The role of correction of hypogonadism in the treatment and prophylaxis of urolithiasis in the men presenting with metabolic syndrome

Abstract

Abdominal obesity is a major component of metabolic syndrome (MS) considered to be the key factor contributing to the development of testosterone deficiency (hypogonadism) in men. Bearing in mind the etiopathogenetic relationship between MS and urolithiasis (UL), the present study was undertaken for the purpose of elucidating the role of the main biochemical risk factors of metabolic syndrome in men, evaluating the influence of correction of hypogonadism on these factors, and optimization of the treatment and prevention of MS in these patients. The study included 90 men presenting with hypogonadism in whom the serum levels and renal excretion of the main lithogenic substances (uric acid, calcium, phosphates, magnesium) and urine pH were measured. At the first stage of the study, the patients were allocated to two groups. Group 1 was comprised of 52 patients with UL, group 2 consisted of 38 patients without UL. The patients of group 1 were found to suffer hyperuricemia (the serum uric acid levels 430 mcmol/l and higher). The patients of both groups exhibited hyperuricosuria (daily uric acid excretion over 4.13 mmol/24 hr) with the urine pH value of 5.5 and lower. The serum uric acid concentration was shown to positively correlate with the insulin and C-peptide levels. At the second stage of the study, 65 randomly selected patients were divided into two groups in one of which (n=40) they were given testosterone therapy. Compensation of hypogonadism in these patients was associated with a significant reduction of the serum uric acid levels and its daily excretion, an increase and normalization of urine pH, and a rise in the serum magnesium concentration, Similar significant changes of the same parameters were absent in the control subjects (n=25). Moreover, testosterone therapy improved characteristics of lipid and carbohydrate metabolism, caused reduction in the body weight, BMI, and the severity of insulin resistance.