DRUG-RELATED LUPUS - INCIDENCE, MECHANISMS AND CLINICAL IMPLICATIONS

被引：36

作者：

ADAMS, LE ^{[1
]}

HESS, EV ^{[1
]}

机构：

[1] UNIV CINCINNATI,MED CTR,DEPT INTERNAL MED,DIV IMMUNOL,231 BETHESDA AVE,ML 564,CINCINNATI,OH 45267

来源：

DRUG SAFETY | 1991年 / 6卷 / 06期

关键词：

D O I：

10.2165/00002018-199106060-00004

中图分类号：

R1 [预防医学、卫生学];

学科分类号：

1004 ; 120402 ;

摘要：

Adverse side effects to drugs and chemicals in which immune mechanisms may be responsible have been described in drug-related lupus (DRL). The spectrum of drugs that may elicit DRL includes such classes as the hydrazines, arylamines, and chemicals that can be metabolised to amines. The 2 major pathways of metabolism - acetylation and N-hydroxylation - are described in detail. The events leading to autoantibody production are not well understood; however, specific consideration of the genetic makeup of patients who are candidates for treatment with these drugs may help identify those at risk of developing DRL.

引用

页码：431 / 449

页数：19

共 163 条

[31]

Drayer D.E., Reidenberg M.M., Clinical consequences of polymorphic acetylation of basic drugs, Clinical Pharmacology and Therapeutics, 22, pp. 251-258, (1977)

[32]

Dubois E.L., Wallace D.J., Drugs that exacerbate and induce systemic lupus erythematosus, Dubois’ lupus erythematosus, pp. 450-453, (1987)

[33]

Edwards C.R.W., Padfield P.L., Angiotensin-converting enzyme inhibitors: past, present, and bright future, Lancet, 1, pp. 30-34, (1985)

[34]

Emery P., Panayi G.S., Husten G., Et al., D-penicillamine induced toxicity in rheumatoid arthritis: the role of sulphoxidation status and HLA-DR3, Journal of Rheumatology, 11, pp. 626-632, (1984)

[35]

Epstein A., Barland P., The diagnostic value of antihistone antibodies in drug-induced lupus erythematosus, Arthritis and Rheumatism, 28, pp. 158-162, (1985)

[36]

Evans D.A.P., White T.A., Human acetylation polymorphism, Journal of Laboratory and Clinical Medicine, 63, pp. 394-403, (1964)

[37]

Facchini V., Timbrell J.A., Future evidence for an acetylator phenotype difference in the metabolism of hydralazine in man, British Journal of Clinical Pharmacology, 11, pp. 345-351, (1981)

[38]

Fielder A.H.L., Walport M.J., Batchelor J.R., Et al., Family study of the major histocompatibility complex in patients with SLE. Importance of null alleles of C4A and C4B in determining susceptibility, British Medical Journal, 286, pp. 425-428, (1983)

[39]

Foad B., Litwin A., Zimmer H., Et al., Acetylator phenotype in systemic lupus erythematosus, Arthritis and Rheumatism, 20, pp. 815-818, (1977)

[40]

Forrester J., Golbus J., Brede D., Hudson J., Richardson B., B cell activation in patients with active procainamide-induced lupus, Journal of Rheumatology, 15, pp. 1384-1388, (1988)

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