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 date4/1/843/31/87


  • National Institutes of Health


  • Medicine(all)

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