Effects of Etidronate Therapy on Osteoporosis in Spinal Cord Injury Patients

Kim, Sang Yoon; Kim, Chang Pyo; Kang, Bong Goo; Lee, Yang Gyun

Abstract

One of the sequelae of spinal cord trauma which start soon after the onset of injury is the loss of the calcium from bone. Bone mineral and matrix resorption causes negative calcium balance, and eventually osteoporosis. Etidronate disodium(etidronate) is an oral diphosphonate compound known to reduce bone resorption through the inhibition of osteoclasic activity. Since continuous oral treatment with high doses of etidronate may lead to the impairment of bone mineralization and the cessation of bone remodeling, a ideal therapeutic regimen consist of the intermittent cyclical administration of the diphosphonate in a dose that inhibits bone resorption. To assess the effect of etidronate on bone metabolism and bone mineral density after spinal cord injury, we studied two groups of 7 spinal cord injury(SCI) patients with etidronate and 7 SCI patients without etidronate. Seven patients of treatment group received oral etidronate (5 mg/kg/day) for 2 weeks followed by a 10-week period in which no drugs were given. This sequence was repeated 4 times, for a total of 48 weeks. The results showed that the patients receiving etidronate had siginificant decrease in the serum osteocalcin(OC), urine deoxypyridinoline(D-PYD) level but no increase in their mean bone density. We can carefully conclude that intermittent cyclical therapy with etidronate siginificantly reduces bone metabolic rate and inhibit bone mineral loss on osteoporosis in spinal cord injury patients.