Inhibition of Sclerostin May Increase Cardiovascular Risk
SOST genetic variants linked to lower risk for fracture and osteoporosis but higher risk for MI, major CV AEs
THURSDAY, June 25, 2020 (HealthDay News) -- Inhibition of sclerostin with romosozumab may increase cardiovascular risk, according to research published in the June 24 issue of Science Translational Medicine.
Jonas Bovijn, M.B.Ch.B., from the University of Oxford in the United Kingdom, and colleagues conducted a meta-analysis of published and unpublished cardiovascular outcome trial data of romosozumab and examined the potential association between genetic variants that mimic therapeutic inhibition of sclerostin and the risk for cardiovascular disease.
The researchers observed a probable higher risk for cardiovascular events with romosozumab in a meta-analysis of up to three randomized controlled trials. Scaled to equivalent romosozumab doses, the SOST genetic variants were associated with a lower risk for fracture and osteoporosis and with an increased risk for myocardial infarction and/or coronary revascularization and major adverse cardiovascular events. There was an association for the same variants with an increased risk for type 2 diabetes mellitus and higher systolic blood pressure and central adiposity.
"Our results warrant a rigorous assessment of the effect of romosozumab (and other sclerostin inhibitors in clinical development) on cardiovascular disease and cardiometabolic risk factors," the authors write. "This adds valuable information to whether pharmacological inhibition of sclerostin should be pursued as a therapeutic strategy for the prevention of fracture."
Several authors disclosed financial ties to the biopharmaceutical industry.