Rapid Changes in Serum Lipid Profiles during Combination Therapy with Daclatasvir and Asunaprevir in Patients Infected with Hepatitis C Virus Genotype 1b

BACKGROUND/AIMS: Changes in lipid profiles in patients infected with hepatitis C virus (HCV) during direct-acting antiviral therapy have been reported in recent years. However, the clinical aspects of disturbed lipid metabolism in chronic HCV infection have not been fully elucidated. METHODS: Dynamic changes in serum total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol and apolipoprotein levels in patients infected with HCV genotype 1b were examined during combination therapy with daclatasvir (DCV) and asunaprevir (ASV). RESULTS: Total, LDL−, and HDL-cholesterol levels increased rapidly and persistently after week 4. Apolipoprotein (apo) A-I, apo B, apo C-II, and apo C-III levels were significantly higher at week 4 than at week 0. In contrast, apo A-II and apo E levels were significantly lower. The differences in LDL− and HDL-cholesterol levels were positively correlated with those of apo B and apo A-I, respectively. Interestingly, in patients with non-sustained virological response, these cholesterol levels decreased rapidly after viral breakthrough or viral relapse. Furthermore, similar changes were observed for apo A-I, apo B and apo C-III levels. CONCLUSIONS: Clearance of HCV using combination therapy with DCV and ASV results in rapid changes in serum lipid profiles, suggesting an influence of HCV infection on disturbed lipid metabolism.

Encephalopathy in type I hyperlipidemia.

Familial chylomicronemia syndrome is a group of rare genetic disorders characterized by deficient activity of an enzyme lipoprotein lipase or apo-protein C-II deficiency. In this paper we present an infant with massive hyperchylomicronemia and severe pancreatitis. Exchange transfusion for controlling hypertriglyceridemia and pancreatitis led to an increase in hyperviscosity which resulted in encephalopathy.

The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate associations between the apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease (CAD).</p><p><b>METHODS</b>apoE genotypes were identified by multiplex amplification refractory mutation system (multi-ARMS) and the polymorphisms of both apoCI and apoCII genes were detected by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 203 cases of CAD and 365 controls. Pairwise linkage disequilibrium coefficients (D, D') were estimated by the LINKAGE program.</p><p><b>RESULTS</b>The frequencies of apoE E3/4 genotype (0.259) and epsilon4 (0.139) in CAD group were significantly higher than that in control group (0.125, 0.069), (P<0.05). The significant difference was also found for the apoCI locus, the frequencies of H2 allele were 0. 205 in the CAD and 0.113 in the control. Linkage disequilibrium coefficient D' was 0.672 (P<0.01) between apoE and apoCI genes. Significant differences for a deficit of epsilon3-H1-T1 and excess of epsilon4-H2-T1 were found in the CAD by estimation of the haplotype frequencies. After adjustment for possible confounding factors, the multivariate Logistic analysis showed a significant interaction among epsilon4, H2 and smoking, OR value was 18.3 (95%CI:2.35-150.81, P<0.05), attributable proportions of interaction (API) was 57.3%, it was a multiplicative model. An additive model was shown among epsilon4, H2 and bibulosity; the odds ratio (OR) (95%CI) and API of their interaction were 12.7(2.8-58.6, P<0.05) and 43.5%, respectively.</p><p><b>CONCLUSION</b>The results suggested that both apoE and apoCI on chromosome 19 were the susceptibility loci for CAD, their linkage disequilibrium should be responsible for the development of CAD. Smoking and bibulosity can significantly increase the risk of CAD.</p>

Expression of apolipoprotein C-II mRNA in cultured HepG2 cell / 대한내분비학회지

No abstract available.