medwireNews: Denosumab, a humanized monoclonal antibody against receptor activator of nuclear factor κB ligand (RANKL), may prevent the development of diabetes, report researchers in JAMA Network Open.
Individuals who adhered to denosumab for the treatment of osteoporosis had a 16% lower risk for incident diabetes than individuals who discontinued denosumab, observe Edward Chia-Cheng Lai (National Cheng Kung University, Tainan City, Taiwan) and co-investigators.
The researchers say that these results have “clinical and public health importance” in light of the “high osteoporosis prevalence, the extensive use of antiosteoporosis medications, and the negative effect of diabetes on both patient health and health care system burdens in the global aging population.”
The team used data from the National Health Insurance Research Database of Taiwan to identify patients who were prescribed denosumab 60 mg for osteoporosis between 2012 and 2019. The patients were free from diabetes and malignancy at the time of treatment.
For the study, 34,255 individuals each were included in the denosumab adherence group (received a second dose 180 days after initial dose with additional 45 grace days) and the comparison group that discontinued denosumab (did not receive second dose within 225 days after initial dose). The mean age of the participants at recruitment was 77.7 years and the majority (84.3%) were women. The participants were followed-up for a mean of 1.9 years.
The incidence of diabetes was lower in patients who continued than discontinued denosumab treatment (35.9 vs 43.6 per 1000 person–years), giving a significant hazard ratio (HR) for diabetes of 0.84.
This gave an estimated number need to treat with denosumab of 130 to prevent an additional case of diabetes, the researchers write.
Stratified analyses confirmed a significantly lower risk for diabetes with continued denosumab treatment in individuals aged at least 65 years (HR=0.80), men and women (HR=0.85 and 0.81, respectively), and irrespective of comorbidities, such as dyslipidemia, hypertension, ischemic heart disease, and kidney failure (HR=0.79–0.86). A significantly lower risk for diabetes with continued denosumab use persisted in sensitivity analyses as well as after taking into account use of other antiosteoporosis medications (HR=0.82) or death as a competing risk (HR=0.83).
Pointing at the putative biological mechanism for prevention of diabetes with denosumab, Lai and colleagues discuss that “mitigating RANKL using denosumab may reduce subacute inflammation and improve insulin resistance.”
They conclude that “[t]hese findings may help physicians choose an appropriate antiosteoporosis medication for patients with osteoporosis while also considering a medication associated with lowering diabetes risk.”
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