Prevention of corticosteroid-induced osteoporosis with salmon calcitonin in sarcoid patients

We assessed the rates of vertebral fracture in patients with postmenopausal osteoporosis. Forty-five patients were not treated (91 person-years of observation); 59 were treated conventionally, with calcium (alone or combined with estrogen) or vitamin D or both (218 years); and 61 were treated with sodium fluoride combined with conventional therapy (251 years). The fracture rate (per thousand person-years) was 834 in untreated patients, 419 in those given calcium with or without vitamin D, 304 in those given fluoride and calcium with or without vitamin D, 181 in those given estrogen and calcium with or without vitamin D, and 53 in those given fluoride, estrogen, and calcium with or without vitamin D. It was reduced in all treatment groups (P less than 0.001 for calcium and P less than 1 x 10(-6) for other combinations); fluoride (one years of treatment) and estrogen (but not vitamin D) independently reduced the rate from that observed with calcium alone (P less than 0.001). The combination of calcium fluoride, and estrogen was more effective than any other combination (P less than 0.001). These results provide grounds for optimism about the efficacy of combinations of available agents with sodium fluoride for fracture in postmenopausal osteoporosis.

All cases of endometrial cancer occurring among the residents of an affluent retirement community were compared with controls chosen from a roster of all women in the same community. Evidence of estrogen and other drug use and of selected medical conditions was obtained from three sources: medical records of the principal care facility, interviews, and the records of the local pharmacy. The risk ratio for any estrogen use was estimated from all available evidence to be 8.0 (95 per cent confidence interval, 3.5 to 18.1). and the for conjugated estrogen use to be 5.6 (95 per cent confidence interval, 2.8 to 11.1). Increased risk from estrogens was shown for invasive as well as noninvasive cancer, and a dose-response effect was demonstrated. For an estrogen user, the risk from endometrial cancer appeared to exceed by far the base-line risk from any other single cancer.

Parathyroid function and calcium metabolism were studied in 44 patients under glucocorticoid therapy (steroid group) and in 25 control subjects. Nephrogenous cAMP and serum immunoreactive parathyroid hormone levels in the steroid group were significantly higher than those in control subjects (p less than 0.001). Nephrogenous cAMP in the steroid group correlated positively with prednisolone dosage (r = 0.424, p less than 0.01), and most patients who showed obvious elevations of nephrogenous cAMP had received over 10 mg/day of prednisolone for at least 2 mo. Fasting urinary calcium in the steroid group [166.1 +/- 78.5 (+/- SD) mg/g creatinine] was about 2 times greater than that in control subjects (74.1 +/- 35.6) (p less than 0.001). Fasting urinary calcium in control subjects correlated negatively with nephrogenous cAMP (r = -0.486, p less than 0.02). In contrast, these values in steroid group showed significant positive correlation (r = 0.631, p less than 0.001), suggesting that increased urinary calcium excretion is an important factor in the development of secondary hyperparathyroidism. Elevated nephrogenous cAMP and serum immunoreactive parathyroid hormone levels decreased after the administration of trichlormethiazide and/or 1 alpha hydroxy-vitamin D3. We conclude that increased urinary calcium excretion plays an important role in the development of secondary hyperparathyroidism in patients under glucocorticoid therapy and that the administration of thiazide and/or vitamin D could improve the secondary hyperparathyroidism caused by glucocorticoid therapy.