Professional Refresher Liver Disease: The Role of Nutrition
The major forms of liver disease are: ▪ Acute viral hepatitis ▪ Fulminant hepatitis ▪ Chronic hepatitis ▪ Alcoholic hepatitis ▪ Cirrhosis
Acute viral hepatitis
▪ Inflammation of the liver ▪ Symptoms of hepatitis include: – Nausea – Vomiting – Anorexia – Abdominal pain – Darkly colored urine – Muscular pain – Jaundice ▪ The five forms of hepatitis are: – Hepatitis A—found in water, food, and sewage. Rarely leads to chronic complications, however 15% of patients will have relapsing symptoms within 6-9 months. Thirty-three percent of the population has evidence of past infection. Vaccination is available. – Hepatitis B and hepatitis C—contracted through blood, semen, or saliva. Can lead to a chronic condition, sometimes resulting in cirrhosis and liver failure. Five percent to 10% of adults with hepatitis B will develop chronic hepatitis, and 10% or more of these cases will develop into cirrhosis. Seventy-five percent to 90% of people with hepatitis C will develop chronic hepatitis, and 20%-30% of these cases will develop into cirrhosis. A 15%-25% fatality rate exists from hepatitis B (the ninth leading cause of death in the world), and a 1%5% fatality rate exists from hepatitis C. Vaccination is available for hepatitis B, but not for hepatitis C. – Hepatitis D—only develops in some people who have hepatitis B. Progression to cirrhosis is common in people with hepatitis B and D. Two percent to 20% of people will develop acute liver failure. Vaccine for hepatitis B is available. – Hepatitis E—rare in the United States (most likely to occur in South Asia and North Africa) and contracted through the oral-fecal route. Hepatitis E is acute, not chronic. No vaccination is available. ▪ The three phases of hepatitis progression are: – First phase (prodromal or preicteric)—only occurs in 25% of all hepatitis cases. Symptoms include fever, weakness, anorexia, fatigue, changes in taste and sleep patterns, abdominal pain, arthralgia, arthritis, rash, and/or angioedema. Lasts 1-21 days. – Second phase (icteric)—when jaundice develops. Lasts 2-4 weeks. – Third phase (convalescent)—when symptoms may subside. Ninety-five percent of hepatitis A, 90% of hepatitis B, and only 15%-30% of hepatitis C result in a full recovery.
▪ Hepatitis also may develop as a result of the Epstein-Barr virus, herpes simplex virus, cytomegalovirus, yellow fever, or rubella.
Fulminant hepatitis
▪ Acute liver failure with hepatic encephalopathy ▪ Seventy-five percent of cases result from acute hepatitis, with 1% of hepatitis A and B patients developing fulminant hepatitis ▪ The remaining 25% of cases result from chemical toxicity, Wilson’s disease, fatty liver pregnancy, Reye’s syndrome, hepatic ischemia, hepatic vein obstruction, or disseminated malignancies ▪ Risks of fulminant hepatitis include: – Brain swelling – Bleeding – Cardiovascular problems – Renal problems – Pulmonary complications – Changes to acid-base balance – Electrolyte imbalances – Sepsis – Pancreatitis ▪ Fifty percent fatality unless timely liver transplantation occurs
Chronic hepatitis
▪ Diagnosed after 6 months of acute hepatitis, with evidence of liver disease and confirmation of unresolved hepatic inflammation through biopsy ▪ Autoimmune, viral, metabolic, and toxicological issues can cause chronic hepatitis
Alcoholic liver disease, alcoholic hepatitis, and cirrhosis
▪ The fourth leading cause of death in middle-aged Americans ▪ Caused by damage to the mitochondrial membrane ▪ Risk factors for developing alcohol-related liver problems include: – Female gender – Genetic predisposition – Exposure to other drugs combined with heavy alcohol consumption – Infection with certain viruses – Immune issues – Poor nutrition ▪ Three stages of alcoholic liver disease – Hepatic steatosis—fatty liver disease, reversible if drinking stops – Hepatitis develops—reversible if drinking stops – Cirrhosis—not reversible
Primary biliary cirrhosis
▪ An immune-mediated disease caused by the progressive destruction of intrahepatic bile ducts ▪ Ninety percent of total incidence occurs in females ▪ A chronic disease that progresses slowly and results in cirrhosis and portal hypertension
▪ People with primary biliary cirrhosis must undergo liver transplantation or the disease becomes fatal ▪ Many nutritional problems develop, including osteopenia, hypercholestrolemia, and deficiency of fat-soluble vitamins
Sclerosing cholangitis
▪ A chronic cholestatic condition ▪ Possibly an immune-mediated disease ▪ Results in portal hypertension, hepatic failure, or cholangiocarcinoma ▪ Seventy-five percent of people with sclerosing cholangitis also have irritable bowel disease, particularly ulcerative colitis ▪ Sixty percent to 70% of total incidence occurs in males ▪ Nutritional problems that are likely to develop include steatorrhea with subsequent fat-soluble vitamin deficiency, hyperparathyroidism, osteomalacia, and rickets ▪ Treated with immunosupressants, but liver transplant is often necessary
Medical nutrition therapy for cirrhosis
▪ Recommend smaller meals because of early satiety and anorexia; smaller meals also may help to promote a positive nitrogen balance and prevention of hypoglycemia ▪ Recommend oral nutritional supplements ▪ Consider nutritional support, if patient is unable to consume 0.8 g protein g/kg/day and 30 kcal/kg/day ▪ Patient may necessitate 120%-140% of REE in end-stage liver disease without ascites; and up to 150%-175% of REE if ascites, malabsorption, or infection is present ▪ Make sure to obtain dry weights for reassessment purposes ▪ Liver failure reduces glucose production and decreases peripheral utilization; coupled with a change in hormones, such as insulin, glucagon, cortisol, and epinephrine, the body develops preference for lipids and amino acids ▪ Twenty-five percent to 40% of total calories should come from lipid ▪ Patient should receive 1.2-1.3 g protein/kg/day to promote positive nitrogen balance; 1.5 g protein/kg/day if patient shows signs of severe ascites or gastrointestinal bleeding ▪ Vitamin and mineral supplementation recommended for end-stage liver disease includes all of the B vitamins and all of the fat-soluble vitamins ▪ Wernicke’s encephalopathy—recommend thiamine, vitamin B6, vitamin B12, folate, and niacin ▪ Iron supplementation recommended in cases of gastrointestinal bleeding ▪ Zinc, magnesium, and copper are malabsorbed in chronic liver disease with steatorrhea ▪ Between 10% and 37% of patients with cirrhosis will develop overt diabetes mellitus
Medical nutrition therapy for portal hypertension
▪ Acute stage—initiation of TPN probably necessary ▪ Repeated endoscopic therapy is likely to cause esophageal stricture or dysphagia ▪ Shunt placement increases the risk of encephalopathy and reduces nutrient metabolism
Medical nutrition therapy for ascites
▪ Recommend fluid restriction
▪ Watch for loop diuretic side effects, including hyponatremia, hypokalemia, hypomagnesemia, hypocalcemia, and hypochloremic acidosis ▪ Monitor weight, abdominal girth, urinary sodium concentration, BUN, creatinine, albumin, uric acid, and electrolyte levels, if patient is prescribed diuretics ▪ Recommend 2 g/day for sodium restriction ▪ Ensure that patient receives adequate protein
Medical nutrition therapy for hepatic encephalopathy (including fulminant hepatitis)
▪ Ammonia is an important causative factor, because the liver can not detoxify ammonia to urea ▪ Some people believe that dietary protein causes an increase in ammonia production, but this is unproven; protein restriction is not recommended, with some studies showing that this practice is possibly quite harmful ▪ A branched-chain amino acid formula is recommended for patients who cannot tolerate standard protein sources and are nonresponsive to medication ▪ Some studies have shown that vegetable protein and casein are the preferred sources of protein for patients with hepatic encephalopathy, because they contain less aromatic amino acids and more branched-chain amino acids than other sources of protein ▪ Monitor glucose regularly ▪ Vitamin K supplementation is recommended
Medical nutrition therapy for fat malabsorption in liver disease
▪ Replace long-chain triglycerides with medium-chain triglycerides, because they are more readily digestible ▪ Recommend a 40-g fat diet; if diarrhea does not resolve quickly as a result of this diet, discontinue the diet because of the risk of furthering malnutrition
Medical nutrition therapy for liver transplant
▪ Pretransplant—malnutrition is common ▪ Recommend small, frequent, nutritionally complete meals, with enteral feedings as necessary ▪ Food-drug interactions are common ▪ Posttransplant—provide nutritional intervention as necessary for obesity, hyperlipidemia, hypertension, diabetes, etc References and recommended resources Hasse JM, Matarese LE. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy. 11th ed. Philadelphia, PA: WB Saunders; 2004:740-756. Marchesini G, Marzocchi R, Noia M, Bianchi G. Branched-chain amino acid supplementation in patients with liver diseases. J Nutr [serial online]. 2005;135:1596S-1601S. Available at: http://jn.nutrition.org/cgi/content/full/135/6/1596S. Accessed March 19, 2008. WebMD. Hepatitis. Available at: http://www.emedicine.com/emerg/topic244.htm. Accessed March 19, 2008.
Centers for Disease Control and Prevention. Viral hepatitis A: fact sheet. Available at: http://www.cdc.gov/NCIDOD/DISEASES/HEPATITIS/a/fact.htm. Accessed March 19, 2008. Centers for Disease Control and Prevention. Viral hepatitis B: fact sheet. Available at: http://www.cdc.gov/NCIDOD/DISEASES/HEPATITIS/b/fact.htm. Accessed March 19, 2008. Centers for Disease Control and Prevention. Viral hepatitis C: fact sheet. Available at: http://www.cdc.gov/NCIDOD/DISEASES/HEPATITIS/c/fact.htm. Accessed March 19, 2008. Centers for Disease Control and Prevention. Viral hepatitis D: fact sheet. Available at: http://www.cdc.gov/NCIDOD/DISEASES/HEPATITIS/d/fact.htm. Accessed March 19, 2008. Centers for Disease Control and Prevention. Viral hepatitis E: fact sheet. Available at: http://www.cdc.gov/NCIDOD/DISEASES/HEPATITIS/e/fact.htm. Accessed March 19, 2008. Liver Transplant Program and Center for Liver Disease, University of Southern California, Dept of Surgery. Current therapy of chronic viral hepatitis. Available at: http://www.surgery.usc.edu/divisions/hep/livernewslettercurrenttherapyofchronicviralhepatitis.html. Accessed March 19, 2008. WebMD. Hepatitis, viral. Available at: http://www.emedicine.com/med/topic3180.htm. Accessed March 19, 2008. Dept of Anaesthesia & Intensive Care, Chinese University of Hong Kong. Fulminant hepatic failure. Available at: http://www.aic.cuhk.edu.hk/web8/fulminant_hepatic_failure.htm. Accessed March 19, 2008. WebMD. Fulminant hepatic failure. Available at: http://www.emedicine.com/ped/topic808.htm. Accessed March 19, 2008. Richardson RA, Davidson HI, Hinds A, Cowans S, Rae R, Garden OJ. Am J Clin Nutr [serial online]. 1999;69:331-337. Influence of the metabolic sequelae of liver cirrhosis on nutritional intake. Available at: http://www.ajcn.org/cgi/content/full/69/2/331. Accessed March 19, 2008. Morgan AG, Kelleher J, Walker BE, Losowsky MS. Nutrition in cryptogenic cirrhosis and chronic aggressive hepatitis. Gut [serial online]. 1976;17:113-118. Available at: http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1411074&blobtype=pdf. Accessed March 19, 2008.
Review Date 4/08 G-0617