In conclusion, the results of the present study show PEG-IFN (40 kDa) administered at a dose of 135 ��g weekly for 48 mo was efficacious but not perfectly tolerable in dialysis patients with HCV infection. COMMENTS Background Our study showed that PEG-IFN (40 kDa) administered at a dose of 135 ��g weekly for 48 mo was efficacious but not perfectly tolerable in dialysis selleck chemicals llc patients with chronic hepatitis C. Research frontiers The present study was carried out in South-east Anatolien/Diyarbakir, Turkey, in hemodialysis patients with chronic hepatitis C. Related publications Yu JW, Wang GQ, Sun LJ, Li XG, Li SC. Predictive value of rapid virological response and early virological response on sustained virological response in hepatitis C virus (HCV) patients treated with pegylated interferon ��-2a and ribavirin.
J Gastroenterol Hepatol. 2007 Jun; 22(6): 832-836. Sporea I, Popescu A, Sirli R, Golea O, Totolici C, Danila M, Vernic C. Pegylated-interferon �� 2a treatment for chronic hepatitis C in patients on chronic hemodialysis. World J Gastroenterol. 2006 Jul 14; 12(26): 4191-4194. Innovations and breakthroughs Many studies published that PEG-IFN treatment is efficacious and tolerable in hemodialysis patients with chronic hepatitis C. In our study we found similar efficacy, but this treatment was not perfectly tolerable in dialysis patients with HCV infection. Peer review Ayaz et al investigated the effects of PEG-IFN for treatment of HCV infection in hemodialysis patients. Eleven of 17 patients had a SVR at wk 24 after end-of-treatment. In 5 patients treatment had to be stopped because of side effects.
The currently available data on this topic are scarce and therefore this is an important study which should be published. Footnotes S- Editor Rivera CA L- Editor Mihm S E- Editor Yin DH
MYH-associated polyposis (MAP) is an autosomal recessive condition (Al-Tassan et al, 2002) associated with the development of multiple adenomas and carcinomas of the colon and rectum, as well as other possible malignancies and extra-colonic manifestations (Enholm et al, 2003; Sampson et al, 2003; Sieber et al, 2003; Gismondi et al, 2004; Nielsen et al, 2005). The syndrome is caused by germline biallelic mutations in MYH, a gene that codes for a DNA glycosylase involved in base excision repair (BER) (Al-Tassan et al, 2002).
MYH mutations have been shown to be ethnically specific, and most (80%) Caucasian individuals with MAP possess the Y165C or G382D mutations (Enholm et al, 2003; Croitoru et al, 2004; Fleischmann et al, 2004; Wang et al, 2004; Farrington et al, 2005; Peterlongo et al, 2005). Italian populations also carry a three base pair deletion (1395delGGA) in exon 14 (Gismondi GSK-3 et al, 2004), whereas non-Caucasian populations harbour a range of different MYH mutations (Jones et al, 2002).