Prospective Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 14, 2016; 22(46): 10226-10231
Published online Dec 14, 2016. doi: 10.3748/wjg.v22.i46.10226
Genotype specific peripheral lipid profile changes with hepatitis C therapy
Mark R Pedersen, Amit Patel, David Backstedt, Myunghan Choi, Anil B Seetharam
Mark R Pedersen, Department of Internal Medicine, Banner University Medical Center, University of Arizona College of Medicine, Phoenix, AZ 85006, United States
Amit Patel, David Backstedt, Department of Gastroenterology, Banner University Medical Center, University of Arizona College of Medicine, Phoenix, AZ 85006, United States
Myunghan Choi, Arizona State University College of Nursing and Health Care Innovation, Phoenix, AZ 85006, United States
Anil B Seetharam, Banner Transplant and Advanced Liver Disease Center, University of Arizona College of Medicine, Phoenix, AZ 85006, United States
Author contributions: Seetharam AB designed the study; Pedersen MR, Patel A and Backstedt D performed the data collection; Choi M analyzed the data; Pedersen MR wrote the paper; and Seetharam AB revised the manuscript for final submission.
Institutional review board statement: This study was reviewed and approved by the Banner University Medical Center - Phoenix Institutional Review Board.
Informed consent statement: The need for informed consent for the prospective study was waived by our institutional review board.
Conflict-of-interest statement: Anil Seetharam has served as a speaker and accepted speaker’s fees for Gilead and Janssen.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Anil B Seetharam, MD, Banner Transplant and Advanced Liver Disease Center, University of Arizona College of Medicine, 1300 N. 12th Street Suite 404, Phoenix, AZ 85006, United States. anil.seetharam@bannerhealth.com
Telephone: +1-602-8397000 Fax: +1-602-8397050
Received: June 23, 2016
Peer-review started: June 24, 2016
First decision: August 29, 2016
Revised: September 27, 2016
Accepted: October 27, 2016
Article in press: October 27, 2016
Published online: December 14, 2016
Processing time: 172 Days and 18.8 Hours
Abstract
AIM

To evaluate magnitude/direction of changes in peripheral lipid profiles in patients undergoing direct acting therapy for hepatitis C by genotype.

METHODS

Mono-infected patients with hepatitis C were treated with guideline-based DAAs at a university-based liver clinic. Patient characteristics and laboratory values were collected before and after the treatment period. Baseline demographics included age, ethnicity, hypertension, diabetes, hyperlipidemia, treatment regimen, and fibrosis stage. Total cholesterol (TCHOL), high density lipoprotein (HDL), low density lipoprotein (LDL), triglycerides (TG), and liver function tests were measured prior to treatment and ETR. Changes in lipid and liver function were evaluated by subgroups with respect to genotype. Mean differences were calculated for each lipid profile and liver function component (direction/magnitude). The mean differences in lipid profiles were then compared between genotypes for differences in direction/magnitude. Lipid profile and liver function changes were evaluated with Levene’s test and student’s t test. Mean differences in lipid profiles were compared between genotypes using ANOVA, post hoc analysis via the Bonferroni correction or Dunnett T3.

RESULTS

Three hundred and seventy five patients enrolled with 321 (85.6%) achieving sustained-viral response at 12 wk. 72.3% were genotype 1 (GT1), 18.1% genotype 2 (GT2), 9.7% genotype 3 (GT3). Baseline demographics were similar. Significant change in lipid profiles were seen with GT1 and GT3 (ΔGT1, p and ΔGT3, p), with TCHOL increasing (+5.3, P = 0.005 and +16.1, P < 0.001), HDL increasing (+12.5, P < 0.001 and +7.9, P = 0.038), LDL increasing (+7.4, P = 0.058 and +12.5, P < 0.001), and TG decreasing (-5.9, P = 0.044 and -9.80 P = 0.067). Among genotypes (ΔGT1 v. ΔGT2 v. ΔGT3, ANOVA), significant mean differences were seen with TCHOL (+5.3 v. +0.1 v. +16.1, P = 0.017) and HDL (+12.3 v. +2 v. +7.9, P = 0.040). Post-hoc, GT3 was associated with a greater increase in TCHOL than GT1 and GT2 (P = 0.028 and P = 0.019).

CONCLUSION

Successful DAA therapy results in increases in TCHOL, LDL, and HDL and decrease in TG, particularly in GT1/GT3. Changes are most pronounced in GT3.

Keywords: Hepatitis C genotypes; Lipids; Metabolic syndrome

Core tip: Different genotypes of the hepatitis C virus (HCV) are associated with differing levels of hepatic steatosis, with genotype 3 (GT3) having the strongest direct association. In this investigation, change in peripheral lipid panels during direct-acting antiviral therapy were assessed in a large HCV treatment cohort with respect to genotype. Total cholesterol in patients with GT3 increased significantly during treatment compared to other genotypes. Associated steatosis and differing lipid kinetics may influence response rates to direct acting therapy and may also influence genotype specific risks of hepatic and systemic complications.