Authors: Albrecht W Popp Juerg Isenegger Elizabeth M Buergi Ulrich Buergi Kurt Lippuner
Publish Date: 2006/02/11
Volume: 15, Issue: 7, Pages: 1035-1049
Abstract
Glucocorticosteroidinduced osteoporosis GIOP is the most frequent of all secondary types of osteoporosis The understanding of the pathophysiology of glucocorticoid GC induced bone loss is of crucial importance for appropriate treatment and prevention of debilitating fractures that occur predominantly in the spine GIOP results from depressed bone formation due to lower activity and higher death rate of osteoblasts on the one hand and from increased bone resorption due to prolonged lifespan of osteoclasts on the other In addition calcium/phosphate metabolism may be disturbed through GC effects on gut kidney parathyroid glands and gonads Therefore therapeutic agents aim at restoring balanced bone cell activity by directly decreasing apoptosis rate of osteoblasts eg cyclical parathyroid hormone or by increasing apoptosis rate of osteoclasts eg bisphosphonates Other therapeutical efforts aim at maintaining/restoring calcium/phosphate homeostasis improving intestinal calcium absorption using calcium supplementation vitamin D and derivates and avoiding increased urinary calcium loss using thiazides prevent or counteract a secondary hyperparathyroidism Bisphosphonates particularly the aminobisphosphonates risedronate and alendronate have been shown to protect patients on GCs from further bone loss and to reduce vertebral fracture risk Calcitonin may be of interest in situations where bisphosphonates are contraindicated or not applicable and in cases where acute pain due to vertebral fracture has to be managed The intermittent administration of 134parathormone may be an appealing treatment alternative based on its documented anabolic effects on bone resulting from the reduction of osteoblastic apoptosis Calcium and vitamin D should be a systematic adjunctive measure to any drug treatment for GIOP Based on currently available evidence fluoride androgens estrogens opposed or unopposed cannot be recommended for the prevention and treatment of GIOP However substitution of gonadal hormones may be indicated if GCinduced hypogonadism is present and leads to clinical symptoms Data using the SERM raloxifene to treat or prevent GIOP are lacking as are data using the promising bone anabolic agent strontium ranelate Kyphoplasty performed in appropriately selected osteoporotic patients with painful vertebral fractures is a promising addition to current medical treatment
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