In a nutshell
This paper studied the effect of elagolix on bone density.
Endometriosis occurs when tissue that normally lines the uterus grows outside of the uterus. There are various types of drugs available to treat endometriosis. However, some of these drugs can cause gradual bone loss.
Elagolix is a drug that is given orally. It is suggested that elagolix could minimize bone loss and reduce endometriosis-associated pain. Thus, the effect of elagolix on bone loss was compared with another drug called subcutaneous depot medroxyprogesterone acetate (Depo-Provera).
Methods & findings
Patients were evaluated in three groups; 32 patients received 150 mg of elagolix daily, 54 patients received elagolix 75 mg twice daily and 37 patients received subcutaneous depot medroxyprogesterone acetate. All patients received a scan which measures bone density.
After 24 weeks, decrease in bone density was similar among patients receiving the different treatments. Bone density of the spine decreased by 11% in patients receiving elagolix daily, 1.29% in patients receiving elagolix twice daily and 0.99% in patients receiving subcutaneous acetate.
Overall, patients in the different treatment groups had similar levels of endometriosis pain. All treatment groups showed improvements in pelvic pain throughout the treatment period. Patients receiving elagolix twice daily had the best improvements in pelvic pain compared to the other patients. The use of painkillers was similar among the three treatment groups.
The overall occurrence of adverse events (undesired effect of treatment) was similar in the three treatment groups. Patients receiving elagolix most commonly experienced headache, nausea, and infection. Patients receiving subcutaneous acetate most commonly experienced headache, nausea, infection, and mood swings.
The bottom line
The authors concluded that elagolix had minimal contribution to bone loss over 24 weeks but was effective in treating pain.
The fine print
Further studies are warranted.
Published By :
Reproductive sciences (Thousand Oaks, Calif.)
Nov 01, 2014