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Hidradenitis Suppurativa Workup

  • Author: Marina Jovanovic, MD, PhD; Chief Editor: William D James, MD  more...
 
Updated: May 19, 2016
 

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.

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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.

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Other Tests

Bacteriologic analysis should include bacteriologic sampling and cultivation. 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.[71] Among the most frequently found species are Staphylococcus aureus and coagulase-negative staphylococci, anaerobic streptococci (eg, microaerophilic Streptococcus milleri), and Bacteroides species.[53, 63]

The microbiologic florae are not consistent and change unpredictably.[71]

Immunohistochemical data obtained for various cytokeratins (CKs) and the 6 desmosomal cadherins (ie, desmogleins [Dsgs] 1-3, desmocollins [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.[72]

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.[72]

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.[55] 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: infundibular-like keratinized epithelium (type-A), noninfundibular keratinized epithelium (type B), and nonkeratinized epithelium (type C).[73] Types A and B were similar to the types I and II reported by Kurzen et al,[72] 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.[74]

CK expression in pilonidal sinus is comparable with that in hidradenitis suppurativa, as previously reported. Moreover, in infundibularlike epithelium, CK17 is also absent.[74]

The overlying epidermis in hidradenitis suppurativa lesions has a more undifferentiated hyperproliferative state than that found in healthy epidermis.[73] In some cases, CK19 is present in the basal layer of the epidermis, and CK19 is thought to be associated with premalignant change.[75]

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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.[71] Some evidence suggests that the occlusion of abnormal hair follicles may play an important part in the initiation of the lesions.[25, 76] Follicular occlusion was found in all specimens compared with controls and regardless of disease duration.[61] 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.[69]

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.[64] 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 inflamed.[13]

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.[41]

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.[77] 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.[72]

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.[78]

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.[72] 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.

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Staging

Clinical staging of hidradenitis suppurativa has diagnostic value. A study has shown that the soluble IL-2 receptor serum level in patients with hidradenitis suppurativa can be used as valuable marker for disease staging.[79] The Hurley clinical staging of hidradenitis suppurativa from 1989 is still relevant today; it has diagnostic value but is not suitable for monitoring the efficacy of interventions in clinical trials.[1] It is as follows:

  • First stage: Solitary/multiple, isolated abscess formation without scarring or sinus tracts
  • Second stage: Recurrent abscesses, single/multiple widely separated lesions, with sinus tract formation and cicatrization
  • Third stage: Diffuse/broad involvement or multiple interconnected sinus tracts/abscesses across the entire area

Dynamic staging system have been used for assessing differences in treatment effects.[6] Uniform outcome variables should take into account the known characteristics of hidradenitis suppurativa, including the following:[6]

  • 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.

A recently developed six-stage physician global assessment (PGA) is defined as follows:

  • Clear: No inflammatory or noninflammatory nodules
  • Minimal: Only the presence of noninflammatory nodules
  • Mild: Fewer than five inflammatory nodules or one abscess or draining fistula and no inflammatory nodules
  • Moderate: Fewer than five inflammatory nodules or one abscess or draining fistula and one or more inflammatory nodules or 2-5 abscesses or draining fistulas and fewer than 10 inflammatory nodules
  • Severe: Two to five abscesses or draining fistulas and 10 or more inflammatory nodules
  • Very severe: More than five abscesses or draining fistulas

However, a Hurley severity grade‒relevant conservative and surgical treatment for hidradenitis suppurativa is recommended.[1, 7] In order to assess any treatment effectiveness, it is very important to standardize relevant endpoints. Defined as at least a 50% reduction in total abscess and inflammatory nodule count with no increase in abscess count and no increase in draining fistula count relative to baseline at week 12, the hidradenitis suppurativa clinical response (HiSCR) is currently the most appropriate clinical endpoint to assess treatment and effectiveness for hidradenitis suppurativa treatment. It does not contradict hidradenitis suppurativa response measured by the modified Sartorius Score or PGA, but rather represents a more sensitive measure of change in disease activity, resulting in a more accurate representation of patient response and treatment evaluation. The HiSCR does not take into account the size or severity of individual lesions and does not measure how treatment response affects a patient’s level of pain or quality of life. However, the threshold of 50% reduction in total abscess and inflammatory nodule count is the defined level that is clinically appropriate and meaningful to the patient regarding improvement in quality of life and pain level.[8]

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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; Professor in Dermatology, Medical Faculty, University of Novi Sad, Vojvodina, Serbia

Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

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, Medical Society of New Jersey

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania 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, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair Research Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Andrea Leigh Zaenglein, MD Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine

Andrea Leigh Zaenglein, MD is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Received consulting fee from Galderma for consulting; Received consulting fee from Valeant for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Anacor for consulting; Received grant/research funds from Stiefel for investigator; Received grant/research funds from Astellas for investigator; Received grant/research funds from Ranbaxy for other; Received consulting fee from Ranbaxy for consulting.

Acknowledgements

Diana Fite, MD, FACEP Clinical Assistant Professor, Department of Emergency Medicine, University of Texas Medical School at Houston, Hermann Hospital

Diana Fite, MD, FACEP is a member of the following medical societies: American Association of Women Emergency Physicians, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Texas Medical Association

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; Ardelyx Ownership interest Board membership

Ravi Pokala Kiran, MBBS, MS, FRCS (Eng), FRCS (Glas) Staff Physician, Department of General Surgery, St Mary's Hospital

Disclosure: Nothing to disclose.

David L Morris, MD, PhD, FRACS Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia

David L Morris, MD, PhD, FRACS is a member of the following medical societies: British Society of Gastroenterology

Disclosure: RFA Medical None Director; MRC Biotec None Director

Naveen Pokala, MBBS, MS, FRCS Staff Physician, Department of Surgery, Bronx Lebanon Hospital

Disclosure: Nothing to disclose.

References
  1. [Guideline] Zouboulis CC, Desai N, Emtestam L, Hunger RE, Ioannides D, Juhász I, et al. European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatol Venereol. 2015 Apr. 29 (4):619-44. [Medline].

  2. Wang SC, Wang SC, Alavi A, Alhusayen R, Bashash M, Sibbald RG. Hidradenitis Suppurativa: A Frequently Missed Diagnosis, Part 2: Treatment Options. Adv Skin Wound Care. 2015 Aug. 28 (8):372-80; quiz 381-2. [Medline].

  3. van der Zee HH, Jemec GB. New insights into the diagnosis of hidradenitis suppurativa: Clinical presentations and phenotypes. J Am Acad Dermatol. 2015 Nov. 73 (5 Suppl 1):S23-6. [Medline].

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

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

  6. 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.

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

  8. Kimball AB, Jemec GB, Yang M, Kageleiry A, Signorovitch JE, Okun MM, et al. Assessing the validity, responsiveness and meaningfulness of the Hidradenitis Suppurativa Clinical Response (HiSCR) as the clinical endpoint for hidradenitis suppurativa treatment. Br J Dermatol. 2014 Dec. 171 (6):1434-42. [Medline].

  9. Blok JL, Spoo JR, Leeman FW, Jonkman MF, Horváth B. Skin-Tissue-sparing Excision with Electrosurgical Peeling (STEEP): a surgical treatment option for severe hidradenitis suppurativa Hurley stage II/III. J Eur Acad Dermatol Venereol. 2015 Feb. 29 (2):379-82. [Medline].

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

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

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

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

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

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

  16. Tierney E, Mahmoud BH, Hexsel C, Ozog D, Hamzavi I. Randomized control trial for the treatment of hidradenitis suppurativa with a neodymium-doped yttrium aluminium garnet laser. Dermatol Surg. 2009 Aug. 35(8):1188-98. [Medline].

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

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

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

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

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

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

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

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

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

  26. Attanoos RL, Appleton MA, Douglas-Jones AG. The pathogenesis of hidradenitis suppurativa: a closer look at apocrine and apoeccrine glands. Br J Dermatol. 1995 Aug. 133(2):254-8. [Medline].

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

  28. Gulliver W, Zouboulis CC, Prens E, Jemec GB, Tzellos T. Evidence-based approach to the treatment of hidradenitis suppurativa/acne inversa, based on the European guidelines for hidradenitis suppurativa. Rev Endocr Metab Disord. 2016 Feb 1. 35(2 Pt 1):191-4. [Medline].

  29. 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. 2008 Oct. 59(4):596-601. [Medline].

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

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

  32. Wang SC, Wang SC, Sibbald RG, Alhusayen R, Bashash M, Alavi A. Hidradenitis Suppurativa: A Frequently Missed Diagnosis, Part 1: A Review of Pathogenesis, Associations, and Clinical Features. Adv Skin Wound Care. 2015 Jul. 28 (7):325-32; quiz 333-4. [Medline].

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

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

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

  36. Blok JL, Boersma M, Terra JB, Spoo JR, Leeman FW, van den Heuvel ER, et al. Surgery under general anaesthesia in severe hidradenitis suppurativa: a study of 363 primary operations in 113 patients. J Eur Acad Dermatol Venereol. 2015 Aug. 29 (8):1590-7. [Medline].

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

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

  39. Hughes R, Kelly G, Sweeny C, Lally A, Kirby B. The medical and laser management of hidradenitis suppurativa. Am J Clin Dermatol. 2015 Apr. 16 (2):111-23. [Medline].

  40. Saunte DM, Boer J, Stratigos A, et al. Diagnostic delay in hidradenitis suppurativa is a global problem. Br J Dermatol. 2015 Dec. 173 (6):1546-9. [Medline].

  41. 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. 1997 Mar. 84(3):375-6. [Medline].

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

  43. 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. 1993 Sep. 8(3):117-9. [Medline].

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

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

  46. 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. 2001 Jul. 52(7):642-5. [Medline].

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

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

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

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

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

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

  53. 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. 1999 Jan. 140(1):90-5. [Medline].

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

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

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

  57. Pink AE, Simpson MA, Desai N, Trembath RC, Barker JN. Gamma-Secretase mutations in hidradenitis suppurativa: new insights into disease pathogenesis. J Invest Dermatol. 2013 Mar. 133(3):601-7. [Medline].

  58. 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. 2006 Jun. 126(6):1302-6. [Medline].

  59. 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. 2001 May. 81(2):96-9. [Medline].

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

  61. 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. 2008 Apr. 158(4):691-7. [Medline].

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

  63. 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].

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

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

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

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

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

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

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

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

  72. 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. 1999 Aug. 141(2):231-9. [Medline].

  73. 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. 2002 Mar-Apr. 30(2):131-6. [Medline].

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

  75. 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. 2007 Sep. 34(9):675-8. [Medline].

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

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

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

  79. Matusiak L, Bieniek A, Szepietowski JC. Soluble interleukin-2 receptor serum level is a useful marker of hidradenitis suppurativa clinical staging. Biomarkers. 2009 Sep. 14(6):432-7. [Medline].

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

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

  82. van Rappard DC, Mooij JE, Mekkes JR. Mild to moderate hidradenitis suppurativa treated with local excision and primary closure. J Eur Acad Dermatol Venereol. 2012 Jul. 26(7):898-902. [Medline].

  83. Yamashita Y, Hashimoto I, Matsuo S, Abe Y, Ishida S, Nakanishi H. Two-stage surgery for hidradenitis suppurativa: staged artificial dermis and skin grafting. Dermatol Surg. 2014 Feb. 40(2):110-5. [Medline].

  84. Jianbing T, Biao C, Qin L, Yanhong W. Topical negative pressure coupled with split-thickness skin grafting for the treatment of hidradenitis suppurativa: a case report. Int Wound J. 2013 Jul 9. [Medline].

  85. Busnardo FF, Coltro PS, Olivan MV, Busnardo AP, Ferreira MC. The thoracodorsal artery perforator flap in the treatment of axillary hidradenitis suppurativa: effect on preservation of arm abduction. Plast Reconstr Surg. 2011 Oct. 128(4):949-53. [Medline].

  86. Alharbi M, Perignon D, Assaf N, Qassemyar Q, Elsamad Y, Sinna R. Application of the inner arm perforator flap in the management of axillary hidradenitis suppurativa. Ann Chir Plast Esthet. 2014 Feb. 59(1):29-34. [Medline].

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

  88. 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. 2002 Aug. 47(2):280-5. [Medline].

  89. 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. 2008 Dec. 159(6):1309-14. [Medline].

  90. 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. 2002 Sep. 55(6):507-9. [Medline].

  91. 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. 2005 Jun. 58(4):441-4. [Medline].

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

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

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

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

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

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

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

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

  100. Kimball AB, Sobell JM, Zouboulis CC, Gu Y, Williams DA, Sundaram M, et al. HiSCR (Hidradenitis Suppurativa Clinical Response): a novel clinical endpoint to evaluate therapeutic outcomes in patients with hidradenitis suppurativa from the placebo-controlled portion of a phase 2 adalimumab study. J Eur Acad Dermatol Venereol. 2015 Jul 22. 27(6):528-9. [Medline].

  101. Yildiz H, Senol L, Ercan E, Bilgili ME, Karabudak Abuaf O. A prospective randomized controlled trial assessing the efficacy of adjunctive hyperbaric oxygen therapy in the treatment of hidradenitis suppurativa. Int J Dermatol. 2016 Feb. 55 (2):232-7. [Medline].

  102. Jemec GB. Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012 Jan 12. 366(2):158-64. [Medline].

  103. Boer J, Nazary M. Long-term results of acitretin therapy for hidradenitis suppurativa. Is acne inversa also a misnomer?. Br J Dermatol. 2011 Jan. 164(1):170-5. [Medline].

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

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

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

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

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

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

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

  111. Grant A, Gonzalez T, Montgomery MO, Cardenas V, Kerdfel FA. Infliximab therapy for patients with moderate to severe hidradenitis suppurativa: A randomized, double blind, placebo-control crossover trial. J Am Acad Dermatol. 2010. 62:205-17.

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

  113. Ingram JR, McPhee M. Management of hidradenitis suppurativa: a U.K. survey of current practice. Br J Dermatol. 2015 Oct. 173 (4):1070-2. [Medline].

  114. Ingram JR, Woo PN, Chua SL, Ormerod AD, Desai N, Kai AC, et al. Interventions for hidradenitis suppurativa: a Cochrane systematic review incorporating GRADE assessment of evidence quality. Br J Dermatol. 2016 Jan 23. 32(2):204-5. [Medline].

  115. 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. 2009 Apr. 60(4):565-73. [Medline].

  116. 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. 2008 Mar. 158(3):567-72. [Medline].

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

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

  119. Boer J, Jemec GB. Resorcinol peels as a possible self-treatment of painful nodules in hidradenitis suppurativa. Clin Exp Dermatol. 2010 Jan. 35(1):36-40. [Medline].

 
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Vulvar hidradenitis suppurativa.
Vulvar and inguinal indurations.
Sinus tract.
Draining sinus tract.
Axillary hidradenitis suppurativa in a patient with pyoderma gangrenosum.
Close-up view of axillary hidradenitis suppurativa in a patient with pyoderma gangrenosum.
Submammary hidradenitis suppurativa in a patient with pyoderma gangrenosum.
Double-ended-comedones. Hidradenitis suppurativa in a patient with pyoderma gangrenosum.
Inguinal hidradenitis suppurativa in a patient with pyoderma gangrenosum.
Close-up view of inguinal hidradenitis suppurativa in a patient with pyoderma gangrenosum.
Pyoderma gangrenosum in a patient with hidradenitis suppurativa.
Close-up view of pyoderma gangrenosum in a patient with hidradenitis suppurativa.
Coexisting hidradenitis suppurativa and pyoderma gangrenosum.
Coexisting hidradenitis suppurativa and pyoderma gangrenosum.
Hidradenitis suppurativa in a patient with pyoderma gangrenosum.
 
 
 
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