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Spontaneous systemic lupus erythematosus and acelylator phenotype
Acta Medica Scandinavica
|January 1, 1977
Summary
Patients with systemic lupus erythematosus (SLE) predominantly exhibit slow acetylator phenotypes. This finding mirrors observations in drug-induced SLE-like syndromes, suggesting a shared genetic predisposition.
Area of Science:
- Rheumatology and Clinical Pharmacology
- Immunogenetics and Drug Metabolism
Background:
- Systemic lupus erythematosus (SLE) is an autoimmune disease with complex etiology.
- Drug-induced SLE-like syndromes share clinical and immunological features with spontaneous SLE.
- Acetylator phenotype, determined by isoniazid (INH) metabolism, is a known genetic marker.
Purpose of the Study:
- To investigate the acetylator phenotype distribution in patients with spontaneous SLE.
- To explore potential correlations between INH half-life, renal function, and SLE.
- To compare acetylator phenotypes in spontaneous SLE with those in drug-induced SLE-like syndromes.
Main Methods:
- Phenotyping of 15 patients with spontaneous SLE using plasma isoniazid (INH) half-life determination.
- Assessment of renal insufficiency in the study cohort.
- Categorization of patients into slow and rapid acetylator groups.
Main Results:
- A significant predominance of slow acetylators (13 out of 15 patients) was observed in spontaneous SLE.
- Only 2 patients were identified as rapid acetylators.
- No significant correlation was found between plasma INH half-lives and the degree of renal insufficiency.
Conclusions:
- Spontaneous SLE exhibits a marked prevalence of the slow acetylator phenotype.
- This finding is consistent with previous observations in drug-induced SLE-like syndromes.
- The results suggest a potential shared genetic predisposition related to drug metabolism in different SLE manifestations.