic Surgery
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey J Miller, MD, Associate Professor of Dermatology, Penn State University College of Medicine; Staff Dermatologist, Penn State Milton S Hershey Medical Center
Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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