Amino acid metabolism in liver cirrhosis]

In patients with liver cirrhosis the fasting plasma alpha-amino nitrogen concentration is high as the rule, due to reduced clearance of total alpha-amino nitrogen. The urea cycle is diminished of its capacity in cirrhotic patients than in the control subject, and to compensate for this, the extrahepatic glutamine cycle capacity is enlarged in the patients. The following important topics were taken up in this mini review: some problems concerning Fischer ratio, amino acids metabolism and pH regulation in the liver, and the supplementation therapy with branched chain amino acids under the condition of organ relationship.     

Alcoholic liver disease

Aggressive management to prevent alcoholic cirrhosis should include the use of biopsy results to diagnose and to monitor alcoholic liver disease. Guidelines for the interpretation of the liver biopsy are highlighted. The diagnosis, course, and treatment of alcoholic hepatitis and cirrhosis are presented in detail.     

Alcoholic liver disease

Liver injury may develop in some people who consume alcohol. The pathogenesis of liver damage in such subjects remains obscure. Major histopathologic features of alcohol-associated liver injury include steatosis, steatonecrosis, and cirrhosis. The clinical manifestations of alcoholic liver disease are nonspecific and range from asymptomatic hepatomegaly to stigmata of portal hypertension with advanced parenchymal failure. The severity of the clinical presentation and the degree of aminotransferase elevation correlate poorly with the liver histopathology, particularly in patients who continue to drink alcohol. Short-term mortality of such patients is best predicted by a composite of clinical and laboratory parameters that are influenced by alcohol consumption as well as by liver disease. Long-term prognosis is determined by residual damage to vital organs (that is, whether or not cirrhosis has developed) and whether or not the patient continues to drink. Current therapy of alcoholic liver disease includes abstinence and correction of nutritional deficiencies. Other therapies are experimental and are best utilized in the setting of controlled clinical trials.     

Alcoholic liver disease

Alcoholic liver disease presents a wide spectrum of clinical manifestations ranging from mild asymptomatic fatty liver to alcoholic hepatitis and severe life-threatening liver failure with ascites, hemorrhaging esophageal varices, and encephalopathy. Although still poorly understood, the mechanism of this injury is probably the result of numerous direct toxic and metabolic effects of alcohol on the hepatocyte. Therapy consists primarily of abstinence and supportive care. However, several newer treatments are actively being studied. These include prednisolone, anabolic steroids, glucagon and insulin, propylthiouracil, and cyanidanol. Colchicine is promising as an agent to inhibit fibrosis. Complications of cirrhosis, including ascites and variceal hemorrhage, are the result of end stage disease. A return to old techniques of ascitic fluid management suggests that therapeutic large-volume paracentesis with albumin infusion is a safe and effective form of therapy. Variceal hemorrhage is best treated with sclerotherapy, vasoconstrictors, and balloon tamponade. Little has been done to alter the ultimately dismal prognosis and long-term survival of alcoholic liver disease.