Comparative cancer risk associated with methotrexate, other non-biologic and biologic disease-modifying anti-rheumatic drugs Daniel H. Solomon, MD, MPH, Joel M. Kremer, MD, Mark Fisher, MD, Jeffrey R. Curtis, MD, MPH, Victoria Furer, MD, MPH, Leslie R. Harrold, MD, MPH, Marc C. Hochberg, MD, MPH, George Reed, PhD, Peter Tsao, MSc, Jeffrey D. Greenberg, MD, MPH Seminars in Arthritis and Rheumatism Volume 43, Issue 4, Pages 489-497 (February 2014) DOI: 10.1016/j.semarthrit.2013.08.003 Copyright © 2014 Elsevier Inc. Terms and Conditions
Fig. 1 This figure illustrates the assembly of the study cohort. The 15,659 included subjects accounted for 17,393 DMARD exposure periods. After trimming, 6806 patients were included with 179 definite or probable cancers. Excluded DMARDs include cyclosporine, gold, minocycline, and d-penicillamine. Seminars in Arthritis and Rheumatism 2014 43, 489-497DOI: (10.1016/j.semarthrit.2013.08.003) Copyright © 2014 Elsevier Inc. Terms and Conditions
Fig. 2 This Forest plot shows the hazard ratios (HR) for the primary analyses across the different cancer end points for each exposure group compared with methotrexate. These analyses were conducted in the propensity score trimmed cohort and include the propensity score as a continuous variable. (A) The adjusted results for nbDMARDs compared with methotrexate. (B) TNF antagonists compared with methotrexate. (C) Abatacept compared with methotrexate. (D) Rituximab compared with methotrexate. Models for other nbDMARDs and TNF antagonists not only included the propensity score but also age, alcohol use, and erosion status. Models for abatacept and rituximab included the propensity score and age, alcohol use, and prior methotrexate. Seminars in Arthritis and Rheumatism 2014 43, 489-497DOI: (10.1016/j.semarthrit.2013.08.003) Copyright © 2014 Elsevier Inc. Terms and Conditions