Abstract
Purpose:
A retrospective study was performed to identify potential metabolic abnormalities and inflammatory abnormalities associated with benign prostatic hyperplasia (BPH) secondary to bladder calculi.
Materials and Methods:
This study enrolled 646 patients with bladder calculi between 2008 and 2022, including 314 patients with benign prostatic hyperplasia (BPH) and 332 without BPH. Demographic characteristics, serum biochemical parameters, prostate volume, maximum bladder calculus diameter, and randomized urinary metabolic profiles were compared between the two groups.
Results:
BPH was associated with increased aspartate aminotransferase/alanine aminotransferase (mean 1.2 vs 1.1, P < 0.05), lower cholinesterase (mean 7240.5 vs 7778.4, P < 0.01), increased systolic pressure (mean 137.2 vs 133.4, P < 0.01). Patients with BPH were significantly older and had higher systolic blood pressure compared to non-BPH patients. BPH group exhibited significantly lower levels of albumin/globulin ratio, cholinesterase, phosphorus, triglycerides, platelet count, neutrophil count, and white blood cell count, while demonstrating higher aspartate aminotransferase/alanine aminotransferase ratio, mean corpuscular volume, monocyte ratio, and urinary red blood cell count. Prostate volume was proportional to body weight and crystal count. Lower phosphorus (OR = 0.207; 95%CI = 0.068, 0.635; P < 0.01) and higher age (OR = 1.065; 95%CI = 1.041, 1.090; P < 0.001) were associated with BPH.
Conclusions:
Advanced age was identified as a significant risk factor for prostate hyperplasia in patients with bladder calculi, whereas elevated phosphorus levels emerged as a protective factor. The pathogenesis of BPH secondary to bladder calculi appears to be multifactorial, primarily influenced by metabolic abnormalities and inflammatory processes. These findings provide valuable insights for the clinical assessment and management of BPH secondary to bladder calculi.
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