2 Patients present with depleted fat stores and varying degrees of muscle wasting and reduced muscle strength. Short-term survival is reduced in malnourished patients with cirrhosis, and PEM can adversely affect outcomes for patients Selleck Trichostatin A on the waiting list for transplantation, as well as post-transplantation morbidity and mortality.3 Malnutrition in cirrhosis is implicated in increased risk for infection,4 increased severity of ascites,5 and the development of hepatic encephalopathy.6 Repeated episodes of overt hepatic encephalopathy might result in recurrent

hospitalizations and persistent cumulative deficits in working memory, response inhibition, and learning.7 The mechanisms of PEM in cirrhosis are complex and multifactorial. They include reduced oral intake secondary

to disease-related INCB024360 supplier anorexia, restrictive diets, including overzealous sodium-restricted diets, altered taste sensations, nausea, early satiety, particularly in the presence of marked ascites, portal-hypertension associated malabsorption, insulin resistance, reduced glycogen storage capacity, increased gluconeogenesis, and alterations in fuel utilization. Repeated episodes of infection and endotoxemia as a result of alterations in gut barrier function might also contribute to the increased energy requirements and reduced intakes in this group via the pro-inflammatory cytokine response.8 Despite studies demonstrating that there is no benefit to a low-protein diet in patients with episodic or chronic hepatic encephalopathy,9 a protein-restricted diet is commonly recommended by health-care practitioners under the misapprehension that it is beneficial

to patients. Protein restriction has further deleterious medchemexpress impacts on the severity of malnutrition,10 while a higher protein intake has positive benefits both on overall nutrition and possibly the severity of hepatic encephalopathy.11 Hospitalization, with frequent prolonged periods of fasting for diagnostic or therapeutic procedures, is another major contributory factor; thus, clinicians should make every effort to minimize periods of fasting and maximize nutritional intake in patients with cirrhosis while they are in hospital. Accurate assessment of nutritional status might also be difficult in patients with cirrhosis. This is because many of the traditional markers of nutritional assessment are dependent on normal hepatic synthetic function. Weight is a poor indicator of nutritional status in the presence of ascites and/or peripheral edema. Nutritional assessment of the cirrhotic patient includes subjective global assessment—liver,12 anthropometrical measurements of mid-arm circumference, triceps skinfold thickness, and mid-arm muscle circumference. In addition, grip strength measurements are an accurate reflection of protein status in those with cirrhosis.