« Previous
Next »
Gastroenterology
Volume 139, Issue 1
, Pages
120-129.e18
, July 2010
Interleukin-28B Polymorphism Improves Viral Kinetics and Is the Strongest Pretreatment Predictor of Sustained Virologic Response in Genotype 1 Hepatitis C Virus
-
Median reductions in viral load from baseline on the basis of IL-28B type. (A) Caucasian, (B) African American, and (C) Hispanic patients. Bars represent 25th and 75th percentiles. P < .001 for all pa
Median reductions in viral load from baseline on the basis of IL-28B type. (A) Caucasian, (B) African American, and (C) Hispanic patients. Bars represent 25th and 75th percentiles. P < .001 for all pairwise comparisons of median viral load for CC vs CT or TT using the Wilcoxon 2-sample test (see ).
-
Virologic responses on treatment on the basis of IL-28B type and ethnicity. (A) Caucasian, (B) African American, and (C) Hispanic patients. EOTR, end-of-treatment response. Statistical comparisons areVirologic responses on treatment on the basis of IL-28B type and ethnicity. (A) Caucasian, (B) African American, and (C) Hispanic patients. EOTR, end-of-treatment response. Statistical comparisons are presented in Table 2.
-
Median reductions in viral load from baseline on the basis of IL-28B genotype in the adherent subset. (A) Caucasians, (B) African Americans, and (C) Hispanics. Bars represent 25th and 75th percentilesMedian reductions in viral load from baseline on the basis of IL-28B genotype in the adherent subset. (A) Caucasians, (B) African Americans, and (C) Hispanics. Bars represent 25th and 75th percentiles. Statistical comparisons are presented in .
-
Virologic responses on treatment on the basis of IL-28B SNP genotype and ethnicity in the adherent subset. (A) Caucasians, (B) African Americans, and (C) Hispanics. EOTR, end-of-treatment response. StVirologic responses on treatment on the basis of IL-28B SNP genotype and ethnicity in the adherent subset. (A) Caucasians, (B) African Americans, and (C) Hispanics. EOTR, end-of-treatment response. Statistical comparisons are presented in .
View this article's video abstract at www.gastrojournal.org.
Conflicts of interest The authors disclose the following: Drs McHutchison, Goldstein, Muir, Afdhal, Jacobson, Esteban, Poordad, Lawitz, McCone, Shiffman, Galler, Lee, Reindollar, King, Kwo, Ghalib, Freilich, Nyberg, Patel, Zeuzem, Poynard, and Sulkowski report having received research and grant support from Schering-Plough; Drs McHutchison, Goldstein, Muir, Afdhal, Jacobson, Esteban, Poordad, Lawitz, Shiffman, Reindollar, Kwo, Zeuzem, Poynard, and Sulkowski have received consulting fees or acted in an advisory capacity for Schering-Plough; Drs Brass, Koury, Pedicone, and Albrecht are employees of Schering-Plough (now Merck & Co, Inc) and are stockholders in this entity; Dr Noviello is a former employee of Schering-Plough and is now a consultant to Merck & Co, Inc; and Drs Goldstein, Ge, Fellay, Shianna, Urban, McHutchison, and Thompson are co-inventors of a patent application based on this finding. David Vock and Karen Pieper declare that they have had access to all data and independent statistical support to allow them to analyze the data independently of the sponsor of the study.
Funding This study was funded by Schering-Plough Research Institute, Kenilworth, NJ; Alexander Thompson received funding support from the Duke Clinical Research Institute, the Richard B. Boebel Family Fund, the National Health and Medical Research Council of Australia, and the Gastroenterology Society of Australia and the Royal Australasian College of Physicians.Jennifer King, PhD, provided editorial assistance in preparing the manuscript; she was funded by the Duke Clinical Research Institute, Duke University. The sponsor did not provide any funding for Dr King or have any contact with her.
PII: S0016-5085(10)00574-3
doi: 10.1053/j.gastro.2010.04.013
© 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Gastroenterology
Volume 139, Issue 1
, Pages
120-129.e18
, July 2010
