AIM: The purpose of this study was to investigate the relationship between -174 G>C IL-6 polymorphism gene on the level of IL-6 and CRP in the population of western Indonesia obese who are obese.
METHODS: In this study, we examined 178 subjects consisting of 89 who are obese with BMI> 25, and controls with BMI between 18.5 and 23. Fasting blood was taken from each subject for the examination of IL-6 and CRP levels by the ELISA method. Determination of genotype -174 G>C IL-6 gene was examined by Polymerase Chain reaction- Restriction Fragment Length Polymorphism (PCR-RFLP) methods.
RESULTS: The results of this study showed increased levels of IL-6 and CRP in the obese group compared to the controls. In the obese group, CC genotype had higher CRP and lower IL-6 levels than the GC and GG genotypes. The frequency of CC genotype in the obese group was 47.2% compared with 28.1% in controls and this genotype was considered a risk factor for obesity. Carriers of the C genotype as a dominant or a recessive model had greater risk of obesity.
CONCLUSION: It was concluded that the polymorphism - 174G>C IL-6 gene is a risk factor for obesity and is associated with increased levels of IL-6 and CRP in an obese group of the Western Indonesian ethnic population.
SETTINGS AND DESIGN: Case-control study at Rheumatology Clinic of Universiti Sains Malaysia Hospital.
SUBJECTS AND METHODS: The sera of SLE patients and HCs were tested for the presence of anti-CLIC2 and anti-HMGB1 autoantibodies using human recombinant proteins and ELISA methodologies. Other serological parameters were evaluated according to routine procedures, and patients' demographic and clinical data were obtained.
STATISTICAL ANALYSIS: Mann-Whitney U-test, Chi-square test, Fisher's exact test, and receiver operating characteristic analysis.
RESULTS: Anti-CLIC2 autoantibody levels were significantly higher in SLE patients compared to HCs (P = 0.0035), whereas anti-HMGB1 autoantibody levels were not significantly elevated (P = 0.7702). Anti-CLIC2 and anti-HMGB1 autoantibody levels were not associated with ANA pattern, anti-dsDNA, and CRP. Interestingly, SLEDAI score (≥6) was associated with anti-CLIC2 (P = 0.0046) and with anti-HMGB1 (P = 0.0091) autoantibody levels.
CONCLUSION: Our findings support the potential of using anti-CLIC2 autoantibodies as a novel biomarker for SLE patients. Both anti-CLIC2 and anti-HMGB1 autoantibody levels demonstrated potential in monitoring SLE disease activity.