Men with pre-existing testicular dysfunction (including renal failure) may be more susceptible to further impairment of steroidogenesis caused by medications or illnesses. HMG-CoA reductase inhibitors inhibit cholesterol synthesis and may, therefore, impair steroidogenesis, particularly because adverse events consistent with androgen deficiency (gynecomastia and impotence) have been reported. A prospective, open-label study of 25 nephrotic, hyperlipidemic men with moderate chronic renal failure treated for 12 mo with lovastatin (40 mg/d) showed no change in baseline and GnRH-stimulated LH, FSH, and testosterone levels (38). A more discerning test of testicular steroidogenesis, such as testosterone response to submaximal hCG stimulation, was not reported. Adrenal steroidogenesis (plasma cortisol before and after adrenocor-ticotropic hormone [ACTH] stimulation) was comparable with age-matched healthy controls at entry and remained unchanged by lovastatin treatment. Not surprisingly, testosterone was lower and gonadotropins were higher than in 25 age-matched untreated healthy controls before and after treatment. This study suggests that concurrent use of HMG-CoA reductase inhibitors in moderate chronic renal failure is not a major contributor to androgen deficiency.
A deleterious effect of secondary hyperparathyroidism has also been postulated as a factor contributing to uremic hypogonadism. However, a recent study examining seven men with severe secondary hyperparathyroidism before and at 3 and 6 mo after subtotal parathyroidectomy (39) reported no change in circulating LH, FSH, or testosterone before or after acute GnRH stimulation, despite dramatic reduction in circulating parathyroid hormone concentrations. These and other findings suggest that secondary hyperparathyroidism is not a major factor in the pathogenesis of uremic hypogonadism.
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