title: Remodeling of the muscle layer (detrusor muscle) of hyperactive bladder disease in patients with benign prostatic hyperplasia.
abstract: We studied remodeling of the detrusor of hyperactive bladder in patients with benign prostatic hyperplasia. Detrusor remodeling was caused by degenerative and atrophic changes and elimination of smooth muscle cells, compensatory hypertrophy of remaining cells, and diffuse or focal-diffuse replacement fibrosis. Focal or diffuse infiltration of all layers of the detrusor with lymphocytes and plasma cells is an important pathologic feature of hyperactive bladder. These changes correlated with pronounced remodeling of the glandular and fibrotic-muscular layers in the prostate gland. We have identified stereotyped patterns of the intracellular reorganization of smooth muscle cells in the detrusor of hyperactive bladder and in the prostate with benign prostatic hyperplasia, which represent both the compensatory and adaptive reactions (hypertrophied cells with minor ultrastructural changes) and the types of smooth muscle cell injury ("dark" electron-dense cells and "light" cells with pronounced lysis of myofilaments and discomplexation of organelles).
authors.affiliation: Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk, Russia. pathol@soramn.ru
authors.forename: L M
authors.initials: LM
authors.lastname: Nepomnyashchikh
authors.forename: E L
authors.initials: EL
authors.lastname: Lushnikova
authors.forename: A I
authors.initials: AI
authors.lastname: Neimark
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001837:Body Weights and Measures; D005355:Fibrosis; D006801:Humans; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009130:Muscle, Smooth / Q000166:cytology* / Q000502:physiology; D010950:Plasma Cells / Q000378:metabolism; D011470:Prostatic Hyperplasia / Q000150:complications / Q000473:pathology*; D053201:Urinary Bladder, Overactive / Q000209:etiology / Q000473:pathology*