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Zoledronic Acid Prevents Poststroke Bone Loss


 

HARROGATE, ENGLAND — A single injection of zoledronic acid can help counteract the loss of bone mass associated with acute stroke and reduce the likelihood of osteoporotic fractures if given soon after the event, a study has shown.

Patients injected with the long-acting, highly potent bisphosphonate within 35 days after suffering a stroke lost significantly less hip bone mineral density than matched control patients who received a placebo, reported Kenneth Poole, B.M., in a presentation at the annual conference of the National Osteoporosis Society.

The findings suggest that taking measures to prevent bone loss as a routine part of stroke management could significantly reduce the high rate of hip fractures among stroke survivors, Dr. Poole said.

“We know that osteoporosis is a significant complication of stroke, particularly when patients become fully or partly immobilized,” said Dr. Poole. “When someone is put to bed and has an immobilized limb, the cells that break down bone are overactive.” The risks are exacerbated by stroke-related lower-limb and vision problems, which lead to more falls and fractures.

Previous studies have shown that stroke survivors are more than four times as likely to suffer hip fractures than individuals in an age-matched reference population.

Most victims of stroke are already at risk for osteoporosis because of their age—more than half of all strokes occur in people older than 70—thus “they can ill afford to lose further bone, said Dr. Poole, who conducted the study with colleagues from the University of Cambridge, England.

The investigators randomly assigned 16 patients to receive 4 mg of zoledronic acid (Zometa) or placebo by intravenous injection within 35 days of acute stroke. All patients also received daily oral calcium and vitamin D supplementation. Bone mineral density (BMD) measurements were obtained in the hemiplegic and unaffected total hip region of all participants at baseline and at months 6 and 12.

At 1 year, patients in the placebo group had a significantly greater reduction of BMD in both hips, compared with those in the zoledronic acid group. The mean percentage decrease in BMD at the hemiplegic and unaffected hips, respectively, of the control patients was 10.2% and 6.0%. By contrast, the patients treated with zoledronic acid group had no decrease in BMD at either site. Zoledronic acid was well tolerated and associated with no serious adverse events. Dr. Poole reported no financial interests relating to zoledronic acid or its manufacturer, Novartis.