Hidradenitis suppurativa (acne inversa): early inflammatory events at terminal follicles and at interfollicular epidermis* |
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Authors: | Maximilian von Laffert Peter Helmbold Johannes Wohlrab Eckhard Fiedler Volker Stadie Wolfgang Christian Marsch |
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Affiliation: | 1. This investigation is part of M.v.L.’s MD thesis at Martin‐Luther‐University Halle‐Wittenberg, Halle (Saale) 2008 and furthermore has been presented at The Hidradenitis Suppurativa Foundation: Abstracts from ‘Directions 2006: The First International Hidradenitis Suppurativa Research Symposium’. Dessau, Germany, March 30 – April 2 2006 [Exp Dermatol 2006;2. 15: 478‐482].;3. Department of Dermatology and Venerology, Martin‐Luther‐University Halle‐Wittenberg, Halle (Saale), Germany |
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Abstract: | Please cite this paper as: Hidradenitis suppurativa (acne inversa): early inflammatory events at terminal follicles and at interfollicular epidermis. Experimental Dermatology 2010; 19: 533–537. Abstract: Hidradenitis suppurativa (acne inversa) is a chronic suppurative and scarring inflammatory disease with predilection in the apocrine gland‐bearing areas. Histological investigations in the 1990s showed keratotic occlusion of the terminal follicle structure to be the initial cause. Our investigations describe and reproduce the morphology and try to figure out very early lesions of HS. A total of 262 operative specimens from 60 patients were investigated by routine histology and 11 operative specimens by immunohistochemistry: HS is dominated by a heterogeneous histological image. 82% of the surgical specimens showed mild or pronounced follicular hyperkeratosis, whereas an isotopic hyperplasia of follicular epithelium was evident in 77%. Pronounced perifolliculitis was seen in 68% and rupture of the follicle structure in 28%. Features which had not so far been described in detail were: epidermal psoriasiform hyperplasia (43%) and subepidermal interfollicular inflammatory infiltrate (78%). In all 11 specimens, immunohistochemical investigations showed a perifollicular and subepidermal inflammation of CD‐3‐, CD‐4‐, CD‐68‐, CD‐79‐ and CD‐8‐cells, the latter with a striking selective epitheliotropism. To conclude, we could show follicular hyperkeratosis and lymphocytic perifollicular inflammation as early patterns in pathogenesis, whereas rupture of the follicle structure takes place later. Finally, it seems that there are two hot spots of inflammatory events (perifollicular and subepidermal) composed of a comparable inflammatory cell mixture. The CD‐8 cell epitheliotropism (follicular and epidermal) described here and its influence in follicular hyperkeratosis, in hyperplasia of follicular epithelium and in epidermal psoriasiform hyperplasia will be of further interest, for instance, concerning early pharmacological intervention. |
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Keywords: | CD‐8 cell epitheliotropism epidermal psoriasiform hyperplasia follicular hyperkeratosis hidradenitis suppurativa (acne inversa) hyperplasia of follicular epithelium |
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