Overview
Inflammatory responses in response to alcohol have been identified as contributing to the development of alcoholic hepatitis. The inflammatory response including that to LippoPolySaccharide is known to lead to progression of alcoholic liver disease. In addition to the inflammatory response mitochondrial perturbations exist and redox homeostasis is altered in patients with alcoholic hepatitis. Though this is known there have been very few studies targeting mitochondrial function in Peripheral Blood Mononuclear Cells (PBMCs). We plan to collect 50 milliliters of blood from healthy control patients so that we can compare the data to that of patients with alcoholic hepatitis and those who are heavy drinkers without liver disease. In addition to studying mitochondrial function we will investigate cytokine response, as well as fatty acid metabolism, glucose, and insulin measurements
Eligibility
Inclusion of Subjects with Alcoholic Hepatitis (AH):
*diagnosis of AH either by imaging, biochemical values or liver biopsy as well as drinking history
Inclusion Heavy Drinking Controls:
*heavy alcohol drinking will be defined as >40 g/day or >280g/week on average for women and >60 g/day or >420 g/week on average for men for a minimum of 6 months [6] and within the 4 weeks prior to study enrollment.
Exclusion Criteria for all groups
- inability or unwillingness to sign informed consent
- cancer
- autoimmune disease that in the opinion of the PI will confound study data
Control subjects (drinking and non drinking) must meet the following criteria:
- INR < 1.4
- total bilirubin levels must <3
- no prior history of known alcoholic liver disease
- absence of hepatosplenomegaly (from physical examination or radiographic imaging) or stigmata of liver disease.