Molecular basis and current treatment for alcoholic liver disease

Abstract

Alcohol use disorders and alcohol dependency affect millions of individuals worldwide. The impact of these facts lies in the elevated social and economic costs. Alcoholic liver disease is caused by acute and chronic exposure to ethanol which promotes oxidative stress and inflammatory response. Chronic consumption of ethanol implies liver steatosis, which is the first morphological change in the liver, followed by liver fibrosis and cirrhosis. This review comprises a broad approach of alcohol use disorders, and a more specific assessment of the pathophysiologic molecular basis, and genetics, as well as clinical presentation and current modalities of treatment for alcoholic liver disease.

Keywords: alcohol; alcoholic liver disease; alcoholism; cirrhosis; fibrosis.

Figure 1.

Main molecular mechanisms by which ethanol causes oxidative stress. NAD Nicotinamide adenine dinucleotide, NADH reduced form of NAD, AMP-K Adenosine monophosphate protein kinase, ROS Reactive oxygen species, ADH Alcohol dehydrogenase, ALDH Acetaldehyde dehydrogenase.

Figure 2.

NK Natural killer, TNF-α Tumor Necrosis Factor alpha, LPS Lipopolysaccharide.

Figure 3.

Steatosis (black arrows) with lipidic cytoplasmic inclusions, it is reversible as long as the harmful stimulus is removed. Nodules circumscribed by fibrous tissue with collagen deposition (red arrows).