Late-onset hypogonadism is defined as a combination of low testosterone levels and typical symptoms and signs. A major area of uncertainty is whether testosterone concentrations are always really sufficient to fully reflect Leydig cell (dys)function. Mild testicular alteration could be diagnosed only by additional biochemical markers, such as luteinizing hormone (LH) and 25-hydroxyvitamin D levels. These markers help in identifying the so-called “subclinical” hypogonadism (normal testosterone, high LH levels). Patients with hypogonadism have frequently low levels of 25-hydroxyvitamin D due to impairment of the hydroxylating enzyme CYP2R1 in the testis. However, no data have been published dealing with the best treatment option (cholecalciferol – the vitamin D precursor, or calcidiol - 25-hydroxylated form of vitamin D) in these patients. We studied 66 patients with classic hypogonadism (total testosterone <12 nmol l-1, LH ≥8 IU l-1) (n=26) and subclinical hypogonadism (total testosterone ≥12 nmol l-1, LH ≥8 IU l-1) (n=40) and low 25-hydroxyvitamin D (<50 nmol l-1). Subjects received cholecalciferol (5000 IU per week) (n=20) or calcidiol (4000 IU per week) (n=46), and 25-hydroxyvitamin D and PTH were evaluated after three months of therapy. Supplementation with calcidiol significantly increased 25-hydroxyvitamin D and significantly decreased PTH levels in both group of men with hypogonadism (primary, n=16 and subclinical, n=30), whereas supplementation with cholecalciferol did not modify their levels. This study shows for the first time that the administration of the 25-hydroxylated form of vitamin D (calcidiol), and not the administration of the precursor cholecalciferol, restores 25-hydroxyvitamin D levels in subjects with hypogonadism.

Keywords: insulin‑like factor 3; late‑onset hypogonadism; male hypogonadism; testosterone; Vitamin D

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