Survival analysis of disease modifying antirheumatic drugs in Spanish rheumatoid arthritis patients

J De La Mata, F J Blanco, J J Gómez-Reino, J De La Mata, F J Blanco, J J Gómez-Reino

Abstract

Objectives: To evaluate the duration of treatment and the reasons for discontinuing therapy with disease modifying antirheumatic drugs in Spanish rheumatoid arthritis patients.

Methods: An observational study was made of 629 patients with rheumatoid arthritis treated with disease modifying antirheumatic drugs between 1979 and 1991. The outcomes (treatment termination because of toxicity and lack of response) of 991 treatment starts with intramuscular gold salts, D-penicillamine, azathioprine, and methotrexate were subjected to survival analysis. Cumulative probability of continuation of each drug (drug survival) was calculated by the Kaplan-Meier method and comparison between the survival curve of each was made by log rank testing.

Results: Median drug survival (95% confidence interval) was 51 (25-76.9) months for methotrexate, 39.9 (19.9-48.2) months for azathioprine, 34.9 (29.4-41.4) months for gold salts, and 16.4 (13.9-21) months for D-penicillamine. The highest cumulative probability of drug survival at five years was for methotrexate (45%); that at 10 years was for gold salts (15%). Up to 60% of the patients discontinued D-penicillamine in the first two years. Lack of response was the major limiting factor for all drugs except D-penicillamine, for which it was toxicity. D-Penicillamine was associated with a greater rate of discontinuations because of toxicity in women and patients older than 65. Previous disease modifying antirheumatic drug administration did not influence current drug survival.

Conclusion: Overall, gold salts remain useful for the treatment of rheumatoid arthritis over long periods of time in the population studied. Because of the high rate of continuation of treatment (survival) and the optimal efficacy and toxicity profiles observed with methotrexate after five years of treatment, it should be the drug of first choice for second line treatment of these RA patients.

References

    1. N Engl J Med. 1980 Aug 7;303(6):300-2
    1. Arthritis Rheum. 1994 Oct;37(10):1492-8
    1. J Rheumatol. 1982 Nov-Dec;9(6):932-4
    1. Ann Rheum Dis. 1984 Jun;43(3):398-401
    1. Arthritis Rheum. 1984 Jul;27(7):721-7
    1. Ann Rheum Dis. 1975 Oct;34(5):416-21
    1. Arthritis Rheum. 1977 Nov-Dec;20(8):1464-72
    1. N Engl J Med. 1985 Mar 28;312(13):818-22
    1. Lancet. 1987 May 16;1(8542):1108-11
    1. Ann Rheum Dis. 1987 Mar;46(3):177-83
    1. Arthritis Rheum. 1987 Apr;30(4):361-8
    1. Scand J Rheumatol. 1987;16(3):177-84
    1. Arthritis Rheum. 1988 May;31(5):577-84
    1. J Clin Epidemiol. 1988;41(11):1037-41
    1. J Rheumatol. 1989 Jan;16(1):1-4
    1. Arthritis Rheum. 1989 Jun;32(6):671-6
    1. Br J Rheumatol. 1990 Apr;29(2):120-5
    1. J Rheumatol. 1990 Aug;17(8):994-1002
    1. Arthritis Rheum. 1990 Oct;33(10):1449-61
    1. Tissue Antigens. 1990 Oct;36(4):174-6
    1. J Rheumatol. 1991 Feb;18(2):188-94
    1. J Rheumatol. 1992 Dec;19(12):1885-94
    1. Arthritis Rheum. 1993 Mar;36(3):297-306
    1. Arthritis Rheum. 1993 Jun;36(6):811-4
    1. Rheum Dis Clin North Am. 1993 Feb;19(1):153-61
    1. Rheum Dis Clin North Am. 1993 Feb;19(1):163-72
    1. J Rheumatol. 1980 Nov-Dec;7(6):825-30

Source: PubMed

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