IL-17 is a novel cytokine that is characterized by an ability to induce several types of cells to secrete proinflammatory cytokines in various inflammatory diseases. This study analyzed the influence of IL-17F gene polymorphisms on disease susceptibility and clinical features. Ninety-nine Behçet's disease (BD) patients and 114 controls were genotyped to analyze three single nucleotide polymorphisms (SNPs) including A126G, G155A, and A161G of the IL-17F gene using automated sequencing. We compared the frequencies of IL-17F alleles, genotypes, and haplotypes in patients with BD and controls using the chi-square or Fisher's exact test. Significant differences in the frequencies of allele and genotype in A126G SNP of IL-17 gene were found between BD patients and controls (P<0.001 and P<0.001, respectively). None of three IL-17F SNPs were associated with diverse clinical features in BD. The frequency of haplotype AA did not differ between patients with BD and controls (P=0.985). The haplotypes, AG, and GG, have positive and inverse association with BD susceptibility (P<0.001 and P<0.001, respectively). These findings suggest that IL-17 gene SNPs may influence the susceptibility of BD.

The aim of this study was to identify any association between serum uric acid and smoking status using data from the Seventh Korea National Health and Nutrition Examination Survey (KNHANES VII-1) 2016 of the Korean population. This study used a cross-sectional design and analyzed 5609 subjects aged ≥ 19 years among 8150 participants enrolled in the KNHANES VII-1 2016. Smoking status was classified into current smokers, never smokers, and ex-smokers. Hyperuricemia was defined as > 7.0 mg/dL for men and > 6.0 mg/dL of serum uric acid for women. Association between smoking and serum uric acid/hyperuricemia was assessed by Pearson's or Spearman's correlation analyses and multivariate logistic regression analysis showing odds ratio (OR) and 95% confidence interval (CI). A significant difference in serum uric acid according to smoking status was identified in female ( P < .001) but not in male subjects ( P = .069). In female subjects, current smokers and ex-smokers showed higher serum uric acid than never smokers ( P < 0.001 of both). Serum uric acid was associated with smoking status in female but not male subjects ( r = 0.057, P = .001 and r = 0.025, P = .220, respectively). There was significant difference of smoking status between female subjects with and without hyperuricemia ( P < .001). Current smokers had 2.7 times higher likely to have hyperuricemia in female, compared to never smokers (OR 2.674, 95% CI 1.578 – 4.531, P < .001). This study revealed that smoking was closely associated with serum uric acid in female but not in male subjects in Korean population.

Our study provides evidence that certain GCH1 haplotypes may be protective against susceptibility and pain sensitivity in FM. Our data suggest that NO is responsible for pain sensitivity in the pathogenesis of FM.