In regression models, several lipid profile parameters at baseline (TG and LDLc, HDLc [with an interaction with gender]) and on-treatment changes (TG and LDLc) were significant predictors of SVR. However, including

this website serum lipid measures did not significantly improve the prediction of SVR compared with models without these measures, nor did serum lipid measures account for the racial difference in treatment efficacy between CAs and AAs. Few studies have assessed in detail changes in serum lipids during and after therapy for chronic HCV infection. Compared with pretreatment, the significant increase in TG levels during therapy found here is consistent with findings in other studies that reported mean increases of 45 mg/dL and 60 mg/dL in TG levels.8, 9 We note that compared with pretreatment, these studies did not report significant changes in TC during or after therapy, whereas our study found significant declines in TC during treatment.8, 9 However, the significant increase in TC levels posttreatment compared with pretreatment is consistent with one study that reported an approximate 10.5 mg/dL significant mean

increase,7 whereas another study did not report significant changes.8 The difference in findings across studies may be due to variable sample sizes, disparate treatment regimens, inclusion of patients with different HCV genotypes, and other participant characteristics. The direct relationship between pretreatment LDLc levels and SVR rate is consistent with findings from several other studies.10-14 Hamamoto https://www.selleckchem.com/products/PLX-4032.html et al.7 reported an association between higher pretreatment TG levels and virological response, which is opposite of the relationship in our study, possibly a reflection of HCV genotype or host

lipid receptor genetic differences. Whereas only individuals infected with HCV genotype 1 were included in Virahep-C, genotype 2 was the predominant genotype in the previously referenced study. Single-nucleotide polymorphisms in the receptors involved in the serum lipoprotein particle uptake into hepatocytes (SR-B1 and LDL receptors) may also account for the different relationships observed in the Sulfite dehydrogenase two study populations. In multivariable analyses, significant interactions between HDLc levels and gender in relation to virological response were found, which have not been previously reported. These relationships warrant further investigation and validation in other cohorts to clarify whether lipid profile measures are important predictors of treatment response. Posttreatment increases from baseline in LDLc and TC were found to be associated with SVR, which may correspond to HCV eradication and the subsequent resolution of HCV-induced liver damage.