N-acetyltransferase 2 polymorphisms in patients with Behcet's disease.

Authors: Tamer, L  Tursen, U  Eskandari, G  Ates, NA  Ercan, B  Yildirim, H  Atik, U 
Citation: Tamer L, etal., Clin Exp Dermatol. 2005 Jan;30(1):56-60.
Pubmed: (View Article at PubMed) PMID:15663505
DOI: Full-text: DOI:10.1111/j.1365-2230.2004.01685.x

It is possible that dietary, environmental factors and/or genetic polymorphisms in xenobiotic-metabolizing enzymes may contribute to the development of Behcet's disease. As N-acetyltransferase (NAT) 2 is an important xenobiotic-metabolizing enzyme and theoretically the nonacetylated xenobiotics may induce an autoimmune mechanism, the aim of the present study was to investigate whether the genetic polymorphism of NAT2 plays a role in susceptibility to Behcet's disease. Forty Behcet's disease patients and 82 control subjects were enrolled in the study. NAT2*5A, NAT2*6A, NAT27*A/B and NAT2*14A polymorphisms were detected by using real time PCR with LightCycler (Roche Diagnostics GmbH, Mannheim, Germany). The NAT2*5A and NAT2*6A mutant genotypes carried an increased risk of developing Behcet's disease [odds ratio (OR) = 66.29, 95% confidence interval (CI) = 8.21-535.33; and OR = 24; 95% CI = 2.04-304.98, respectively]. The NAT2*7A/B and NAT2*14A gene polymorphisms were not an increased risk for developing Behcet's disease. As a result of this study we conclude the NAT2 slow acetylator status may be a determinant in susceptibility to Behcet's disease. This finding may have implications for the theories of the pathogenesis of the disease as well as for therapeutic aspects.

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CRRD ID: 8552650
Created: 2014-04-23
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Last Modified: 2014-04-23
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.