Forty-five postmenopausal osteoporotic women with at least one osteoporotic vertebral crush fracture were randomized into three treatment groups. Each patient was on calcitonin, 50 U, on alternate days for 2 weeks monthly (350 U/month), and 500 mg/day oral calcium supplementation. In group II, this therapy was supplemented with phosphate (750 mg/day), and in group III, norandrostenolone decanoate (50 mg/month) was added to the calcitonin+calcium therapy. Bone mineral content, by single photon absorptiometry, of the radius midshaft and distal site (3 cm), as well as the lumbar and metacarpal radiomorphometrical indices were estimated seminannually. The therapeutic trial lasted 36 months except in the phosphate supplementation group, where, due to unfavorable results, treatment was discontinued after 24 months. Calcitonin practically prevented further bone loss for 24 months even in this relatively small and intermittent dosage. Phosphate supplementation was without benefit; however, according to the majority of the examined parameters, combination of calcitonin with the anabolic steroid norandrostenolone decanoate extended efficacy up to 36 months. This latter combination seems to be a promising, relatively inexpensive therapeutic regimen in the treatment of established postmenopausal osteoporosis.

Greater than normal bone mineral content, bone width of the radius measured by photon absorptiometry and bone mineral content to bone width ratio found in women with hyperostosis frontalis interna pointed on a generalized alteration of the skeletal system. An increase in serum dehydroepiandosterone, its sulphate and testosterone levels and a significant correlation between serum free dehydroepiandosterone and bone mineral content in subjects without any sign of hirsutism or obesity suggested an involvement of androgens in pathogenesis of this metabolic bone disorder.

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Osteoporosis in one of the most common complications of streak gonad syndrome (SGS), however, its pathogenesis is still unclear. To test whether SGS is associated with calcitonin (CT) deficiency, 11 affected individuals and 8 age-matched healthy women were studied. Calcium, 3.6 mg/kg b.w. as a 10% solution of calcium chloride, was given intravenously for 3 minutes. Serum levels of CT and calcium were measured before and at 5, 30, 60, and 120 minutes after the injection. There was a statistically significant rise in serum calcium levels both in the control subjects and patients with SGS, with significantly lower levels prior to and at 30, 60, and 120 minutes following calcium load in the control group. The CT rise following calcium load was also significant at 5, 30, and 60 minutes in the controls and at 5 and 30 minutes in patients with SGS, with a significantly lower baseline and 30, 60, and 120 minutes levels in the latter group. Maximum levels of calcium and CT occurred 5 minutes after the calcium load and were statistically indistinguishable. There were no significant differences in either the calcium or the CT incremental changes between the two groups. These findings are consistent with decreased basal (and 30-120 minute) CT levels in SGS and suggest that CT deficiency may be involved in the development of osteoporosis in patients with SGS. The possible causal relationship of estrogen deficiency to the reduced CT levels in SGS is discussed.