Oxidative Stress and Fatty Acids in Hepatitis C

NCT00444002 | Completed

• 1 other identifier: 05-0305 AE
• Study Type: observational
• Target: 105
• Locations: 1 country
• Sites: 1

Brief Summary

Hepatitis C virus infection (HCV) is a major health concern in Canada and worldwide. Chronic HCV can cause progressive liver damage leading to inflammation, scarring and, in some cases, cirrhosis or liver cancer. It has been shown that fat accumulation in the liver can accelerate the disease progression and is therefore a risk factor in HCV patients. However, the exact mechanism(s) by which fat accumulation in the liver is involved in disease progression are not clear yet. It is possible that the presence of fat provides a liver susceptible to a second injurious process which leads to scarring. Candidates for this second "hit" may include insulin resistance, leading to accumulation of fat within the liver cells and secondly oxidation of these lipids. In turn, lipid peroxidation can lead to production of reactive oxygen species (unstable molecules that can damage cells) and cytokines (signal molecules that promote inflammation) resulting in more oxidative stress and liver damage. Aim of the study is to find out, whether patients with HCV and fatty liver have increased oxidative stress and inflammation than patients with HCV without fatty liver, and whether this is associated with a different nutritional status.

Conditions

Hepatitis C; Hepatic Steatosis

Keywords

Hepatitis C; Steatosis; Oxidative Stress; Antioxidants; Inflammation; Fatty acids

Outcome Measures

Primary Outcomes (1)

• Lipid peroxidation (LPO) in the liver

  LPO by commercially available kit

  Single time point

Secondary Outcomes (4)

• Hepatic fatty acid composition

  Single time point

• Antioxidant power in the liver

  Single time point

• Plasma vitamin C

  Single time point

• Tocopherols in plasma

  Single time point

Other Outcomes (2)

• Insulin resistance

  Single time point

• Dietary intake

  single time point

Study Arms (2)

Hepatitis C - Steatosis

Patients with chronic Hep C infection undergoing liver biopsy with \>=5% steatosis on liver biopsy

Hepatitis C - no steatosis

Patients with chronic Hep C infection without steatosis on liver biopsy (\<5% of hepatocytes involved)

Eligibility Criteria

• Age: 18 Years+
• Sex: all
• Healthy Volunteers: No
• Age Groups: Adult (18-64), Older Adult (65+)
• Sampling Method: Non-Probability Sample

Study Population

Patients with chronic Hep C infection undergoing routine pre-treatment liver biopsy

You may qualify if:

• Male and female patients, age \>18 y
• Established hepatitis C infection as confirmed by positive serology and positive hepatitis C RNA in serum
• Convincing evidence of negligible alcohol consumption (\<20g of ethanol per day) obtained from a detailed history, confirmed by at least one close relative
• Absence of any other possible cause for liver dysfunction.
• Undergoing routing liver biopsy (usually pre-treatment)

You may not qualify if:

• Findings highly suggestive of liver disease of other etiology (e.g. other viral hepatitis, auto-immune chronic hepatitis, primary biliary cirrhosis and genetic liver diseases such as hemochromatosis, alpha-1 antitrypsin deficiency, Wilsons disease and biliary obstruction)
• Anticipated need for liver transplantation in one year or complications of liver disease such as recurrent variceal bleeding, spontaneous porto- systemic encephalopathy, resistant ascites or bacterial peritonitis
• Concurrent medical illnesses contraindicating a liver biopsy (history of unexplained bleeding, hemophilia or abnormal coagulation results as per routine laboratory work-up or other reasons judged by the hepatologist to contraindicate a percutaneous liver biopsy)
• Medications known to precipitate steatohepatitis (corticosteroids, high dose estrogens, methotrexate, amiodarone, calcium channel blockers, sulfasalazine or cloxacillin) in the 6 months prior to entry
• Antioxidant vitamin or n-3 supplementation, ursodeoxycholic acid or any other experimental drug in the 6 months prior to study entry
• Pregnant or lactating

Sponsors & Collaborators

• Johane Allard: lead
• Canadian Association of Gastroenterology: collaborator

Study Sites (1)

University Health Network (Toronto General Hospital & Toronto Western Hospital)

Toronto, Ontario, Canada

Location

Related Publications (1)

• Arendt BM, Mohammed SS, Aghdassi E, Prayitno NR, Ma DW, Nguyen A, Guindi M, Sherman M, Heathcote EJ, Allard JP. Hepatic fatty acid composition differs between chronic hepatitis C patients with and without steatosis. J Nutr. 2009 Apr;139(4):691-5. doi: 10.3945/jn.108.101782. Epub 2009 Feb 11.

  PMID: 19211827 RESULT

MeSH Terms

Conditions

Hepatitis C; Fatty Liver; Inflammation

Condition Hierarchy (Ancestors)

Blood-Borne Infections; Communicable Diseases; Infections; Hepatitis, Viral, Human; Virus Diseases; Flaviviridae Infections; RNA Virus Infections; Hepatitis; Liver Diseases; Digestive System Diseases; Pathologic Processes; Pathological Conditions, Signs and Symptoms

Study Officials

• Johane P Allard, MD, FRCPC

  University Health Network, Toronto General Hospital

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Observational Model: CASE ONLY
• Time Perspective: CROSS SECTIONAL
• Sponsor Type: OTHER
• Responsible Party: SPONSOR INVESTIGATOR
• PI Title: Prof. Dr.

Study Record Dates

• First Submitted: March 6, 2007
• First Posted: March 7, 2007
• Study Start: July 1, 2005
• Primary Completion: July 1, 2008
• Study Completion: July 1, 2010
• Last Updated: January 10, 2014

Record last verified: 2014-01

Locations

CA (1)