Investigation of the relationship between apolipoprotein E gene polymorphisms and hepatitis B virus infection in northern China.

BACKGROUND: Certain genetic polymorphisms can lead to differences in immunity function, resulting in different clinical outcomes for hepatitis B virus (HBV) patients. The aim of this study was to investigate the association between apolipoprotein E (ApoE) gene polymorphisms and HBV infection status in northern Chinese individuals. METHODS: Genomic DNA was extracted using an improved sodium iodide (NaI) method from the peripheral blood of 270 patients with hepatitis B and 112 healthy controls. Multiplex Amplification Refractory Mutation System (Multi-ARMS) was performed to analyze ApoE gene polymorphisms with three alleles (ɛ2, ɛ3, ɛ4) in patients and controls. A chemiluminescence assay was used to detect serological markers for hepatitis B infection status. RESULTS: An improved PCR system for the detection of ApoE gene polymorphisms was established successfully. The frequency of the ɛ2 allele in patients with HBV infection was higher than that of normal controls (p<0.05). The ɛ2 allele, compared with the ɛ3 and ɛ4 alleles, showed positive correlation with the different HBV infection models [odds ratio (OR)=1.735, 95% confidence interval (CI): 1.509-1.999, p<0.01; OR=1.768, 95% CI: 1.554-2.011, p<0.01]. The OR for the ApoE ɛ2 allele was 1.503 in a multivariate unconditional logistic regression model (OR=1.503, 95% CI: 1.212-1.754, p<0.01). CONCLUSIONS: Our results indicated that the ApoE gene polymorphism was associated with HBV infection, and the ɛ2 allele showed positive correlation with HBV infection in northern China.

[The effect of different dosage of aspirin on inflammatory biomarkers and prognosis in acute coronary syndrome.].

OBJECTIVE: To observe and assess the effect of different dosages of aspirin on inflammatory biomarkers, hemorheology (platelet aggregation rate) and clinical prognosis in patients with acute coronary syndrome (ACS). METHODS: ACS patients were randomly assigned to receive different dosages of aspirin treatment orally. Patients in group A, B and C took 100 mg, 500 mg and 1000 mg of aspirin per day respectively. They were treated and followed-up for 1 year. High-sensitivity C-reactive protein (hsCRP), IL-6, tumor necrosis TNFalpha and platelet aggregation rate were examined and major adverse cardiac events (MACE) were recorded. RESULTS: A total of 312 patients with ACS were enrolled in the study. The baseline characteristics of the three groups were not different with respect to age, gender, cardiovascular risk profile, level of inflammatory biomarkers and concomitant treatment before and after randomization. The levels of baseline serum hsCRP, IL-6 and TNFalpha were higher in subjects of the study as compared with normal reference value (P < 0.05, < 0.05, < 0.01) and they decreased significantly after therapy with 3 different doses of aspirin (detected at 30 days, 6 months and 12 months, P < 0.001), but there were no significant differences among the three groups (P > 0.05). Rehospitalization, MACE and the change of platelet aggregation ratio were not significantly different among the three groups. The incidence of gastrointestinal complaints was significantly higher in groups B and C than in group A (P < 0.05). CONCLUSIONS: The levels of serum inflammatory biomarker increase in patients with ACS. Aspirin therapy may decrease the level of inflammatory markers significantly, but increasing the dosage of aspirin from 100 mg to 1000 mg daily does not decrease the level of inflammatory markers and the clinical MACEs further. However, the incidence of gastrointestinal complaints increase significantly with the increase of aspirin dosage.

The E23K polymorphism in Kir6.2 gene and coronary heart disease.

BACKGROUND: The G to A mutation in the Kir 6.2, the ATP-sensitive potassium channel subunit, resulted a glutamate (E) to lysine (K) substitution at codon 23, and the A allele was shown to have a relationship with high risk to type 2 diabetes in previous study. Their role in coronary heart disease (CHD) has not been evaluated. We hypothesized that the polymorphism would be associated with increased susceptibility to CHD. METHODS: The E23K gene polymorphism of Kir6.2 gene was analyzed by PCR-restriction site polymorphism (PCR-RSP) methods in 101 controls and 119 CHD patients. Serum lipids and C reactive protein concentrations were measured in all subjects. RESULTS: Among the CHD patients, the frequency of the G allele was higher (63.4% vs. 56.9%, P>0.05) and the frequency of the A allele was lower (36.6% vs. 43.1%, P>0.05) than among controls. No significant differences were found in allele frequencies between CHD and controls (P>0.05), but there were significant differences in GG and combined (GA+AA) genotypes frequencies (42.0% vs. 28.7%, and 58.0% vs. 71.3%, P<0.050). CONCLUSIONS: The E23K gene polymorphism in Kir6.2 gene appeared to be related to high susceptibility to CHD.

[Polymorphisms in the apolipoprotein A5 gene and apolipoprotein C3 gene in patients with coronary artery disease].

OBJECTIVE: To investigate the association between the -1131T/C and 56C/G polymorphism in the APOA5 gene as well as the -482C/T in the APOC3 gene and susceptibility to coronary artery disease (CAD) in a Chinese Han population. METHODS: Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and polyacrylamide gel electrophoresis (PAGE) methods, we analyzed the genotypes in 312 CAD patients diagnosed by angiography and 317 healthy controls. The levels of serum lipid profiles were also studied by biochemical methods. RESULTS: The frequency of the APOA5 -1131 C allele in CAD patients was significantly higher than that of the control group (39.9% vs. 33.3%, P = 0.02). Compared with the wild type TT, CC homozygotes had a significantly increased CAD risk (OR = 1.93 and OR = 1.80 using unadjusted and adjusted logistic regression models, respectively). This association still existed after adjustment for the APOC3-482 variant. The APOA5-1131C allele also showed a correlation with increasing plasma TG levels (P < 0.01). CONCLUSIONS: The APOA5-1131T/C polymorphism but not APOC3-482C/T might contribute to an increased risk of CAD among Chinese accompanied by an elevation of serum TG levels; this effect was found to be independent of the APOC3-482C/T variant.

[Investigation of the relationship between apolipoprotein gene polymorphism and hepatitis B virus infection in China].

OBJECTIVE: To explore the gene polymorphisms of ApoAI-75 Msp1, ApoB Msp1, ApoCIII Sst1, LRP5, and ApoE genotypes in two pairs of semi different modes of hepatitis B for HBV markers. METHODS: The patients are divided into 9 groups. There were a total of 720 cases, 80 patients in each group, The patients was carried out by SnaPshot method (single-base multilocus micro-sequencing), and different genotypes of each locus were conducted by the method of sequencing in order to support the final evidence of the accuracy of test results. RESULTS: There was association between gene polymorphisms of ApoAI-75Msp1 and ApoE and different modes of two pairs of semi-hepatitis B (P < 0.05), while there wasn't any association between gene polymorphisms of ApoB-Msp1, ApoCIII-Sst1, LRP5 and different modes of two pairs of semi-hepatitis B (P > 0.05). CONCLUSION: The gene polymorphism of ApoAI-75Msp1 and ApoE was associated with the different modes of HBV markers.

A single nucleotide polymorphism -1131T>C in the apolipoprotein A5 gene is associated with an increased risk of coronary artery disease and alters triglyceride metabolism in Chinese.

The disorder of triglyceride (TG) metabolism leading to hypertriglyceridemia is an independent risk factor for coronary artery disease (CAD). Variants in the newly identified apolipoprotein APOA5 gene were found to be strongly associated with elevated TG levels in different racial groups. In this study, we investigated the phenotypic effects of two polymorphisms (APOA5-1131T>C and APOC3-482C>T) on susceptibility to CAD in 312 Chinese CAD patients diagnosed by angiography. The frequency of the APOA5-1131C allele in these patients was significantly higher than that of the control group (39.9 vs. 33.3%, P=0.02). Compared with the wild type TT, CC homozygotes had a significantly increased CAD risk (OR=1.93 and OR=1.80 using unadjusted and adjusted logistic regression models, respectively). This association still existed after adjustment for the APOC3-482 variant. The APOA5-1131C allele also showed a correlation with increasing plasma TG levels (P<0.001). These data suggest that the APOA5-1131T>C polymorphism might contribute to an increased risk of CAD among Chinese as a result of its effect on TG metabolism; this effect was found to be independent of the APOC3-482C>T variant.