The interaction between insulin resistance, liver fibrosis and early virological response in Egyptian patients with chronic hepatitis C.
BACKGROUND
Hepatitis C virus (HCV) infection may induce insulin resistance (IR) irrespective of the severity of liver disease, and there is evidence of a central role for IR in failure to achieve sustained virological response (SVR) in HCV patients.


OBJECTIVE
To assess IR as a predictor of the severity of hepatic fibrosis in Egyptian HCV patients, and its effect on early viral kinetics and virological response to HCV therapy.


METHODS
A total of 140 chronic HCV patients were divided into two groups according to the homeostasis model assessment-IR (HOMA-IR). Group 1 consisted of 48 chronic HCV patients with HOMA-IR >=2, and group 2 consisted of 92 chronic HVC patients without IR (HOMA IR <2). All patients were treated with combination therapy (pegylated interferon-alpha 2a plus ribavirin) for 48 weeks and studied for viral kinetics throughout the period of therapy.


RESULTS
The study revealed that older age, higher body mass index and HOMA-IR >=2 were significantly associated with advanced fibrosis. Rapid virological response, complete early virological response and SVR were significantly lower in the IR-HCV group compared with the non-IR-HCV group. Univariate and multivariate analyses revealed that older age, fibrosis (F>=3), high viral load (>600,000 IU⁄mL) and HOMA-IR >=2 were significantly associated with a lack of viral kinetics as well as SVR. However, HOMA-IR >=2 was the main independent variable associated with lack of SVR. On the other hand, body mass index, plasma insulin level and HOMA-IR decreased significantly compared with starting levels in patients who achieved SVR. This suggests a cause and effect relationship between HCV infection and IR.


CONCLUSIONS
IR in chronic HCV patients is associated with progressive fibrosis and slow viral kinetics, and could be a predictor for lack of rapid and early virological response. Therefore, HOMA-IR levels should be measured and improved before starting antiviral treatment.
Department of Tropical Medicine, Tanta University, Tanta, Egypt. dhz646@hotmail.com
Dina Hazem
DH
Ziada
Sherif
S
El Saadany
Mohamed
M
Enaba
Medhat
M
Ghazy
Azza
A
Hasan
D000328:Adult; D000367:Age Factors; D000998:Antiviral Agents / Q000627:therapeutic use; D001706:Biopsy; D016009:Chi-Square Distribution; D018450:Disease Progression; D004359:Drug Therapy, Combination; D004534:Egypt; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy; D006801:Humans; D007333:Insulin Resistance; D016898:Interferon-alpha / Q000627:therapeutic use; D008103:Liver Cirrhosis / Q000150:complications*; D016015:Logistic Models; D008297:Male; D011092:Polyethylene Glycols / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use; D012307:Risk Factors; D012720:Severity of Illness Index; D019562:Viral Load
D000998:Antiviral Agents; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a