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Arch Hellen Med, 34(1), January-February 2017, 10-26


Nutrition in liver disease

I. Mani, S.P. Dourakis
Second Department of Internal Medicine, "Hippokration" General Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece

As the liver is a crucial modulator of metabolism, liver dysfunction results in changes in the basic metabolic rate, the nutritional status and the adequacy of the available micro- and macronutrients. Malnutrition is the most common, potentially reversible complication of cirrhosis, especially in the case of alcoholic etiology. It occurs in 20% of decompensated and 50–100% of non-decompensated cases of cirrhosis, representing a significant cause of comorbidity and deterioration of the quality of life of patients with cirrhosis of the liver. The term hepatic cachexia is used to describe both sarcopenia and lipopenia. Another manifestation is sarcopenic obesity, especially abdominal, seen in the cirrhosis of nonalcoholic fatty liver disease. The causes of malnutrition and cachexia in liver cirrhosis are reduced food intake, malabsorption and or poor digestion and increased energy needs resulting from altered metabolic rate and increased catabolism. Sarcopenia, which is caused by reduced protein synthesis, but mainly by an increased catabolic rate, is associated with the severity of the liver disease. It is also an independent risk factor for morbidity and mortality, particularly in end-stage cirrhosis and in liver transplant patients. Assessment of the nutritional status in patients with liver disease is difficult using traditional tools such as anthropometric criteria because of the presence of ascites and edema in many cases. Imaging tests, particularly abdominal computed tomography (CT) scan and dual energy X-ray absorptiometry (DEXA) are the most accurate. The daily caloric needs in patients with cirrhosis are estimated to be 35–45 kcal/kg. Calorie intake must be ingested in the form of fat (25–30% of daily calories) and carbohydrates (45–65%), and it is of great importance to also enhance protein consumption (1.2–1.5 g/kg). Restriction of protein intake is indicated only in the case of hepatic encephalopathy and only for a limited time. In addition, studies show that supplementation with branched chain amino acids and frequent feeding improve the nutritional status and optimize the clinical outcome. Potential therapeutic strategies such as the use of leucine and inhibitors of myostatin are still under investigation.

Key words: Cirrhosis, Malnutrition, Nutrition, Sarcopenia.

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