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Immunohistochemical evaluation of epidermal proliferation, differentiation and melanocytic density in symmetrical acrokeratoderma
Author(s) -
Yang P.P.,
Peng J.,
Wu Y.Y.,
Liu Z.,
Sheng P.,
Zhou Y.,
Li S.J.,
Fan Y.M.
Publication year - 2017
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/ced.13118
Subject(s) - involucrin , filaggrin , immunohistochemistry , keratinocyte , keratin , loricrin , acanthosis , epidermis (zoology) , hyperplasia , pathology , hyperkeratosis , biology , medicine , dermatology , atopic dermatitis , cell culture , anatomy , genetics
Summary Background Symmetrical acrokeratoderma ( SAK ) is characterized by brown to black hyperkeratotic patches on acral regions. Although epidermal hyperkeratosis and acanthosis are consistent pathological changes, the nature of epidermal hyperplasia is unknown. Aim To evaluate epidermal proliferation and differentiation and melanocytic density in skin lesions of SAK . Methods Expression of keratin 10 (K10), K14, K16, involucrin, filaggrin, Ki‐67, and Melan‐A was detected by immunohistochemistry in eight patients with SAK , seven patients with ichthyosis vulgaris ( IV ) and six healthy controls ( HC s). Results Expression of K14, K16, involucrin and filaggrin was upregulated in patients with SAK compared with patients with IV and the HC s ( P < 0.01–0.05), but K10 expression was similar for the three groups ( P > 0.05). Numbers of Ki‐67+ and Melan‐A+ cells were higher in patients with SAK than in patients with IV and the HC s ( P < 0.05). Conclusions These results demonstrate that excessive keratinocyte proliferation and abnormal differentiation contribute to epidermal hyperplasia, while melanocytic proliferation is responsible for the pigmented lesions in SAK .