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#Gastroenterology #Hepatology #Multispeciality
Plethora of evidence suggests that deficiency of protein can be associated with liver disease which is mainly attributed to decreased dietary intake. The deficiency of protein is more frequently encountered in alcoholic liver disease, owing to the disturbances in digestion and absorption in alcoholics. Although the requirement of protein in most patients with compensated chronic liver disease are similar to those of healthy counterparts, it increases during episodes of hepatocellular deterioration. This raised demand for protein after liver injury causes depletion of nitrogen from other organs such as muscle. Excessive amount of aromatic amino acids released from muscle accumulate in the circulation of patients with chronic liver disease due to their reduced hepatic metabolism. Moreover, these branched chain amino acids further decrease in the circulation due to increased uptake by extrahepatic tissues.
Besides, an increase in accumulation of ammonia is observed in patients with liver disease which is caused due to the decrease in urea synthesis attributed to the decrease in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. This increase in ammonia in combination with an increased accumulation and intake of aromatic amino acids into the brain are considered important factors implicated in the pathogenesis of hepatic encephalopathy. Additionally, circulating proteins synthetized by the liver, such as albumin and clotting factors, are known to get reduced in chronic liver disease. Apart from protein deficiency, vitamin deficiencies are a common finding in liver disease that also play a significant role in abnormalities of protein metabolism. Thus, success of hepatic regeneration after a hepatic resection or injury is negatively affected by protein and vitamin deficiencies along with alcohol consumption.
Source: Mezey E. Liver disease and protein needs. Annu Rev Nutr. 1982;2:21-50.