Hepatic encephalopathy diet therapy

The mainstay of therapy of hepatic encephalopathy involves therapy to lower blood ammonia concentrations, and includes diet therapy, lactulose, and antibiotics alone or in combination with lactulose. 

As hyperammonemia is considered to be the main cause of hepatic encephalopathy, specific therapy for HE is aimed at the reduction of anunonia production and resorption. Protein restriction has been recommended for a long time to reduce ammonia production. But patients with cirrhosis are hypercatabolic. They may require up to 1.5 g/kg protein per day. Therefore protein restriction has been limited to patients with severe hepatic encephalopathy, and a reduction to less than 1 g protein per kg body weight has been discouraged in the past. A recent clinical study even showed no benefits of protein restriction (Cordoba et al., 2004). 30 cirrhotics who were admitted to the hospital with hepatic encephalopathy were randomized to a low-protein diet or normal protein diet. After two weeks of treatment, the groups did not significantly differ with regard to the course of hepatic encephalopathy. 

Freund, H., Yoshimura, N., Fischer, J.E. Chronic hepatic encephalopathy. Long-term therapy with a branched-chain amino-acid-enriched elemental diet. X. Amer. Med. Ass. 1979 242 347-349... 

Nitrogen requirements for the patient with liver failure are not unlike those of normal subjects, but intolerance to protein is common, and protein restriction has been used successfully as part of the therapy. A dilemma arises when the diet becomes so restrictive that malnutrition results, and the patient becomes susceptible to infection and other comphcations. Overzealous use of protein to correct nutritional deficits invariably results in hepatic encephalopathy. 

There has been considerable interest in the use of vegetable-protein diets in the chronic management of patients with cirrhosis and hepatic encephalopathy. Enthusiasm for this therapy is based on the reduced amounts of AAAs and methionine in vegetable protein. The... 

Fortunately, bed rest, rehydration, parenteral nutrition, and therapy directed at decreasing the production of toxins that result from bacterial degradation of nitrogenous substrates in the gut lumen (e.g., administration of lactulose, which reduces gut ammonia levels by a variety of mechanisms, the use of enemas and antibiotics to decrease the intestinal flora, a low-protein diet) prevented Percy Veere from progressing to the later stages of hepatic encephalopathy. As with most patients who survive an episode of fulminant hepatic failure, recovery to his previous state of health occurred over the next 3 months. Percy s liver function studies returned to normal, and a follow-up liver biopsy showed no histologic abnormalities. 

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See also in sourсe #XX -- [ ]

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