Liver Diseases by Alcohol and Hepatitis C: Early Detection and New Insights in Pathogenesis Lead to Improved Treatment

Abstract

Much progress has been made in the understanding of the pathogenesis of alcoholic liver disease, resulting in improvement of treatment. Therapy must include correction of nutritional deficiencies, while taking into account changes of nutritional requirements. Methionine is normally activated to S-adenosylmethionine (SAMe). However, in liver disease, the corresponding enzyme is depressed. The resulting deficiencies can be attenuated by the administration of SAMe but not by methionine. Similarly, phosphatidylethanolamine methyltransferase activity is depressed, but the lacking phosphatidylcholine (PC) can be administrated as polyenylphosphatidylcholine (PPC). Chronic ethanol consumption increases CYP2E1, resulting in increased generation of toxic acetaldehyde and free radicals, tolerance to ethanol and other drugs, and multiple ethanol-drug interactions. Experimentally, PPC opposes CYP2E1 induction and fibrosis. Alcoholism and hepatitis C infection commonly co-exist, with acceleration of fibrosis, cirrhosis, and hepatocellular carcinoma. PPC is being tested clinically as a corresponding antifibrotic agent. Available antiviral agents are contraindicated in the alcoholic. Anti-inflammatory agents, such as steroids, may be selectively useful. Finally, anticraving agents, such as naltrexone or acamprosate, should be part of therapy.

Hepatitis C: Magnitude of the problem

“…[3][4][5] A similar observation has been found among obese patients with hepatic steatosis. These investigators also found that steatosis was observed more commonly in association with genotype 3 independent of body mass index.…”

Effect of Alcohol Consumption On Platelets Count, Intrinsic and Extrinsic Pathways of Blood Coagulation

“…Alcohol is a drug that depresses the central nervous system like sedative and anesthetics. It is not a stimulant as widely believed but speech becomes free and social inhibition may be forgotten since it affects the portion of the brain that control judgment (Leiber, 2000). It infiltrates the brain, liver heart, pancrease, lung and kidney within minutes and passes into the blood stream (Epstein, 1992).…”

Does Diversity Matter? The Need for Longitudinal Research on Adolescent Alcohol and Drug Use Trajectories

“…Finally, it is important to better understand how outcomes related to AOD use may differ across racial/ethnic groups. Although research has shown that non-whites often have worse health outcomes (Caetano & Clark, 1998; Herd, 1989; Lieber, 2001; NIDA, 1998; Stinson, Grant, & Dufour, 2001; Sutocky, Shultz, & Kizer, 1993) and more problems (e.g., with family, accidents) associated with AOD use compared to whites (Galvan & Caetano, 2003) even with less AOD use, it is not clear why this occurs (NIAAA, 2002). …”