摘要
It is possible that dietary, environmental factors and/or genetic polymorphism s in xenobiotic-metabolizing enzymes may contribute to the development of Behce t’s disease. As N-acetyltransferase (NAT) 2 is an important xenobiotic-metabo lizing enzyme and theoretically the nonacetylated xenobiotics may induce an auto immune mechanism, the aim of the present study was to investigate whether the ge netic 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 st udy. NAT2.5A, NAT2.6A, NAT27.A/B and NAT2.14A polymorphisms were detected by usi ng real time PCR with LightCycler (Roche Diagnostics GmbH, Mannheim, Germany). T he NAT2.5A and NAT2.6A mutant genotypes carried an increased risk of developing Behcet’s disease [odds ratio(OR) =66.29,95%confidenceinterval(CI) =8.21-535. 3 3; and OR = 24; 95%CI = 2.04-304.98, respectively]. The NAT2.7A/B and NAT2.14 A 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 implic ations for the theories of the pathogenesis of the disease as well as for therap eutic aspects.
It is possible that dietary, environmental factors and/or genetic polymorphism s in xenobiotic-metabolizing enzymes may contribute to the development of Behce t's disease. As N-acetyltransferase (NAT) 2 is an important xenobiotic-metabo lizing enzyme and theoretically the nonacetylated xenobiotics may induce an auto immune mechanism, the aim of the present study was to investigate whether the ge netic 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 st udy. NAT2.5A, NAT2.6A, NAT27.A/B and NAT2.14A polymorphisms were detected by usi ng real time PCR with LightCycler (Roche Diagnostics GmbH, Mannheim, Germany). T he NAT2.5A and NAT2.6A mutant genotypes carried an increased risk of developing Behcet's disease [odds ratio(OR) =66.29,95%confidenceinterval(CI) =8.21-535. 3 3; and OR = 24; 95%CI = 2.04-304.98, respectively]. The NAT2.7A/B and NAT2.14 A 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 implic ations for the theories of the pathogenesis of the disease as well as for therap eutic aspects.
