Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

5. Alcohol 91The small intestine shows histological changes and contractual patternchanges even with adequate nutrition. Acute alcohol consumption impairsabsorption of folate, vitamin B 12, thiamine, and vitamin A, as well as someamino acids and lipids. Intestinal enzyme activity is altered as well (Hauge,Nilsson, Persson, & Hultberg, 1998).Alcohol consumption and gallstones are the two most common causes ofacute pancreatitis. Alcohol in moderate amounts does not increase the risk foracute pancreatitis, but consumption of 35 or more drinks per week increases theodds ratio to 4.1 (Blomgren et al., 2002). Acute pancreatitis presents as a dull,steady epigastric pain that may radiate to the back. Bending or sitting may partiallyrelieve the pain, confirming its retroperitoneal origin. Pain may be precipitatedor aggravated by meals and relieved by vomiting. A serum amylase of 1.5to 2.0 times the upper limit of normal has a sensitivity of 95% and a specificityof 98% for acute pancreatitis. Ethanol-induced acute pancreatitis is the result ofthe toxic effect of ethanol on pancreatic acinar cells, leading to inflammationand release of proteolytic enzymes. Chronic pancreatitis is caused most commonlyby alcoholism. The common presenting symptoms are abdominal pain,weight loss, nausea, vomiting, jaundice, and diarrhea. Surgical procedures areavailable for treatment of chronic pancreatitis, with favorable long-term results(Sohn et al., 2000).LiverThree histological distinct lesions occur in the evaluation of alcohol-inducedliver disease. The most common, occurring in 90% of heavy drinkers, is fattyliver (hepatic steatosis); 10–35% of heavy drinkers acquire alcoholic hepatitis,and 10–20% acquire alcohol cirrhosis (fibrosis, nodules, loss of normal structure).Alcohol leads to liver damage by several mechanisms: the production ofacetaldehyde, free radicals, and cytokines as alcohol is metabolized; the passageof bacterial endotoxins through the intestinal wall is enhanced by the presenceof alcohol; and alcohol-induced cell death and inflammation, which lead toscarring (Lieber, 1998).Hepatic steatosis is a common, reversible condition that may progress tocirrhosis in about 7% of cases (Gish, 1996). Signs and symptoms of alcoholicsteatosis include nausea, vomiting, hepatomegaly, right-upper-quadrant pain,and tenderness. Ascites and jaundice are uncommon. Laboratory data mayreveal mild elevation of transaminases, alkaline phosphatase, or bilirubin.Clinically, fatty liver may mimic or coexist with alcoholic hepatitis. Symptomsof alcoholic fatty liver, as well as alcoholic hepatitis, should resolve with abstinence.Alcoholic hepatitis frequently coexists with fatty liver and cirrhosis.Symptoms include anorexia, nausea, vomiting, fever, chills, and abdominalpain. Hepatomegaly and right-upper-quadrant tenderness are common.