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Acetylator polymorphism in discoid lupus erythematosus
J M Ladero1, L C Jiménez, M J Fernández
1Department of Medicine, Hospital Universitario San Carlos, Facultad de Medicina, Universidad Complutense, Madrid, Spain.
European Journal of Clinical Pharmacology
|January 1, 1988
Summary
Slow acetylator phenotype, a genetic trait, does not appear to increase the risk for developing discoid lupus erythematosus. This finding suggests acetylator polymorphism is unrelated to the development of this autoimmune skin condition.
Area of Science:
- Pharmacogenetics
- Dermatology
- Immunology
Background:
- Discoid lupus erythematosus (DLE) is an autoimmune disease primarily affecting the skin.
- The role of genetic factors, such as drug metabolism, in DLE susceptibility is not fully understood.
- Acetylator phenotype influences the metabolism of various drugs, including sulfonamides.
Purpose of the Study:
- To investigate the association between acetylator phenotype and the risk of developing discoid lupus erythematosus.
- To determine if slow acetylator phenotype is a risk factor for pure cutaneous DLE.
Main Methods:
- Acetylator phenotype was assessed using sulphamethazine.
- The study included 37 patients with histologically confirmed discoid lupus erythematosus (DLE) and no visceral involvement.
- A control group of 157 healthy subjects was also analyzed.
Main Results:
- The prevalence of slow acetylators was similar in both the DLE patient group (54%) and the control group (57.4%).
- The difference in the proportion of slow acetylators between patients and controls was not statistically significant (p > 0.05).
Conclusions:
- Acetylator polymorphism does not appear to be associated with an increased risk of developing pure cutaneous discoid lupus erythematosus.
- These findings suggest that genetic variations in drug metabolism, specifically acetylator phenotype, are unlikely to be a major determinant in the pathogenesis of DLE.