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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.

Background: Behçet's disease (BD) is a multisystemic disease of unknown etiology characterized by chronic relapsing oral-genital ulcers and uveitis. Some abnormalities in lipoprotein metabolism have been described in patients with BD., Methods: In this study, apolipoprotein E (apo E) polymorphism and lipoprotein cholesterol concentrations in 30 patients with BD were compared with those of 27 control subjects., Results: Both patients and controls were found to be normolipidemic. Patients with BD had significantly higher concentrations of high-density lipoprotein (HDL) cholesterol than those of controls (P < 0.05); however, there was no difference in serum triglyceride, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol concentrations. The distribution of apo E genotypes and alleles was the same in both groups. There were slight differences in allele frequency between the groups, but this was not statistically significant., Conclusions: The high HDL cholesterol levels observed in our patients were not related to abnormalities in apo E alleles.

Superficial mycosis, including dermatophytic infections, tinea versicolor, and cutaneous candidiasis is mostly limited to the outer layers of the skin, nails, and mucous membranes. In this study, Apolipoprotein E (ApoE) polymorphism and lipoprotein cholesterol concentrations were compared between 42 patients with superficial fungal disease and 27 control subjects. Both the patients and controls were found to be normolipemic. The patients with superficial fungal disease had significantly higher concentrations of high-density cholesterol (HDL) compared to the control group (p=0.0462). However, there was no difference in the serum triglyceride, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol concentrations. A significantly higher incidence of heterozygosity E2/3 was found in the patients (p=0.0228), and significantly lower incidence of homozygosity E3/3 in all patients, and those with candidiasis and dermatophytosis (p=0.0139, 0.0194 and 0.0337, respectively) compared to the control group. The E3/4 genotype differences between patients and controls were not statistically significant. There were slight differences in the allele frequencies between the two groups, but these did not reach statistically significant levels. It was concluded that the presence of apoE2/3 genotype, high HDL-cholesterol levels and the absence of apoE3/3 genotype can be regarded as risk factors for superficial fungal disease, especially dermatophytosis.

Glutathione S-transferase (GST) enzymes play an important role in drug metabolism. GST is a multigene family of enzymes involved in the detoxification and in a few instances activation of a wide variety of chemicals. Detoxification features make it plausible to search for GST polymorphism in patients with drug eruption. The GSTM (mu), GSTT (theta) and GSTP (pi) have been shown to be polymorphically distributed. The GSTT1, GSTM1 and GSTP1 gene polymorphism were detected using real-time PCR. GSTM1 and GSTT1 null genotypes were found to be associated with an increased risk of drug eruption (OR 2.27, 95% CI 1.20-5.21; OR 2.48, 95% CI 1.12-6.39, respectively). No relationship was observed between the null combination of the GSTM1 and GSTT1 genotype polymorphisms and drug eruption risk (OR 2.65, 95% CI 0.62-11.25). Our results show that GSTP1 polymorphism is not a significant contributor to drug eruption risk. The GSTM1 and GSTT1 gene polymorphisms seem to be associated with the development of drug eruption. Further studies may shed additional light on the role of GSTM1, GSTT1 and GSTP1 in drug eruption.