摘要
Aim： To investigate the frequency of atypical adenomatous hyperplasia （AAH） and its associations with benign prostate hypertrophy （BPH） and latent histological carcinoma of the prostate （LPC） in autopsy material. Methods： Two hundred and twelve prostate specimens obtained from autopsy material were subjected to whole mount analysis in an attempt to investigate the associations among BPH, AAH and LPC. Results： Most histological carcinomas and AAH lesions were found in enlarged prostates with intense hypertrophy. No statistically significant relation was found between BPH and the main characteristics of LPC, such as tumor volume, histological differentiation and biological behavior. Our data regarding multi-focal tumors showed a tendency for multi-focal carcinomas to develop in larger prostates, and a tendency of AAH lesions to develop in larger prostates. No statistically significant relation was found between AAH and LPC. Conclusion： There seems not any causative aetiopathogenetical or topographical relation between AAH lesions and prostate adenocarcinoma. AAH lesion seems to be a well-defined mimicker of prostatic adenocarcinoma, and the reported association of AAH with prostatic carcinoma could probably be an epiphenomenon.
Aim： To investigate the frequency of atypical adenomatous hyperplasia （AAH） and its associations with benign prostate hypertrophy （BPH） and latent histological carcinoma of the prostate （LPC） in autopsy material. Methods： Two hundred and twelve prostate specimens obtained from autopsy material were subjected to whole mount analysis in an attempt to investigate the associations among BPH, AAH and LPC. Results： Most histological carcinomas and AAH lesions were found in enlarged prostates with intense hypertrophy. No statistically significant relation was found between BPH and the main characteristics of LPC, such as tumor volume, histological differentiation and biological behavior. Our data regarding multi-focal tumors showed a tendency for multi-focal carcinomas to develop in larger prostates, and a tendency of AAH lesions to develop in larger prostates. No statistically significant relation was found between AAH and LPC. Conclusion： There seems not any causative aetiopathogenetical or topographical relation between AAH lesions and prostate adenocarcinoma. AAH lesion seems to be a well-defined mimicker of prostatic adenocarcinoma, and the reported association of AAH with prostatic carcinoma could probably be an epiphenomenon.
