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  • Title: Increased genotype frequency of N-acetyltransferase 2 slow acetylation in patients with rheumatoid arthritis.
    Author: Pawlik A, Ostanek L, Brzosko I, Gawroska-Szklarz B, Brzosko M, Dabrowska-Zamojcin E.
    Journal: Clin Pharmacol Ther; 2002 Sep; 72(3):319-25. PubMed ID: 12235453.
    Abstract:
    OBJECTIVES: Acetylation polymorphism can alter therapeutic responses and toxicity to certain xenobiotics and may also be a factor that influences a patient's susceptibility to certain diseases. We investigated whether patients with rheumatoid arthritis (RA) differed from healthy individuals with regard to genotype of the polymorphic enzyme N-acetyltransferase 2 (NAT2). METHODS: NAT2 polymorphism was compared in 118 healthy subjects and 82 patients with RA. NAT2 alleles (*4, *5, *6, and *7) were determined by polymerase chain reaction-restriction fragment length polymorphism methods with deoxyribonucleic acid extracted from peripheral blood. RESULTS: A statistically significant increase in the proportion of homozygous slow acetylators with 2 mutated alleles (84.1%) was found among patients with RA in comparison with healthy subjects (52.5%; P <.0001). The risk of development of RA was almost 5-fold greater in slow acetylators than in fast acetylators (odds ratio, 4.79; 95% confidence interval, 2.28-10.21). There was no correlation between NAT2 polymorphism and presence of rheumatoid factor, extra-articular manifestations, and age at first occurrence of disease symptoms. CONCLUSIONS: NAT2 slow acetylation genotype may be a risk factor of individual susceptibility to RA.
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