medwireNews: Treatment with adalimumab does not improve pain or inflammation among patients with erosive hand osteoarthritis (OA) and magnetic resonance imaging (MRI)-defined synovitis, phase III trial results suggest.
Previous data have “consistently shown” that tumor necrosis factor (TNF) inhibition does not improve erosive hand OA symptoms, but a post-hoc analysis suggested that adalimumab may suppress disease progression in a subset of patients with synovitis at baseline, say Graeme Jones (University of Tasmania, Hobart, Australia) and study co-authors.
However, the present HUMOR trial findings indicate that “TNF α may not be the right treatment target, even in those with definite synovitis,” they write.
As reported in Osteoarthritis and Cartilage, the investigators randomly assigned 43 patients to receive adalimumab 40 mg or placebo every other week for 12 weeks, followed by an 8-week washout period. The treatment groups were then switched over for the final 12 weeks of the study.
Patients receiving adalimumab did not experience significantly greater improvements in visual analog scale (VAS) pain scores from baseline to week 12 than patients receiving placebo, with corresponding mean decreases of 3.2 versus 0.8 mm on a 100 mm scale.
Jones and team note that patients who received adalimumab during the first 12 weeks of the study experienced a 1.9 mm decrease in the average VAS pain score, but this increased by 5.1 mm after switching to placebo in the second treatment phase. By comparison, participants who started with placebo treatment experienced a mean 5.0 mm decrease in score that decreased by a further 4.2 mm when they switched to adalimumab. However, they say that “[t]hese changes are small and are not considered clinically important.”
There were also no significant differences in patient-reported function and stiffness, and MRI-detected synovitis and bone marrow lesions, among patients treated with adalimumab versus placebo.
“Anti-TNF α therapies have been very successful for treating pain and structural disease progression in inflammatory arthritis such as RA [rheumatoid arthritis],” write the researchers. They hypothesize that unlike RA, “inflammation in OA may be present as a result of joint damage as opposed to primary immune activation,” and may not be driving disease pathogenesis.
And the team concludes that “pain and inflammation are not responsive to TNF α inhibition in this patient population.”
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