Project Details


Systemic lupus erythematosus (SLE) is a chronic inflammatory disease which may affect any or all major organ systems of the body. Although numerous risk factors have been postulated, there is a conspicuous absence of controlled human studies which would enable us to draw causal inferences about presumptive etiologic factors. A number of drugs have been implicated as causing SLE. Several investigators have observed that most patients with drug-induced lupus are slow acetylators of these drugs. Preliminary work by one of the investigators indicates that a disproportionate number of patients with native SLE may also be slow acetylators. Other work by this investigator indicates that the chemical structure common to those drugs which cause lupus is also a common environmental exposure. Thus, the hypothesis has been raised that native SLE is a function of environmental chemical exposures combined with a genetic predisposition toward slow metabolism of these chemicals. In order to test this hypothesis, a case-control study is planned. Three hundred patients with SLE will be compared to 300 control patients from a general medical group practice and to 300 "friend controls," both control groups matched for age and sex. Acetylator phenotype will be determined by administering dapsone and measuring the ratio of dapsone to mono-acetyldapsone in the serum. Exposures to environmental agents, drug exposures, demographic characteristics, and previous medical histories will be determined from personal interview, medical record review, and obtaining information from prior physicians. Univariate analysis, including calculation of odds ratios with confidence intervals, will be followed by stratification and multiple logistic regression, enabling us to evaluate the importance of each variable while adjusting for the others as confounders, as well as the relative importance of each variable as a risk factor. This research, involving the disciplines of internal medicine, clinical epidemiology, and clinical pharmacology, should contribute to our understanding of, treatment of, and, ultimately, prevention of SLE.
Effective start/end date4/1/8611/30/88


  • National Institute of Arthritis and Musculoskeletal and Skin Diseases


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