Rishi J Desai1, Jaya K Rao1, Richard A Hansen1, Gang Fang1, Matthew Maciejewski1, Joel Farley2. 1. From the Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill; Department of Medicine, Division of General Internal Medicine, Duke University Medical Center, Durham, North Carolina; Department of Pharmacy Care Systems, Harrison School of Pharmacy, Auburn University, Auburn, Alabama, USA.R.J. Desai, PhD, Graduate Student, Research Fellow, Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, University of North Carolina, and Department of Medicine, Division of Pharmacoepidemiology and Pharmacoeconomics, Harvard Medical School, Brigham and Women's Hospital; J.K. Rao, MD, Associate Professor; G. Fang, PhD, Assistant Professor; J.F. Farley, PhD, Associate Professor, Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, University of North Carolina; R.A. Hansen, PhD, Professor, Department of Pharmacy Care Systems, Harrison School of Pharmacy, Auburn University; M. Maciejewski, PhD, Associate Professor, Department of Medicine, Division of General Internal Medicine Durham, Duke University. 2. From the Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, University of North Carolina, Chapel Hill; Department of Medicine, Division of General Internal Medicine, Duke University Medical Center, Durham, North Carolina; Department of Pharmacy Care Systems, Harrison School of Pharmacy, Auburn University, Auburn, Alabama, USA.R.J. Desai, PhD, Graduate Student, Research Fellow, Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, University of North Carolina, and Department of Medicine, Division of Pharmacoepidemiology and Pharmacoeconomics, Harvard Medical School, Brigham and Women's Hospital; J.K. Rao, MD, Associate Professor; G. Fang, PhD, Assistant Professor; J.F. Farley, PhD, Associate Professor, Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, University of North Carolina; R.A. Hansen, PhD, Professor, Department of Pharmacy Care Systems, Harrison School of Pharmacy, Auburn University; M. Maciejewski, PhD, Associate Professor, Department of Medicine, Division of General Internal Medicine Durham, Duke University. jffarley@email.unc.edu.
Abstract
OBJECTIVE: To compare the risk of cardiovascular (CV) events between use of tumor necrosis factor-α inhibitors (TNFi) and nonbiologic disease-modifying antirheumatic drugs (DMARD) in patients with early rheumatoid arthritis (RA). METHODS: A nested case-control study was conducted using data from Truven's MarketScan commercial and Medicare claims database for patients with early RA who started treatment with either a TNFi or a nonbiologic DMARD between January 1, 2008, and December 31, 2010. Date of CV event diagnosis for cases was defined as the event date, and 12 age-matched and sex-matched controls were sampled using incidence density sampling. Drug exposure was defined into the following mutually exclusive categories hierarchically: (1) current use of TNFi (with or without nonbiologics), (2) past use of TNFi (with or without nonbiologics), (3) current use of nonbiologics only, and (4) past use of nonbiologics only. Current use was defined as any use in the period 90 days prior to the event date. Conditional logistic regression models were used to derive incidence rate ratios (IRR). RESULTS: From the cohort of patients with early RA, 279 cases of incident CV events and 3348 matched controls were identified. The adjusted risk of CV events was not significantly different between current TNFi users and current nonbiologic users (IRR 0.92, 95% CI 0.59-1.44). However, past users of nonbiologics showed significantly higher risk compared to current nonbiologic users (IRR 1.47, 95% CI 1.04-2.08). CONCLUSION: No differences in the CV risk were found between current TNFi and current nonbiologic DMARD treatment in patients with early RA.
OBJECTIVE: To compare the risk of cardiovascular (CV) events between use of tumor necrosis factor-α inhibitors (TNFi) and nonbiologic disease-modifying antirheumatic drugs (DMARD) in patients with early rheumatoid arthritis (RA). METHODS: A nested case-control study was conducted using data from Truven's MarketScan commercial and Medicare claims database for patients with early RA who started treatment with either a TNFi or a nonbiologic DMARD between January 1, 2008, and December 31, 2010. Date of CV event diagnosis for cases was defined as the event date, and 12 age-matched and sex-matched controls were sampled using incidence density sampling. Drug exposure was defined into the following mutually exclusive categories hierarchically: (1) current use of TNFi (with or without nonbiologics), (2) past use of TNFi (with or without nonbiologics), (3) current use of nonbiologics only, and (4) past use of nonbiologics only. Current use was defined as any use in the period 90 days prior to the event date. Conditional logistic regression models were used to derive incidence rate ratios (IRR). RESULTS: From the cohort of patients with early RA, 279 cases of incident CV events and 3348 matched controls were identified. The adjusted risk of CV events was not significantly different between current TNFi users and current nonbiologic users (IRR 0.92, 95% CI 0.59-1.44). However, past users of nonbiologics showed significantly higher risk compared to current nonbiologic users (IRR 1.47, 95% CI 1.04-2.08). CONCLUSION: No differences in the CV risk were found between current TNFi and current nonbiologic DMARD treatment in patients with early RA.
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