11.07.2015 Views

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

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

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

SHOW MORE
SHOW LESS
  • No tags were found...

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

92 III. SUBSTANCES OF ABUSETransaminase levels rarely exce<strong>ed</strong> 500 international units (IU), with a typicalratio <strong>of</strong> aspartate aminotransferase to alanine aminotransferase <strong>of</strong> 2:1 to 5:1.Liver biopsy can be helpful in distinguishing fatty liver from hepatitis and fromcirrhosis. Ascites, encephalopathy, high bilirubin levels, and prolongation <strong>of</strong>the prothrombin time are poor prognostic indicators that portend an increas<strong>ed</strong>mortality. Treatment consists <strong>of</strong> abstinence and nutritional support. Treatmentwith steroids, propylthiouracil, and colchicines has yield<strong>ed</strong> mix<strong>ed</strong> results. Thereis a relative-risk increase <strong>of</strong> 14–20 for individuals who drink more than fiv<strong>ed</strong>rinks per day, although wine drinkers are at a lower risk than beer or liquordrinkers (Becker, Gronbaek, Johansen, & Sorensen, 2002). Women have ahigher incidence <strong>of</strong> alcoholic hepatitis and cirrhosis than men, although themechanisms underlying these gender differences is not known. Alcoholiccirrhosis develops as a result <strong>of</strong> prolong<strong>ed</strong> hepatocyte damage, leading tocentrilobular inflammation and fibrosis. The latter pathology causes portalhypertension and the development <strong>of</strong> varices. Esophageal varices may ble<strong>ed</strong>spontaneously, or ble<strong>ed</strong>ing may be precipitat<strong>ed</strong> by respiratory tract infections,nonsteroidal anti-inflammatory drugs, and alcohol. Cirrhosis also leads toascites, clotting deficiencies, secondary malnutrition, and hepatic encephalopathy(Sutton & Shields, 1995).NutritionAlcoholics are especially susceptible to deficiencies <strong>of</strong> thiamine, folate, Bvitamins, and ascorbic acid. Alcohol intake leads to negative nitrogen balance,increas<strong>ed</strong> protein turnover, and inhibition <strong>of</strong> lipolysis (Bunout, 1999).Deficiencies in folate, vitamin B 6, and vitamin B 12play a role in elevat<strong>ed</strong> levels<strong>of</strong> homocysteine, which in turn promotes atherosclerosis and thrombosisformation (Cravo & Camilo, 2000). Ethanol can suppress appetite through itseffect on the CNS. Gastric, hepatic, and pancreatic disease my furtherdecrease enteral intake and contribute to maldigestion or malabsorption.Signs <strong>of</strong> malnutrition include thinning <strong>of</strong> the hair, ecchymosis, glossitis,abdominal distention, peripheral <strong>ed</strong>ema, hypocalcemic tetany, and neuropathy.Nutritional management consists <strong>of</strong> abstinence and institution <strong>of</strong> a wellbalanc<strong>ed</strong>diet and multivitamins, plus thiamine and vitamin B supplementswhen indicat<strong>ed</strong>.Cardiovascular SystemIt is well establish<strong>ed</strong> that alcoholic heart muscle disease is a complication <strong>of</strong>long-term alcoholism and not malnutrition or other possible causes <strong>of</strong> dilat<strong>ed</strong>cardiomyopathy. In a dose-dependent fashion, left ventricular systolic functiondeclines, implicating alcohol in at least 30% <strong>of</strong> all dilat<strong>ed</strong> cardiomyopathies(Lee & Regan, 2002). The contractility <strong>of</strong> heart muscle is decreas<strong>ed</strong> through

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!