Determining Treatment Response to Rheumatoid Arthritis Drugs


Presence of different antibodies in the blood can influence response to abatacept regimen.

The presence of an anti-CCP antibody in the blood stream of rheumatoid arthritis (RA) patients was associated with an improved response to the T cell co-stimulation blocker abatacept during a recent trial.

However, being positive for anti-CCP antibodies did not correlate with the efficacy of a tumor necrosis factor-inhibitor (TNFi). Patients who are positive for anti-CCP are known to have a more severe form of RA.

There have even been some prior studies that have shown anti-CCP and RF antibodies as independent predictors of disease progression, while others show only anti-CCP antibodies as an independent predictor.

The study’s findings were presented at the European League Against Rheumatism Annual Congress (EULAR 2016), providing further understanding of anti-CCP status in RA patients.

“Our findings have shown that the effects of TNF inhibitors are not dependent on the ACPA antibody status,” said researcher Leslie R. Harrold. “However, the outcomes of patients receiving the T cell co-stimulation modulator abatacept were dependent on ACPA status with better responses observed in those who were positive for anti-CCP antibodies, compared to those who didn't have these antibodies.”

During the study, researchers sought to evaluate the impact anti-CCP and RF antibodies had on treatment responses separately in patients starting abatacept or TNFi. Of 566 patients who initiated abatacept, double positive status was associated with a significantly greater response compared with a double negative status on all outcomes.

Furthermore, single positive status was associated with an increased likelihood of remission compared with double negative status in abatacept users. There were no significant differences in response between anti-CCP and RF groups in the 1715 TNFi users.

When researchers examined the relationship separately, they found that the responses were driven by seropositivity to anti-CCP antibodies alone, while RF was found to not be an independent factor that influenced a response. The findings suggest that the different effects of anti-CCP status on treatment could be due to differences in the mechanism of action between the different drugs.

“These findings are exciting as anti-CCP antibodies are a marker of disease severity and detectable early in the course of the disease,” Harrold concluded. “A better understanding of the relationship between anti-CCP antibodies and treatment response has the potential to advance patient care. Specifically, patients with RA can spend years trying different treatments until their disease is properly controlled. Therefore, identifying subsets of patients likely to respond to a specific drug or class of drugs is so critical.”

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