Channeling Bias and Cancer Risk with Biologic or Targeted Synthetic DMARDs Save
A retrospective US administrative claims cohort study of Rheumatoid arthritis (RA) patients on tumor necrosis factor inhibitors (TNFis), non-TNFi biologics, or Janus kinase inhibitors (JAKis) found a statistically significantly higher risk of incident cancer in patients receiving rituximab, abatacept, or JAKis (compared with TNFis).
New initiations of TNFis, abatacept, interleukin 6 inhibitors (IL-6is), rituximab, or JAKis in RA were observed for outcomes of incident cancer, excluding nonmelanoma skin cancer, after at least 90 days and within 2 years of drug initiation. Outcomes were associated with the most recent drug exposure.
From a total of 25 305 RA patients included, there were 20 586 TNFi exposures (74%), 2570 JAKi exposures (9%), 2255 abatacept exposures (8%), 1182 rituximab exposures (4%), and 1068 IL-6i exposures (4%). Cancer risk (by multivariable Cox proportional hazards regression analysis) showed :
- rituximab incident cancer was higher than TNFis (hazard ratio [HR], 1.91; 95% CI, 1.17-3.14)
- abatacept CA risk (HR, 1.47; 95% CI, 1.03-2.11)
- JAKis CA risk (HR, 1.36; 95% CI, 0.94-1.96)
These findings are likely to represent channeling bias, as in the first first 2 years of use, rituximab, abatacept, and JAKis demonstrated higher cancer incidence rates compared to TNFi. The data is clear that rituximabs incident cancer risk is channeling bias, rather than from the drug itself.
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