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J Rheum Dis.  2011 Sep;18(3):161-167. 10.4078/jrd.2011.18.3.161.

Treatment Persistence with TNF Blocker in Korean Rheumatoid Arthritis Patients

Affiliations
  • 1Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, Korea. scbae@hanyang.ac.kr

Abstract


OBJECTIVE
To estimate drug persistency and the safety of TNF blocker in Korean patients with rheumatoid arthritis.
METHODS
Data were extracted from medical records of rheumatoid arthritis patients who had treated with TNF blocker or are currently using TNF blocker at Hanyang University Hospital for Rheumatic Diseases from December 2000 to November 2009 (REtrospective study for Safety and Efficacy of Anti-RA treatment with biologiCs, RESEARCh). Comprehensive chart reviews were undertaken on all patients and data on drug usages and response of TNF blocker was collected at initiation, 3 months and the time of data collection. Persistency with treatment was examined using life-table analysis and multivariate Cox proportional hazard models were developed to examine potential predictors of discontinuation of TNF blocker.
RESULTS
A total of 268 patients were enrolled in this retrospective study. Among them 180 patients were included in the analysis of drug persistency. The 1-year and 5-year drug persistency of TNF blocker was 74% and 46%, respectively. Concomitant use of methotrexate (hazard ratio 0.46, 95% CI 0.27-0.80) was associated with higher persistence. Comparing to etanercept, adalimumab is an independent risk factor for discontinuation (hazard ratio 2.63, 95% CI 1.43-4.84).
CONCLUSION
Five-year drug persistency of TNF blocker was 46% and concomitant use of methotrexate is associated with higher persistence.

Keyword

Rheumatoid arthritis; TNF-blocker; Drug persistency

MeSH Terms

Antibodies, Monoclonal, Humanized
Arthritis, Rheumatoid
Biological Agents
Data Collection
Humans
Immunoglobulin G
Medical Records
Methotrexate
Proportional Hazards Models
Receptors, Tumor Necrosis Factor
Retrospective Studies
Rheumatic Diseases
Risk Factors
Adalimumab
Etanercept
Antibodies, Monoclonal, Humanized
Biological Agents
Immunoglobulin G
Methotrexate
Receptors, Tumor Necrosis Factor
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