Liver Disease and Protein Needs

Abstract

Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

Possible Role of Endogenous Retinoid (Vitamin A) Toxicity in the Pathophysiology of Primary Biliary Cirrhosis

“…These decreased serum levels in the face of high liver levels of retinoids are not due to malabsorption or retinoid de"ciency but due to decreased mobilization of retinoids from the liver (Mezey, 1982). Decreased mobilization may be due in part to the known inhibitory e!ect of increased retinoic acid levels on the hepatic secretion of RBP (Keilson et al, 1979;Barua et al, 1997).…”

“…Retinoid intoxication is also associated with dry skin and alopecia which, however, are not seen typically in PBC. Splenomegaly and 50 (Bodenheimer, 1995;Sherlock, 1994;Mezey, 1982).…”

Effect of Quail Egg Administration on Some Liver Function Related Parameters

“…This can only imply that the damage to the liver may not have taken a chronic course as to impair the protein synthetic function of the liver. Researchers have reported that such functions like protein production can be affected in the cases of chronic hepatic impairment (Mezey, 1982). The plasma half-life of plasma proteins is 2-3 weeks.…”

Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective

“…In studies of infective hepatitis, the RBP-prealbumin complex and plasma vitamin A were decreased in association with reduced hepatic mobilization and very high liver levels of vitamin A, resulting in a mixed symptom pattern of hypo-and hypervitaminosis A [202].…”