Apoptosis and apoptotic pathway in actinic prurigo by immunohistochemistry.
Med Oral Patol Oral Cir Bucal. 2015 Nov 30;:0
Authors: Cuevas-González JC, Vega-Memíje ME, García-Vázquez FJ, Rodríguez-Lobato E, Farfán-Morales JE
Abstract
BACKGROUND: Actinic prurigo (AP) is an idiopathic photodermatosis, this entity requires exposure to UV-B and -A to develop lesions. Apoptosis is a physiological death program that can be initiated by a permanently active mechanism (extrinsic pathway) or irreparable damage (intrinsic pathway).
MATERIAL AND METHODS: Descriptive study, the sample size comprised 64 paraffin blocks of tissue with a diagnosis of AP. In H&E-stained slides, the diagnosis of AP was corroborated, and 1-µm-thick sections were processed for immunohistochemistry (IHC). A database was constructed with SPSS version 20, Inc., Chicago, IL, USA, and descriptive statistics were analyzed by X2 test and comparison of means.
RESULTS: A total of 64 cases were processed, of which 40 (62.5%) were cheilitis AP and 24 (37.5%) were AP in the skin. Of the 40 cheilitis samples, 27 were positive for Bcl-2 and caspase 3 (67.5%), p53 was expressed in 30 (75%). Of the skin lesions, p53 and caspase 3 were expressed in 18 of 24 cases (75%), and 13 were positive for Bcl-2 (54%).
CONCLUSIONS: We propose that apoptosis is the last step in the type IV subtype a-b hypersensitivity response-activation of the intrinsic pathway indicates that external factors, such as UV-A and -B are the trigger.
PMID: 26615506 [PubMed - as supplied by publisher]
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