Ignite Creation Date:
2024-05-05 @ 5:22 PM
Last Modification Date:
2024-10-26 @ 9:31 AM
Study NCT ID:
NCT00444002
Status:
COMPLETED
Last Update Posted:
2014-01-10
First Post:
2007-03-06
Brief Title:
Oxidative Stress and Fatty Acids in Hepatitis C
Sponsor:
Johane Allard
Organization:
University Health Network Toronto
Study Overview
Official Title:
Hepatitis C Infection With Liver Steatosis Compared to Hepatitis C Infection Without Liver Steatosis Is There a Difference in Lipid Peroxidation and Indicators of Inflammation
Status:
COMPLETED
Status Verified Date:
2014-01
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
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 mechanisms 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
However the exact mechanisms 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
Detailed Description:
Hypothesis Patients with Hepatitis C and steatosis are more oxidatively stressed than those without steatosis This is associated with 1 increased liver lipid peroxides and cytokines TNF-alpha TGF-beta 2 altered unsaturated fat status intake tissue storage as measured in red blood cells 3 reduced antioxidant status
Objectives To assess oxidative stress and nutritional status in patients with Hepatitis C and steatosis on liver biopsy and to compare the results to the same parameters measured in patients with Hepatitis C and no steatosis
Measurements
Primary outcome Liver lipid peroxides LPO
Secondary outcomes
Liver TNF-alpha liver pathology and immunohistochemistry for adducts of malondialdehyde MDA a product of lipid peroxidation LP alpha-smooth muscle actin alpha-SMA a marker of hepatic stellate cell activation and transforming growth factor TGF-beta a profibrogenic cytokine involved in fibrogenesis liver fatty acid composition substrate for lipid peroxidation
Oxidative stress and nutrition Plasma lipid peroxides plasma antioxidant vitamins antioxidant status and power and red blood cell fatty acid composition 7 day food record anthropometry
Other measurements
Insulin resistance parameters such as blood glucose insulin c-peptide hemoglobin A1c HbA1c Blood lipid profile liver enzymes as part of standard medical assessment Subject demographics and medical history will also be recorded
Objectives To assess oxidative stress and nutritional status in patients with Hepatitis C and steatosis on liver biopsy and to compare the results to the same parameters measured in patients with Hepatitis C and no steatosis
Measurements
Primary outcome Liver lipid peroxides LPO
Secondary outcomes
Liver TNF-alpha liver pathology and immunohistochemistry for adducts of malondialdehyde MDA a product of lipid peroxidation LP alpha-smooth muscle actin alpha-SMA a marker of hepatic stellate cell activation and transforming growth factor TGF-beta a profibrogenic cytokine involved in fibrogenesis liver fatty acid composition substrate for lipid peroxidation
Oxidative stress and nutrition Plasma lipid peroxides plasma antioxidant vitamins antioxidant status and power and red blood cell fatty acid composition 7 day food record anthropometry
Other measurements
Insulin resistance parameters such as blood glucose insulin c-peptide hemoglobin A1c HbA1c Blood lipid profile liver enzymes as part of standard medical assessment Subject demographics and medical history will also be recorded
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None