Discussion The major findings of the present study are, serum EPO levels of all individuals increased significantly 5 fold at week 4 and 14 fold at week 8 compared to baseline, EPO rs1617640 G homozygotes showed significantly lower serum EPO levels during antiviral treatment compared to T allele carriers, besides age, baseline Hb levels and selleck inhibitor RBV dose, EPO rs1617640 G allele is independently asso ciated with Hb decline during antiviral treatment, in EPO rs1617640 G homozygotes the need of RBV dose reduction as well as epoetin supplementation was sig nificantly higher compared to T allele carriers, Inhibitors,Modulators,Libraries ITPA rs1127354 gene variant rather associated with Hb reduc tion at week 4 but not at week 12 and did not increase the risk of epoetin supplementation, RBV dose reduction or blood transfusion.

Hb decline during antiviral treatment is a frequent side effect and the reason for it is probably multifactorial. IFN induces a significant and rapid dose dependent Hb decline in CHC patients probably by causing an inhibition of hematopoietic stem cell proliferation. Accumulation of RBV in Inhibitors,Modulators,Libraries red blood cells may aggravate anemia by inducing hemolysis. The most important mediator of erythropoiesis is EPO. Several reports have examined serum EPO levels during antiviral treatment and could Inhibitors,Modulators,Libraries show that serum EPO levels are increasing up to 4 fold at week 4 in patients treated with PEG IFN and RBV while Hb levels are declining. Our present study is consistent with these results in this respect. Here, we examined for the first time a sin gle nucleotide polymorphism within the EPO gene promoter, rs1617640, in chronic hepatitis C patients who were undergoing antiviral treatment.

The T allele of this polymorphism had been shown to be associated with higher levels of EPO in the Inhibitors,Modulators,Libraries vitreous body fluid of non diabetic patients than the G allele. The present study found EPO rs1617640 G homozygotes to have an attenu ated serum EPO response compared to T allele carriers. Moreover, EPO rs1617640 G homozygotes also had higher incidence of significant Hb reduction at week 4 and 12. Finally, EPO rs1617640 G homozygotes had a significantly higher need of RBV dose reduction or epoetin supple mentation, but not blood transfusion. The reason for this might be the relatively small sample number of patients who achieved blood transfusion.

Although this study investigated the EPO rs1617640 Inhibitors,Modulators,Libraries SNP with regard to a common side effect such as Hb decline of antiviral therapy in CHC patients, our findings might not be specific for therapy of CHC with RBV. This SNP might directly be involved in the regulation of the EPO response to acute Hb decline in other conditions as well. Here, the role of RBV might just be in inducing an erythropoietic stress test taking advantage of con trolled conditions which are not typically achievable Cisplatin structure in human research. Therefore, further research should investigate the role of the EPO gene vari ation in various anemic diseases.