Nutritional Support in Chronic Liver Disease

Anne S Henkel; Alan L Buchman


Nat Clin Pract Gastroenterol Hepatol. 2006;3(4):202-209. 

In This Article


The primary etiology of malnutrition is poor oral intake, stemming from multiple factors. Many patients with advanced liver disease have an altered sense of taste, which might be related to vitamin A and/or zinc deficiency.[19] Patients with cirrhosis often experience early satiety that is related to mechanical compression from massive ascites. Early satiety can also result from an increased serum concentration of leptin, which has been found in patients with advanced liver disease.[20] The dietary restrictions that are commonly recommended to these patients, such as restriction of sodium, protein, and fluids, can discourage adequate oral intake. In addition, weakness, fatigue, and low-grade encephalopathy can contribute to decreased oral intake.

Malabsorption is another important factor in the development of malnutrition in this patient population. A number of mechanisms contribute to malabsorption. There might be a reduction in the bile-salt pool in patients with advanced liver disease, leading to fat malabsorption,[21] which is particularly problematic in patients with cholestatic liver disease. Another potential mechanism that contributes to malabsorption in patients with advanced liver disease is bacterial overgrowth resulting from impaired small-bowel motility.[22] The presence of portal hypertension has also been implicated as a cause of malabsorption and gastrointestinal protein loss.[23,24] An additional factor is the administration of medications that lead to malabsorption, such as neomycin, which is used in the treatment of hepatic encephalopathy.[25] Fat malabsorption not only contributes to undernourishment, but also results in a deficiency in fat-soluble vitamins.

Another factor that might contribute to malnutrition, around which there has been considerable debate, is increased energy expenditure. Although several studies have suggested that cirrhosis does not significantly alter resting energy expenditure (REE),[26,27] other studies suggest that patients with cirrhosis are actually hypermetabolic when measurements of REE are corrected for lean body mass.[28,29] Hypermetabolism is found in as many as a third of patients with stable cirrhosis; however, it seems that there is significant variability in REE among patients with cirrhosis. In fact, it has been suggested that up to 30% of patients with cirrhosis are actually hypometabolic.[30,31]

The exact cause of hypermetabolism remains unclear, but certain predisposing factors have been identified. Infection, a common complication in patients with advanced liver disease, tends to induce a state of hypermetabolism. Ascites has also been shown to increase energy expenditure; this effect tends to be reversed with the removal of ascitic fluid.[32] Muller et al. demonstrated that hypermetabolism cannot be readily identified by clinical or biochemical markers of liver disease, suggesting that hypermetabolism might be an extrahepatic manifestation of liver disease.[31] It has also been demonstrated that an increase in energy expenditure caused by hypermetabolism seems to be matched by a reduction in activity-related energy expenditure.[33] Successful treatment of portal hypertension with transjugular intrahepatic portosystemic shunt placement results in a reduction of the hypermetabolic state.[34]

Patients with advanced liver disease also have an altered pattern of fuel consumption, in which there is a more rapid transition from the use of carbohydrates to the use of fat stores as a substrate for metabolism. This increased use of lipids is a metabolic pattern that is seen in starvation.[6,35,36] Chang et al. showed that, after an overnight fast, 58% of the energy used by patients with cirrhosis was derived from fat oxidation, whereas control participants derived 55% of their energy from carbohydrates.[36]


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