DISRUPTION OF THE UROTHELIAL BARRIER UNDER BENIGN PROSTATIC HYPERPLASIA AS A COMPONENT OF BLADDER DECOMPENSATION

Abstract

Introduction. The urothelial barrier resists the aggressive effect of urine on the bladder tissues. Chronic retention of urine causes the development of an infectious and non-infectious inflammatory process with metaplasia and desquamation of the urothelial layer of the bladder. With long-term infravesical obstruction, the contact density between urothelial cells is disturbed, which leads to the loss of the barrier function of the mucous membrane of the urinary bladder.
 The purpose of the study is to investigate the role of urothelial barrier disruption in the development of urinary bladder decompensation in patients with BPH.
 Materials and methods. 70 patients with BPH were selected, their average age was 67.94±7.42 years. They underwent a bladder biopsy during the operation, followed by a pathomorphological examination.
 According to clinical manifestations, patients were divided into three groups: group I included 20 patients with bladder compensation (I-PSS – 16±4.5, Qmax – 15.8±2.4 ml/s, Qave – 12.8±2.8 ml/s, without post void residual); group II involved 20 patients with bladder subcompensation (I-PSS – 26±3.9, Qmax – 10.8±2.5 ml/s, Qave – 4.4±1.4 ml/s, post void residual – 150.1 ±80.8 ml.); and III group included 30 patients with bladder decompensation (before the cystostomy I-PSS – 33.1±1.88, post void residual – 1093.3±458.8 ml).
 Results. In the compensation stage of the bladder there is found multilayer transitional cell urothelium that often forms folds, causing pseudoepithelial outgrowths. The detrusor is represented by hypertrophied smooth muscle cells, with the phenomena of moderate hydropic dystrophy in individual myocytes, with isolated small foci of sclerosis. In the stage of bladder subcompensation we observe foci of desquamation of the surface layers of the urothelium and dystrophic changes in epitheliocytes. Areas of atrophy are combined with foci of hyperplasia of epitheliocytes with stratification of the epithelium (up to 14 - 18 layers or more). The lamina propria of the mucous membrane is swollen in most cases, the formation of lacuniform slits is seen. There are often foci of lymphoplasmacytic infiltration. The detrusor is mostly represented by hypertrophied smooth muscle cells, a significant number of which have signs of hydropic dystrophy.
 In the stage of bladder decompensation the foci of total desquamation of all layers of the urothelium can be observed; pronounced dystrophic changes of epitheliocytes also take place. The own plate of the mucous membrane is sharply thickened: due to the formation of numerous lacuniform slits it has a porous appearance. Erosive changes in the mucous membrane of the urinary bladder are accompanied by pronounced sclerosis of the stroma. In places of desquamation of the urothelium, submucosal foci of sclerosis are observed, which penetrate into the detrusor. The latter is represented by hypotrophied smooth muscle cells with signs of hydropic dystrophy. Due to the massive proliferation of connective tissue, muscle fibres are divided into separate bundles. Diffuse lymphoplasmacytic infiltration is observed in all layers of the bladder.
 Conclusion: The results of pathomorphological studies in the context of clinical and functional characteristics enables to distinguish three stages of SM remodelling in BPH: compensation, subcompensation and decompensation. Long-term chronic retention of urine causes a violation of the urothelial barrier, urine impregnation of all layers of the CM with the development of aseptic inflammation. A progressive increase in the specific weight of connective tissue, dystrophic changes in myocytes and nerve fibres become the cause of decompensation of the CM with a violation of the contractile ability of the detrusor.