 |
|
|
 |
Cost-Effectiveness Analysis of MTHFR Polymorphism Screening by Polymerase Chain Reaction in Korean Patients with Rheumatoid Arthritis Receiving Methotrexate
SEONG-KYU KIM, JAE-BUM JUN, AHMED EL-SOHEMY, and SANG-CHEOL BAE ABSTRACT. Objective. To determine whether a strategy based on methylenetetrahydrofolate reductase (MTHFR) genotype screening is more cost-effective than the conventional strategy in reducing the risk of methotrexate (MTX)-related toxicity in patients with rheumatoid arthritis (RA). Methods. We consecutively enrolled 385 patients with RA (355 female, 30 male) who had received MTX and identified toxicity associated with MTHFR C677T genotypes. We designed a hypothetical decision model to compare the genotype-based strategy with the conventional strategy. The time horizon was set as 1 year, and direct medical costs were used. The measured outcomes were the total expected cost, the effectiveness, and the incremental cost-effectiveness ratio. Results. MTHFR genotype distribution revealed 133 patients (34.6%) with 677CC, 193 (50.1%) with 677CT, and 59 (15.3%) with 677TT. A total of 154 patients (40.0%) exhibited MTX-related toxicity. Compared to RA patients with the CC genotype, the odds ratio (95% confidence interval) for risk of toxicity was 3.8 (2.29–6.33) for the CT genotype, and 4.7 (2.40–9.04) for the TT genotype. In the base-case model, the total expected cost and the probability of continuing MTX medication for the conventional and genotype-based strategies were 851,415 Korean won (US$ 710) and 788,664 Korean won (US$ 658), and 94.03% and 95.58%, respectively. Conclusion. The MTHFR C677T polymorphism may be an important predictor of MTX-related toxicity in patients with RA. The cost-effectiveness analysis suggests that the genotype-based strategy is both less costly and more effective than the conventional strategy for MTX therapy. (First Release June 1 2006; J Rheumatol 2006;33:1266–74) Key Indexing Terms:
METHYLENETETRAHYDROFOLATE REDUCTASE RHEUMATOID ARTHRITIS
From the Department of Internal Medicine, Division of Rheumatology, the Hospital for Rheumatic Diseases, Hanyang University, Seoul, Korea; Department of Nutritional Sciences, University of Toronto, Toronto, Canada; and Division of Rheumatology, Department of Internal Medicine, College of Medicine, Dankook University, Cheonan, Chungcheong Nam Do, Korea. Supported in part by grants from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea (grant numbers 03-PJ10-PG13-GD01-0002, 01-PJ3-PG6-01GN11-0002, and 01-PJ1-PG1-01CH10-0007). S-K. Kim, MD, Assistant Professor of Medicine, Department of Internal Medicine, Division of Rheumatology, Hospital for Rheumatic Diseases, Hanyang University and Division of Rheumatology, Department of Internal Medicine, College of Medicine, Dankook University; J-B. Jun, MD, PhD, Associate Professor of Medicine, Department of Internal Medicine, Division of Rheumatology, Hospital for Rheumatic Diseases, Hanyang University; A. El-Sohemy, PhD, Assistant Professor of Nutritional Sciences, Department of Nutritional Sciences, University of Toronto; S-C. Bae, MD, PhD, MPH, Professor of Medicine, Department of Internal Medicine, Division of Rheumatology, Hospital for Rheumatic Diseases, Hanyang University. Address reprint requests to Dr. S-C. Bae, Department of Internal Medicine, Division of Rheumatology, The Hospital for Rheumatic Diseases, Hanyang University, Seoul 133-792, Korea. E-mail: scbae@hanyang.ac.kr Accepted for publication February 27, 2006.
|
