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
None
inability or unwillingness to sign informed consent
cancer
autoimmune disease that in the opinion of the PI will confound study data
INR < 1.4
Patients with alcoholic hepatitis as diagnosed by liver biopsy, imaging, or biochemical values with noted encounter in Cleveland Clinic Electronic Medical Record, Heavy Drinking Controls - patients who lack any evidence (biochemical, imaging, and/or biopsy) of alcoholic liver disease who consume \>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 Healthy Controls - patients without any form of liver disease nd do not meet the criteria for "Heavy Drinking Controls"
Cohort
Prospective
Blood Draw
Other interventionBlood Draw Only
Quantify mitochondrial respiration
Mitochondrial Respiration will be quantified by using a standard substrate, uncoupler, inhibitor titration protocol using high resolution respirometry
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