Elevated Serum Low-Density Lipoproteins-Cholesterol Levels and B1B2/B2B2 CETP Genotype Are Positively Associated with Nonalcoholic Fatty Liver Disease in Women with Gallstone Disease.

Background: Nonalcoholic fatty liver disease (NAFLD) is generated by the interaction between environmental and genetic factors, and the presence of metabolic alterations. Since Taq1B cholesteryl ester transfer protein (CETP) polymorphism is associated with abnormal serum lipid values, it could be related to NAFLD. The aim of this study was to determine the role of the Taq1B CETP polymorphism with serum lipids, anthropometric variables, and the extent of steatosis in Mexican-mestizo women with gallstone disease (GD). Methods: Sixty-two women were enrolled in this cross-sectional study. Serum lipids were determined by dry chemistry. The Taq1B CETP polymorphism was determined by allelic discrimination. CETP serum levels were measured by enzyme-linked immunosorbent assay, and the extent of steatosis with a biopsy staining with Oil-Red-O. Results: Subjects with the B1B2/B2B2 genotype had higher percentage of degree of steatosis than those with B1B1 (11.95% vs. 2.19%, P = 0.008). The B1B2/B2B2 genotype (odds ratio [OR] 3.90 [confidence interval {CI} 95% 1.891-8.536], P = 0.04) and an elevated low-density lipoproteins (LDL)-cholesterol (OR 3.54 [CI 95% 1.042-2.058, P = 0.039) significantly increase the risk for NAFLD. Conclusions: This study provides evidence that the B1B2/B2B2 genotype of CETP and the elevated LDL-cholesterol serum levels increase the risk of NAFLD in women with GD.

Effect of the ADIPOQ Gene -11391G/A Polymorphism Is Modulated by Lifestyle Factors in Mexican Subjects.

BACKGROUND/AIMS: Single nucleotide polymorphisms (SNPs) in the ADIPOQ gene could explain the adiponectin level. However, the knowledge about the influence of genetic and lifestyle factors is not sufficient. The aim was to analyze whether the effect of the -11391G/A SNP in the ADIPOQ gene is modulated by lifestyle factors in Mexican subjects. METHODS: A cross-sectional study was performed in which 394 participants were analyzed. Genetic, anthropometric, biochemical, dietary, clinical and physical activity parameters were measured. Statistical analysis was performed with SPSSv19 software. RESULTS: The distribution of the -11391G/A SNP genotypes was 55.6 and 44.4% for GG and AG, respectively. The adiponectin level was modulated by the -11391G/A SNP in response to the body mass index (BMI); A allele carriers showed a higher adiponectin level compared to G homozygous carriers but only in the minor BMI tertile group (p=0.032). Adiponectin level variability was explained by gender [(r)=1.5, 95% CI 1.1-1.9, p=0.000], insulin resistance [(r)=-1.2, 95% CI -0.8 to -1.6, p=0.000], physical activity [(r)=0.6, 95% CI 0.2-0.9, p=0.002] and monounsaturated fat intake [(r)=0.5, 95% CI 0.38-1.0, p=0.047]. CONCLUSIONS: The adiponectin level was modulated by the interaction between BMI and -11391G/A SNP; this suggests that the lifestyle rather than genetic factors modulates serum adiponectin.

Prevalence of hepatitis A, B and C serological markers in children from western Mexico.

INTRODUCTION: Viral hepatitis in children is a major public health problem worldwide. AIM: To evaluate the prevalence of serological markers for hepatitis A, B and C infections in Mexican children diagnosed with hepatitis during a five-year period. MATERIAL AND METHODS: A total of 31,818 children admitted to a tertiary level hospital in Mexico from 2005 to 2009 were evaluated for hepatitis. RESULTS: Hepatitis was found in 215 (0.7%) of the children. Serum samples from hepatitis-positive children were screened for anti-HAV IgM, HBsAg, total anti-HBc and anti-HCV. HAV was the leading cause of viral hepatitis (81%), followed by HBV and HCV (3.1 and 2%, respectively), whereas no serological marker was observed in 13.9% of the analyzed samples. Furthermore, when children were categorized by age, a significant increase in anti-HAV detection was observed in school-aged children (7-11 years old) (p < 0.001) and a reduction in adolescents (12-15 years old). CONCLUSION: In conclusion, hepatitis A is the most prevalent viral hepatitis infection detected in children, followed by HBV and HCV. In addition, the high percentage of hepatitis infections without a known etiological agent and the serological test limitations require the detection of occult HBV, HCV and hepatitis E infections. The age-dependent vulnerability of groups with HAV infections emphasizes the importance of HAV vaccination in young children in Mexico.

sE-Selectin expression and A561C polymorphism in relation to rheumatoid arthritis clinical activity.

OBJECTIVE: To investigate the relationship of A561C polymorphism and sE-selectin levels with rheumatoid arthritis (RA) clinical activity. METHODS: In a case-control study, we compared 60 patients with RA and 60 healthy subjects. Patients fulfilled the 1987 American College of Rheumatology criteria. Soluble E-selectin levels were measured from serum samples using the ELISA kit. We investigated E-selectin A561C polymorphism by the restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique. The disease activity was recorded with Spanish Health Assessment Questionnaire Disability Index (HAQ-DI), Spanish Arthritis Impact Measurement Scales (AIMS), and Disease Activity Score (DAS28) scores. A p value < 0.05 was considered significant. RESULTS: Patients with RA showed higher sE-selectin levels than controls (mean 91.7 vs 39 ng/ml; p = 0.002). A positive correlation between sE-selectin and rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), Spanish HAQ-DI, and DAS28 scores was found. The E-selectin polymorphism analysis showed diminished frequency in RA of heterozygous A/C genotype and increased frequency of homozygous wild-type A/A genotype (p = 0.043, OR 1.45; 95% CI 1.125-16.167) versus A/C and A/A genotype in healthy subjects. No significant association between A561C polymorphism and clinical activity was present. CONCLUSION: The sE-selectin, RF, and ESR, in addition to clinical indices, were associated with clinical activity in RA. We highlighted the presence of A/A genotype A561C polymorphism in our patients with RA.