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
The five forms of acute viral hepatitis are hepatitis A, B, C, D, and E.
Hepatitis A: Hepatitis A is found in water, food, and sewage, It is spread via the oral-fecal route.
It rarely leads to chronic complications. However, 15% of patients will have relapsing symptoms
within 6–9 months. Complete recovery occurs in 95% of cases. Thirty-three percent of the
population has evidence of past infection. Vaccination is available.
Hepatitis B: Hepatitis B is contracted through blood, semen, or saliva. It can lead to a chronic
condition sometimes resulting in cirrhosis and liver failure, with 5%–10% of adults with hepatitis
B developing chronic hepatitis and 10% or more of these cases developing into cirrhosis. A
15%–25% fatality rate exists from hepatitis B. Vaccination is available.
Hepatitis C: Hepatitis C is contracted through blood, semen, or saliva. It can lead to a chronic
condition, sometimes resulting in cirrhosis and liver failure, with 75%–90% of people with
hepatitis C developing chronic hepatitis and 20%–30% of these cases developing into cirrhosis.
A 1%–5% fatality rate exists from hepatitis C. Vaccination is not available for hepatitis C.
Hepatitis D: Hepatitis D only develops in some people who have hepatitis B. Progression to
cirrhosis is common in people with hepatitis B and D, and 2%–20% of people will develop acute
liver failure. Vaccine for hepatitis B is available.
Hepatitis E: Hepatitis E is rare in the United States (most likely to occur in South Asia and
North Africa) and is contracted through the oral-fecal route. Hepatitis E is acute, not chronic. No
vaccination is available.
Hepatitis also is caused by the Epstein-Barr virus, cytomegalovirus, herpes simplex, yellow
fever, and rubella.
Hepatitis progresses in four phases:
 First phase (early prodromal phase): Symptoms include fever, arthralgia, arthritis, rash, and/or
angioedema.
 Second phase (preicteric phase): Symptoms include malaise, fatigue, myalgia, anorexia, and
nausea and vomiting.
 Third phase (icteric phase): Jaundice occurs.
 Forth phase (convalescent): Symptoms may subside.
Fulminant hepatitis
 Acute liver failure with hepatic encephalopathy
 75% 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 of
pregnancy, Reye’s syndrome, hepatic ischemia, hepatic vein obstruction, or disseminated
malignancies
 Risks of fulminant hepatitis include:
– Cerebral edema
– Bleeding
– Cardiovascular problems
– Renal problems
– Pulmonary complications
– Changes to acid-base balance
– Electrolyte imbalances
– Sepsis
– Pancreatitis
 50% fatal 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 (most
common causes are hepatitis B, hepatitis C, and autoimmune hepatitis)
Alcoholic liver disease, alcoholic hepatitis, and cirrhosis
 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 status
 Three stages of alcoholic liver disease:
– Hepatic steatosis—fatty liver disease, reversible if drinking stops
– Alcoholic hepatitis—reversible if drinking stops
– Cirrhosis—not reversible
Primary biliary cirrhosis
 An immune-mediated disease caused by the progressive destruction of intrahepatic bile ducts
 95% 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
 70%–90% of people with sclerosing cholangitis also have irritable bowel disease, particularly
ulcerative colitis
 More common in men than in women
 Nutritional problems that are likely to develop include steatorrhea with subsequent fat-soluble
vitamin deficiency, hyperparathyroidism, osteomalacia, and rickets
 Treated with immunosuppressants, but liver transplant is often necessary
Hepatic encephalopathy
 Characterized by impaired mental status, neuromuscular disturbances, and altered
consciousness
 Ammonia accumulation is thought to be a causal factor
 Amino acid imbalance exists in which branched chain amino acids (BCAAs) valine, leucine,
and isoleucine are decreased, changing the plasma ratio of BCAA to aromatic amino acid
(AAA).
Medical nutrition therapy for cirrhosis
 Serve smaller meals because of early satiety and anorexia:
– Smaller meals also may help to promote a positive nitrogen balance and prevention of
hypoglycemia
 Offer oral nutritional supplements to meet nutrient needs, if needed
 Consider nutritional support, if patient is unable to consume 0.8 grams (g) protein /kilogram
(kg)/day and 30 kilocalories (kcal)/kg/day
 May necessitate 120%–140% of resting energy expenditure (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
 Understand that 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
 Have 25%–40% of total calories from lipid
 Provide 1.2–1.3 g protein/kg/day to promote positive nitrogen balance, or 1.5 g protein/kg/day
if patient shows signs of severe ascites or gastrointestinal bleeding
 Recommend:
– Vitamin and mineral supplementation for end-stage liver disease, including all of the B and
fat-soluble vitamins
– Thiamine, vitamin B6, vitamin B12, folate, and niacin for Wernicke’s encephalopathy
– Iron supplementation for gastrointestinal bleeding
 Know that zinc, magnesium, and copper are malabsorbed in chronic liver disease with
steatorrhea
 Realize that 10%–37% of patients with cirrhosis will develop overt diabetes mellitus
Medical nutrition therapy for portal hypertension
 Know that in the acute stage, initiation of total parenteral nutrition (TPN) probably is necessary
 Realize that repeated endoscopic therapy is likely to cause esophageal stricture or dysphagia
 Understand that 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, blood urea nitrogen (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)
 Understand that ammonia is an important causative factor, because the liver can not detoxify
ammonia to urea
 Realize that even though some people believe that dietary protein causes an increase in
ammonia production, this is unproven:
– Protein restriction is not recommended, with some studies showing that this practice is
possibly quite harmful
 Recommend a BCAA formula for patients who cannot tolerate standard protein sources and are
nonresponsive to medication
 Know that vegetable protein and casein are the preferred sources of protein for patients with
hepatic encephalopathy (according to some studies), because they contain less AAA and more
BCAA than other sources of protein
 Monitor glucose regularly
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
 Know that malnutrition is common pretransplant
 Recommend small, frequent, nutritionally complete meals, with enteral feedings as necessary
 Realize that food-drug interactions are common
 Provide nutritional intervention post-transplant, as necessary, for comorbid conditions, such as
obesity, hyperlipidemia, hypertension, and diabetes
References and recommended readings
Centers for Disease Control and Prevention. Hepatitis A information for health professionals.
Available at: http://www.cdc.gov/hepatitis/HAV/index.htm. Accessed April 16, 2012.
Centers for Disease Control and Prevention. Hepatitis B information for health professionals.
Available at: http://www.cdc.gov/hepatitis/HBV/index.htm. Accessed April 16, 2012.
Centers for Disease Control and Prevention. Hepatitis D information for health professionals.
Available at: http://www.cdc.gov/hepatitis/HDV/index.htm. Accessed April 16, 2012.
Centers for Disease Control and Prevention. Hepatitis E information for health professionals.
Available at: http://www.cdc.gov/hepatitis/HEV/index.htm. Accessed April 16, 2012.
Centers for Disease Control and Prevention. Viral hepatitis C: fact sheet. Available at:
http://www.cdc.gov/hepatitis/HCV/index.htm. Accessed April 16, 2012.
Hasse JM, Matarese LE. Medical nutrition therapy for hepatobiliary and pancreatic disorders. In:
Mahan LK, Escott-Stump S, Raymond JL. Krause’s Food and the Nutrition Care Process. 13th
ed. St Louis, MO: Saunders Elsevier; 2012:645-674.
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 April 16, 2012.
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 April 16, 2012.
Review Date 4/12
G-0617