PROSPECTIVE CASE-CONTROL STUDY TO DETERMINE THE EFFECT OF LOVASTATIN ON SERUM TESTOSTERONE AND CORTISOL CONCENTRATIONS IN HYPERLIPIDEMIC NEPHROTIC PATIENTS WITH CHRONIC-RENAL-FAILURE

Citation
A. Segarra et al., PROSPECTIVE CASE-CONTROL STUDY TO DETERMINE THE EFFECT OF LOVASTATIN ON SERUM TESTOSTERONE AND CORTISOL CONCENTRATIONS IN HYPERLIPIDEMIC NEPHROTIC PATIENTS WITH CHRONIC-RENAL-FAILURE, Nephron, 73(2), 1996, pp. 186-190
Citations number
27
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00282766
Volume
73
Issue
2
Year of publication
1996
Pages
186 - 190
Database
ISI
SICI code
0028-2766(1996)73:2<186:PCSTDT>2.0.ZU;2-L
Abstract
In order to investigate the effects of lovastatin on adrenal and gonad al function, we prospectively determined the basal and gonadorelin-sti mulated concentrations of testosterone, follicle-stimulating hormone ( FSH) and luteinizing hormone (LH) and the cortisol response to adrenoc orticotropic hormone (ACTH) in a sample of 25 male patients with advan ced chronic renal failure, hypercholesterolemia and proteinuria. Hormo ne studies were done prior to and after lovastatin treatment. The valu es of these patients were compared with those of a matched healthy con trol group. Before starting treatment with lovastatin, the patients sh owed significantly lower testosterone concentration and higher LH conc entration than the control group. After stimulation with gonadorelin, they also showed a lower increase in testosterone and LH. After 12 mon ths of lovastatin treatment, a significant decrease in the concentrati on of cholesterol, LDL C, VLDL C and apo B was observed, but neither t he basal testosterone concentration nor the response to gonadorelin st imulation was modified, Before treatment, basal and ACTH-stimulated se rum cortisol levels did not differ from those of the control group. Af ter lovastatin treatment, neither the basal serum cortisol levels nor the response to ACTH was modified, We conclude that in the patients st udied, although the decrease in testosterone concentration may be part ially attributable to a decrease in its synthesist lovastatin treatmen t does not increase testosterone deficit. This is either because this drug does not inhibit gonadal hydroxymethylglutaryl CoA reductase at t he dose given or because the cholesterol which LDL C provides the cell with is enough to maintain testosterone synthesis.