Liver diseases by alcohol and hepatitis C: Early detection and new insights in pathogenesis lead to improved treatment

Much progress has been made in the understanding of the pathogenesis of alc oholic liver disease, resulting in improvement of treatment. Therapy must i nclude correction of nutritional deficiencies, while taking into account ch anges of nutritional requirements. Methionine is normally activated to S-ad enosylmethionine (SAMe). However, in liver disease, the corresponding enzym e is depressed. The resulting deficiencies can be attenuated by the adminis tration of SAMe but not by methionine. Similarly, phosphatidylethanolamine methyltransferase activity is depressed, but the lacking phosphatidylcholin e (PC) can be administrated as polyenylphosphatidylcholine (PPC). Chronic e thanol consumption increases CYP2E1, resulting in increased generation of t oxic acetaldehyde and free radicals, tolerance to ethanol and other drugs, and multiple ethanol-drug interactions. Experimentally, PPC apposes CYP2E1 induction and fibrosis. Alcoholism and hepatitis C infection commonly, co-e xist, with acceleration of fibrosis, cirrhosis, and hepatocellular carcinom a. PPC is being tested clinically as a corresponding antifibrotic agent. Av ailable antiviral agents are contraindicated in the alcoholic. Anti-inflamm atory agents, such as steroids, may be selectively useful: Finally, anticra ving agents, such as naltrexone or acamprosate, should be part of therapy.