Introduction. One of the key characteristics of the lower urinary tract is its hormone dependence. Pathophysiological mechanisms of lower urinary tract symptoms in patients with benign prostatic hyperplasia include infravesical obstruction, formation of a fibrous framework in the urinary bladder, disruption of the urothelial barrier, and changes in the nervous and vascular networks of the pelvis. However, to date, there is a lack of data on the pathophysiological relationship between testosterone deficiency and morpho-functional changes of the bladder. The purpose of this study is to investigate the role of age-related hypogonadism in the pathogenesis of morpho-functional changes in the urinary bladder among patients with benign prostatic hyperplasia. The results of the examination of 70 patients with benign prostatic hyperplasia, aged from 47 to 83 years (mean age 67.94 ± 7.42 years), were analyzed. The first group consisted of 20 patients, whose disease duration was 4 ± 1.8 years. They had an International Prostate Symptom Score (IPSS) of 16 ± 4.5 points, a maximum flow rate (Qmax ) of 15.8 ± 2.4 ml/s, an average flow rate (Qave) of 12.8 ± 2.8 ml/s, and no post-void residual. The second group included 20 patients with incomplete bladder emptying, with a disease duration of 5.8 ± 3.5 years. Their IPSS was 26 ± 3.9 points, Qmax was 10.8 ± 2.5 ml/s, Qave was 4.4 ± 1.4 ml/s, and post-void residual was 150.1 ± 80.8 ml. The third group comprised 30 patients who had undergone cystostomy, with a disease duration of 10.6 ± 3.3 years. Before cystostomy, their IPSS was 33.1 ± 1.88 points, and post-void residual was 1093.3 ± 458.8 ml. During surgery, all patients with benign prostatic hyperplasia were taken a biopsy from the anterior wall of the bladder. In benign prostatic hyperplasia patients in the stage of bladder compensation, the level of testosterone was 15.39±1.44 nmol/l, the Aging Males Symptoms indicator was 24.80±5.78 points. Morphometric analysis of bladder tissue demonstrated the following: the diameter of the lumen of arterioles was 27.96±2.14 μm, the thickness of the arteriole wall was 16.03±1.83 μm, the Kernoghan index for arterioles was 1.22±0.17, the specific gravity of connective tissue made 4.48±0.82%, the diameter of SMCs was 7.46±1.66 μm. In benign prostatic hyperplasia patients in the stage of bladder subcompensation, the level of testosterone was 10.92±2.24 nmol/l, the Aging Males Symptoms index was 37.9±8.0 points. Morphometric analysis of bladder tissue revealed the following: the diameter of the arteriole lumen was 23.78±1.62 μm, the thickness of the arteriole wall was 18.30±1.32 μm, the Kernoghan index for arterioles was q1.65±0.18, the specific gravity of the connective tissue made up 11.80±1.22%, the diameter of SMCs was 7.07±1.93 μm. In benign prostatic hyperplasia patients in the stage of bladder decompensation, the level of testosterone is 9.66±2.13 nmol/l, the Aging Males Symptoms index is 55.80±6.69 points. Morphometric analysis of bladder tissue showed the following: the diameter of the arteriole lumen was 19.0±2.08 μm, the thickness of the arteriole wall – 21.01±1.57 μm, the Kernoghan index for arterioles was 2.41±0.32, the specific gravity of the connective tissue made up 29. 46±1.35%, the diameter of SMCs was 4.75±1.87 μm. The obstructive component is not the only causal factor of bladder decompensation in patients with benign prostatic hyperplasia. A decrease in the level of testosterone triggers a cascade of pathological processes that negatively affect the morpho-functional state of the prostate gland and worsen the results of surgical treatment of patients with benign prostatic obstruction.
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Open Access
Jun 1, 2024
Farhan Khan + 5
