Molecular Insights into Alcohol-Induced Hepatocarcinogenesis and
Comorbidities: Unravelling the Clinical Markers Symphony
Abstract
This review delves into the molecular mechanism that drives
alcohol-induced liver cancer and associated comorbidities, emphasizing
on the role of specific biomarkers that help in diagnosing these
conditions. Chronic alcohol consumption triggers oxidative stress by
generating reactive oxygen species (ROS), which disrupt mitochondrial
function and cause cell death ultimately. Elevated levels of alanine
aminotransferase (ALT) in relation to aspartate aminotransferase (AST)
are key indicators of liver injury, shedding light on significant marker
for alcoholic liver disease (ALD). Enzymes such as gamma-glutamyl
transferase (GGT) and alkaline phosphatase (ALP) further provide
insights into bile duct function and potential risks for hepatocellular
carcinoma (HCC) and cholestasis. Hyaluronic acid (HA), procollagen III
peptide (Pro-C3), and fibrosis-4 (FIB-4) index also emerge as important
biomarkers for liver fibrosis, offering a non-invasive method for
assessing the degree of fibrosis through the analysis of ALT, AST, and
platelet counts. The review also explores how alcohol accelerates liver
damage in individuals with hepatitis B or C infection, by enhancing
viral replication and suppressing immune responses. Advanced imaging
technologies, such as ultrasound, computed tomography (CT), and magnetic
resonance imaging (MRI) reveal the structural changes and tumour
presence in the liver, improving the accuracy of diagnosing and
monitoring liver diseases with the help of these biomarkers. The other
key signatures in alcohol-induced liver disease such as pro-inflammatory
cytokines production, insulin resistance, dyslipidaemia, blood pressure,
cholesterol levels, and cognitive functions are crucial in assessing
liver pathogenesis. These holistic approaches highlight the importance
of molecular markers and imaging techniques, allowing for earlier
intervention and better patient outcomes.