Reduced calcitonin reserve in young hypogonadic osteoporotic men.

Calcitonin is a potent inhibitor of bone resorption and in both sexes, plasma levels progressively decrease with age: therefore, a relative deficiency of calcitonin may be involved in the pathogenesis of osteoporosis in the elderly. Calcitonin plasma levels of young hypogonadic men with osteoporosis are significantly lower than controls: the hypothesis that the decreased calcitonin plasma levels in the elderly are due to a reduced secretory capacity of the "C" cells of the thyroid gland, related to age, does not explain the low calcitonin plasma levels found in young hypogonadic osteoporotic men. Our hypothesis is that gonadal steroid deficiency may participate in the mechanisms regulating calcitonin secretion. Therefore, we studied ten males affected by hypogonadotropic hypogonadism and ten normal men, of comparable age, as controls: we measured plasma levels of testosterone, 17 beta estradiol, androstenedione and calcitonin, and the response of calcitonin to an i.v. bolus of pentagastrin, a well known "C" cells stimulatory drug. Testosterone and calcitonin plasma levels and the response of calcitonin to pentagastrin were also evaluated after 6 months of replacement therapy with testosterone. Basal levels of testosterone, 17 beta estradiol, androstenedione and calcitonin, and the response of calcitonin to pentagastrin, are significantly lower in our patients than in controls, demonstrating that hypogonadotropic hypogonadic subjects have a lower secretory reserve of calcitonin. After testosterone therapy the basal calcitonin plasma levels and its response to pentagastrin stimulus did not differ from controls, suggesting that gonadal steroids influence the calcitonin secretion and reserve. Our data cannot clarify whether osteoporosis of hypogonadotropic hypogonadic patients is related to androgen or estrogen deficiency; however, they suggest that the mechanisms by which gonadal steroid influence bone metabolism may involve calcitonin secretion.

Testosterone and calcitonin plasma levels in hypogonadal osteoporotic young men.

The aim of this study was to ascertain whether there was an interrelationship between male osteoporosis, calcitonin and androgens. Ten young hypogonadal osteoporotic men were studied: testosterone and calcitonin plasma levels were measured before and after therapy with testosterone enanthate (200 mg im every three weeks for four months). In these patients testosterone and calcitonin plasma levels were significantly lower than controls, before therapy (p less than 0.001 and p less than 0.01 respectively). Testosterone treatment significantly increased (p less than 0.05) serum calcitonin. The conclusion was that androgen deficiency may cause osteoporosis also by decreasing calcitonin secretion.

Twenty-four hour variations of triiodothyronine (T3) levels in patients who had thyroid ablation for thyroid cancer, receiving T3 as suppressive treatment.

Measurements of serum triiodothyronine (T3) concentrations were made in 46 patients who had thyroid ablation for thyroid cancer and who were receiving T3 three times a day as suppressive treatment. In all patients thyrotropin (TSH) suppression was confirmed by the inhibition of TSH response to thyrotropin releasing hormone (TRH). The suppressive dose of T3 varied from 40 to 100 micrograms/day (mean +/- SD 72.39 +/- 13.07 micrograms/day). Related to body weight the dose varied from 0.95 to 1.35 micrograms/kg/day (mean +/- SD 1.13 +/- 0.13 micrograms/kg/day). In ten hospitalized patients serum T3 levels were measured at hourly intervals from 08:00 to 23:00. Before the first dose of T3, serum T3 levels were 153 +/- 43 mg/100 ml; after T3 the levels increased promptly reaching after 4 h a peak of 264 +/- 90 ng/100 ml. Afterwards T3 levels showed a similar peak after each dose: 262 +/- 77 and 266 +/- 78 ng/100 ml, slightly decreasing in the intervals between the doses: 227 +/- 63 and 255 +/- 69 ng/100 ml. After the last peak T3 levels showed a slow decline during the night. TSH response to TRH was completely inhibited both at 08:00 and at 16:00. In 36 outpatients T3 levels were measured twice a day and T3 levels were found similar to the ones of the first group. In these patients also TSH response to TRH evaluated at 08:00 was completely inhibited. No important side effect was noted in both groups of patients.