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New research published in the Journal of Bone and Mineral Research suggests that non-steroidal anti-inflammatory drugs (NSAIDs) may block the beneficial effects of bisphosphonates.
In the study of 5,212 community-dwelling women aged 75 years and older, the use of NSAIDs did not seem to have a direct impact on individuals’ bone fracture risk, but the medications appeared to negate the bone-protective effects of the oral bisphosphonate clodronate on preventing osteoporotic fractures.
“We need to exercise some caution in extrapolating these data to more widely used bisphosphonates in osteoporosis, but given that concomitant usage of NSAIDs and bisphosphonates is relatively common, this could have major clinical consequences and result in a failure to reduce fracture risk as much as we had hoped,” said senior author Eugene McCloskey, MD, Northern General Hospital, Sheffield, United Kingdom.
Only verified, incident fractures were included in the analysis. Of the women, 1,082 (20.8%) reported use of NSAIDs at baseline. In an adjusted model, NSAID use was associated with a significant increase in osteoporotic fracture risk over the 3-year study period (hazard ratio [HR] = 1.27; 95% confidence interval [CI], 1.01-1.62; P = .039). However, this increase in risk was not statistically significant in the placebo group (HR = 1.11; 95% CI, 0.81-1.52).
In women receiving clodronate, the effect of the bisphosphonate to reduce osteoporotic fracture risk was not observed in those receiving NSAIDs (HR = 0.95; 95% CI, 0.65-1.41; P = .81) in contrast to those not using NSAIDs (HR = 0.71; 95% CI, 0.58-0.89; P = .002).
In a subset of women in which hip bone mineral density (BMD) was repeated at 3 years, BMD loss during clodronate therapy was greater among women receiving NSAIDs than in nonusers (total hip, -2.75% vs -1.27%, P = .078; femoral neck, -3.06% vs -1.12%, P = .028), and was not significantly different from that observed in women receiving placebo.
“The efficacy of the bisphosphonate, clodronate, to reduce fracture risk was largely negated in those receiving NSAIDs,” the authors wrote. “Although the mechanism is unclear, this clinically significant observation requires exploration in studies of commonly used bisphosphonates.”
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