Antibodies Predict Response to Biologics in RA | Arthritis Information

Patients with rheumatoid arthritis who develop antibodies against the tumor necrosis factor (TNF) antagonist infliximab (Remicade) are also likely to develop antibodies against adalimumab (Humira), a Dutch cohort study found.

During 28 weeks of follow-up, 33% of patients with anti-infliximab antibodies also developed anti-adalimumab antibodies, compared with only 18% of patients who had never received a TNF blocker (P=0.039), according to Geertje M. Bartelds, MD, of the Jan van Breemen Institute in Amsterdam, and colleagues.

Patients who developed antibodies to both TNF blockers also had a smaller decrease in their disease activity score compared with TNF-naive patients (1.1 versus 1.7 points, P=0.007), a difference that persisted after adjustment for baseline disease activity (95% CI −1.166 to −0.351, P<0.0001), the researchers reported online in the Annals of the Rheumatic Diseases.

Some 30% to 40% of patients with rheumatoid arthritis fail to respond to anti-TNF therapy. Some, though not all of this failure can be explained by immunogenic antibody responses to the drugs.

When patients don't respond to one TNF antagonist, doctors frequently switch to another, the researchers noted, but the choice of drug is generally not evidence-based, and there is considerable variability in subsequent response.

To investigate factors determining response after switching, Bartelds and colleagues prospectively followed a consecutive cohort of 235 patients with rheumatoid arthritis being treated with adalimumab.

http://www.medpagetoday.com/Rheumatology/Arthritis/18141So, it seems this would also be true of Enbrel and Humira, because if you develop antibodies to one TNF, you are likely to develop antibodies to other TNF's.

The findings of this study suggest that nonresponders could be treated according to their antibody status, with antibody-positive patients likely deriving greater benefit from switching to a less immunogenic drug acting on the same principle, or from optimizing concomitant methotrexate therapy.

In nonresponders without antibodies, it may be more useful and cost-effective to try a drug with a different mechanism of action, they suggested.