Wien Med Wochenschr. 1993;143(14-15):395-7.

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Abstract

Severe osteoporosis represents a major complication of corticosteroid (CST) excess. Steroid-induced osteoporosis is characterized by both increased bone resorption and inhibition of bone formation. Excessive bone resorption is attributed to hyperparathyroidism which is secondary to calcium malabsorption. Calcium and vitamin D supplementation or treatment with inhibitors of bone resorption are of benefit but they usually lead to further inhibition of bone formation. The inhibition of bone formation in CST treated patients is due in part to suppression of adrenal androgen secretion. Thus the suppressed circulating levels of osteocalcin, a biochemical marker of osteoblast activity, in patients on CST can be reverted to normal by administration of anabolic steroids. In a prospective controlled trial in patients on long-term CST therapy we have observed that nandrolone decanoate therapy, 50 mg intramuscularly every 3 weeks for 18 months, induces a transient increase in bone mass within the first 6 months of treatment and prevent further losses thereafter. The sequential biochemical changes indicate that nandrolone decanoate in patients on CST inhibits bone resorption without affecting or even increasing bone formation. Furthermore in patients on CST treatment the virilizing activity of nandrolone decanoate was virtually negligible at least within the 18 months of treatment. These results indicate that anabolic steroid administration may represent a rational and convenient strategy for preventing and treating CST-induced osteoporosis.
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