What causes hidradenitis suppurativa?

Hidradenitis suppurativa (HS)--a rather common, very chronic and debilitating inflammatory skin appendage disorder with a notoriously underestimated burden of disease--has long been a playground for the high priests of nomenclature: Ask a bunch of eminent dermatologists and skin pathologists to publicly share their thoughts on what causes HS, and they will soon get entrenched in a heated debate on whether this historical term is a despicable misnomer. Fortunately, the recently founded Hidradenitis Suppurativa Foundation (HSF; http://www.hs-foundation.org), to which EXP DERMATOL serves as home journal, has broken with this unproductive tradition and has encouraged publication of the current CONTROVERSIES feature. This is exclusively devoted to discussing the pathobiology of this chronic neutrophilic folliculitis of unknown origin. Although traces of terminological bickering remain visible, it does the HS experts in our virtual debate room credit that they engage in a constructive and comprehensive dissection of potential pathogenesis pathways that may culminate in the clinical picture we know under the competing terms HS or acne inversa. These experts sketch more often complementary than mutually exclusive pathogenesis scenarios, and the outlines of a conceivable consensus on the many open pathobiology questions begin to emerge in these CONTROVERSIES. Hopefully, this heralds a welcome new tradition: to get to the molecular heart of HS pathogenesis, which can only be achieved by a renaissance of solid basic HS research, as the key to developing more effective HS therapy.

Cytokeratin expression in subungual squamous cell carcinoma.

Cytokeratin expression in subungual squamous cell carcinoma was investigated in order to evaluate the origin and state of differentiation of the tumour. The tumour nests contained cytokeratin 14, 16 and 17, which were also expressed in the nail bed. Therefore, cytokeratin expression in subungual squamous cell carcinoma may reflect its indolent clinical prognosis.

Keratinizing squamous epithelium associated with Syringocystadenoma papilliferum differentiates towards infrainfundibulum: case report with immunohistochemical study of cytokeratins.

We describe a case of Syringocystadenoma papilliferum (SCAP) with keratinizing squamous epithelium in a 26-year-old female presenting with a dark brown to black nodule on her forehead. After surgical excision, the specimen was examined immunohistochemically using antibodies against cytokeratin (CK) 1, 8, 10, 14, 17, 18 and 19. Within the keratinizing squamous epithelium, CK1, 10, 14 and 17 were present, whereas the other CKs were absent. Based on CK expression, keratinizing squamous epithelium in SCAP seems to differentiate towards the infrainfundibulum.

Trichilemmoma: an immunohistochemical study of cytokeratins.

BACKGROUND: The histogenesis of trichilemmoma remains unclear. OBJECTIVES: To clarify the histogenesis of trichilemmoma by evaluating its cytokeratin (CK) expression. METHODS: In three cases of trichilemmoma, CK expression was studied immunohistochemically using seven antikeratin antibodies against CK1, 10, 14-17 and 19, respectively. RESULTS: CK1 and CK10 were present in keratinizing ductal epithelium. CK14 was present in the whole layer. CK15 was present in suprabasal layers in two cases. CK16 was present in the suprabasal layer, but was absent in keratinizing ductal epithelium. CK17 was present in suprabasal layers and the sebaceous duct-like structure. CK19 was totally absent. CONCLUSIONS: These results showed that trichilemmoma may differentiate mainly towards two directions: infundibular keratinization and proliferation of the outer root sheath with undifferentiated and pluripotent characteristics.

A therapy-resistant chronic leg ulcer treated successfully with topical basic fibroblast growth factor.

We report a patient with rheumatoid arthritis who had a chronic leg ulcer with long-standing resistance to therapy. Topical basic fibroblast growth factor (bFGF) at a dose of 30 micrograms/day for 3 months was clinically effective in reducing the ulcer area by promoting angiogenesis, re-epithelization, granulation and scar formation. bFGF may be an effective treatment for therapy-resistant leg ulcers.

Immunohistochemical study of cytokeratins in hidradenitis suppurativa (acne inversa).

In 14 cases of hidradenitis suppurativa, cytokeratin (CK) expression was studied immunohistochemically, using six antikeratin antibodies against CK1, CK10, CK14, CK16, CK17 and CK19, respectively. The draining sinus tract epithelium of hidradenitis suppurativa lesions was divided into three components: infundibular-like keratinized epithelium (type A), non-infundibular keratinized epithelium (type B), and non-keratinized epithelium (type C). In type A samples, CK17 (which is found in normal infundibulum) was not detected, suggesting fragility of this epithelial type. Keratin expression in types B and C epithelia was similar to that observed in the outer root sheath in normal hair follicles. Our results suggest that the draining sinus epithelium may possess characteristics of fragility, undifferentiation and hyperproliferation, as shown with CK expression.

Cytokeratin expression in pilonidal sinus.

BACKGROUND: Pilonidal sinus (PS) is considered to belong in the category of follicular occlusion diseases (acne triad). OBJECTIVES: The aim of our study was to elucidate the pathogenesis of PS by evaluating its cytokeratin (CK) expression. METHODS: CK expression in nine cases of PS was studied immunohistochemically using six antikeratin antibodies. RESULTS: Infundibular-like epithelium contained CK1, 10 and 14 similar to normal infundibulum, but it did not contain CK17. In non-infundibular-like epithelium, CK14, 16 and 17 were detected similar to that in normal outer root sheath. CK expression in PS was similar to that in hidradenitis suppurativa, suggesting that sinus epithelium may be fragile, hyperproliferative and undifferentiated. CONCLUSIONS: PS can be classified in the same entity as follicular occlusion diseases based on CK expression.

Varicella zoster virus antigens in the epidermis of patients with herpes zoster before and after treatment with acyclovir: an immunohistochemical study.

Using a monoclonal antibody to varicella zoster virus (VZV), an immunohistochemical study was performed before and after treatment with acyclovir (750 mg/day intravenously for 5 - 7 days) to investigate the distribution of VZV antigens in the epidermis of four in-patients with herpes zoster, and to correlate their presence with clinical manifestations of the disease. Biopsy specimens were obtained from epidermal lesions on admission to hospital prior to acyclovir administration, and again following treatment. In all cases, VZV antigens were found extensively in the erythematous and vesicular lesions before treatment, but they were not detected 5 - 7 days later in the ulcerative, crusted or pigmented lesions after acyclovir therapy. Further controlled studies will be necessary to compare the distribution of epidermal VZV antigens in acyclovir-treated patients with that in a placebo group to determine whether the loss of VZV antigens was due to acyclovir or to a natural decrease over time.