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STRUCTURAL CHANGES OF THE GI TRACT IN LIVER CIRRHOSIS However, not all studies have found defective active absorption in these patients. This may be related to the cholestasis often present in cirrhosis, but a reduction in the area of the intestinal absorptive surface has also been proposed in cirrhotics. Last, fat malabsorption has been reported to be frequent (especially in those with evidence of malnutrition). Increased energy expenditure, although not a constant feature of cirrhosis, has also been reported to contribute to a negative energy balance. Postprandial glucose and ghrelin alterations are probably associated with insulin resistance which is common in these patients. Increased glucose and lower ghrelin levels postprandially have also been suggested to be related to poor food intake and weight loss in cirrhosis. Potential reasons for low energy intake include reduced appetite possibly associated with increased brain tryptophan availability, satiety due to ascites, poor palatability of low-sodium diets, and hepatic encephalopathy, GI symptoms, and gut dysfunction. The pathogenesis of malnutrition in liver cirrhosis is not fully understood but poor dietary intake, increased energy expenditure, malabsorption and poor synthetic capacity of the cirrhotic liver may be involved.
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Lean-mass depletion is also related to hepatic encephalopathy in liver transplant candidates with cirrhosis.
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Recently, severe muscle wasting (sarcopenia) has been shown to be present in 30%-41% of patients with cirrhosis and to be independently related to mortality in general as well as in patients with hepatocellular cancer and those listed for liver transplantation in particular.
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It is associated with increased morbidity and mortality and it can compromise liver transplantation results. Malnutrition is common in cirrhosis with a reported prevalence as high as 80%. Finally, several studies have reported intestinal barrier dysfunction in patients with cirrhosis (especially those with portal hypertension), which is related to bacterial translocation and permeation of intestinal bacterial products, e.g., endotoxin and bacterial DNA, thus potentially being involved in the pathogenesis of complications of liver cirrhosis. Furthermore, small bowel manometry disturbances and delayed gut transit may be associated with the development of small bowel bacterial overgrowth. This may be related to disturbances in postprandial glucose, insulin, and ghrelin levels, which, in turn, appear to be associated to insulin resistance, a common finding in cirrhosis. Gastric emptying and small bowel transit have generally been shown to be prolonged. Although tense ascites appears to have a negative impact on meal-induced accommodation of the stomach, published data on gastric accommodation in cirrhotics without significant ascites are not unanimous. They may lead to reduced food intake and, thus, may contribute to the nutritional status deterioration in cirrhotic patients. Gastrointestinal symptoms are common in cirrhosis and their pathophysiology probably involves factors related to liver disease severity, psychological distress, and gut dysfunction ( e.g., increased gastric sensitivity to distension and delayed gut transit). Patients with liver cirrhosis exhibit several features of gut dysfunction which may contribute to the development of cirrhosis complications as well as have an impact on nutritional status and health-related quality of life.