HEPATIC ENCEPHALOPATHY AND DIET

Dr. Alberto Frosi, Responsabile Unità Operativa di Epatogastroenterologia, Ospedale di Sesto S. Giovanni, Az. Osp. Istituti Clinici di Perfezionamento, Ospedale di rilievo nazionale e di alta specializzazione convenzionato con l’Università di Milano 

a.frosi@libero.it

Since the suspected toxins involved are thought to arise from the gut and its contents, diet should assume a position of central importance in the treatment of hepatic encephalopathy (HE). However, dietary modification is extremely difficult as it implies the reversal of lifelong habits; dietary recommendations are therefore interesting but very difficult to implement in daily practice. Protein restriction or even abstinence was once recommended for this condition but is not longer practised, as it creates a protein catabolic situation in which ammonia formation is increased and the reduction of muscle mass also restricts the extent of extrahepatic ammonia detoxification. General susceptibility to infections is also increased due to catabolic conditions.
Patients with liver cirrhosis require a daily intake of 0.8 to 1.0 g/kg or even 1 to 1,2 g/kg, bodyweight protein to maintain a satisfactory nitrogen and energy balance since hepatic protein synthesis depends heavily on substrate supply for export and structural proteins. Susceptibility to infections also decreases under these conditions.
Only in acute episodic encephalopaty will it be temporarily necessary to initially limit protein supply to 20 g/day. After an improvement in HE, protein supply should be increased by 10 g every 3 to 5 days until the patient's protein tolerance has been reached. During the period with insufficient protein supply, an adequate caloric intake should be ensured, preferably by increasing dietary carbohydrate.
Increased intake of vegetable proteins is recommended. In patients with protein intolerance below 1 g/kg bodyweight, an increase in total protein intake can usually be achieved by switching to more vegetable proteins. Vegetable proteins are considered to improve the nitrogen balance without causing deterioration in HE. They are better tolerated than fish, meat or milk proteins. The beneficial effect appears to be due to the higher dietary fibre content of vegetable as compared with animal protein diets. Dietary fibres accelerate gastrointestinal transit and, by promoting fermentation by intestinal bacteria, induce a reduction in the pH of the intestinal lumen similar to that observed with non-absorbable disaccharides. Most patients accept a diet containing 30 to 40 g vegetable protein daily. A small group of patients with HE exhibit pronounced protein intolerance and cerebral function is adversely affected by increasing protein intake. Patients are titrated to maximal daily protein intake, for which the clinical symptoms are evaluated and appropriated psychometric tests are performed after test meals. In patients with proven protein intolerance, branched-chain amino acids should also be administered orally in amounts of up to 0,25 g/kg bodyweight to create the best possible nitrogen balance (1).

The table below synthesize all published studies comparing vegetable and animal diets in cirrhotic patients were searched in two on-line data bases (Medline, Embase), by Index Medicus, and by references of reviews and papers dealing with this topic (2, 3, 4, 5, 6, 7, 8, 9, 10).

Comment to the Table

Despite the fact that pathophysiological reasoning suggests that vegetarian diets might represent a low-cost therapeutic approach for cirrhotic patients with HE, evidence emerging from clinical studies is not yet conclusive. This is mainly due to: the heterogeneity of the diets used, the small number of the patients treated, their different clinical conditions, and the poor assessment of encephalopathy.
Moreover, the possible harmful effects of long-term use of vegetarian diets have not been considered in detail. In fact, exclusively vegetarian diets hardly provide sufficient calcium, iron, energy and protein intake so that long-term malnutrition is avoided. Indeed, vegetarian diet has a low energy density, and, therefore, may facilitate a rapid sense of satiety. In addition, the low palatability of a monotonous diet regiment might even lead to a long-term reduction of food intake, eventually deteriorating the nutritional status. Such limits may be overcome by a supplementation of vegetable with cheese and other dairy products in order to obtain more palatable and varied diet regiments which provide a high energy content, a high quantity and quality of proteins, and sufficient calcium (2).

References

1. Gerber T, Schomerus H. Drugs 2000;60(6):1353-70.
2. Amodio P, Caregaro L, Pettenò E, Marcon M, Del Piccolo F, Gatta A. Digestive and Liver Disease 2001; 33: 492-500.
3. Fenton JCB, Knight EJ, Humpherson PL. Lancet 1966;1: 164-6.
4. Greenberger NJ, Carley J, Schenker S, Bettinger I, Stamnes C, Beyer P. Am. J Dig Dis 1977;22:845-55.
5. Uribe M, Marquez MA, Garcia RG, Ramos-Uribe MH, Vargas F, Villabos A, et al. Dig Dis Sci 1982; 27:1109-16.
6. Shaw S, Worner TM, Lieber CS. Am J Clin Nutr 1983;38:59-63.
7. de Bruijn KM, Blendis LM, Zilm DH, Carlen PL, Anderson GH. Gut 1983; 24: 53-60.
8. Keshavarzian A, Meek J, Sutton C, Emery VM, Hughes EA, Hodgson HJ. Gastroenterology 1984;79:945-9.
9. Chiarino C, Frosi A, Vezzoli F, Sforza m, Rusca M. Minerva Gastroenterol Dietol 1992;38:7-14.
10. Bianchi GP, Marchesini G, Fabbri A, Rondelli A, Bugianesi E, Zoli M. J Intern Med 1993; 233:385-92.
11. Keeffe EB et al. Current Concepts in the Management of Hepatic Encephalopathy. Seminars in Liver Disease 2007; 27 (2): 1-32.
12. Hepatic Encephalopathy in Chronic Liver Disease: 2014 Practice Guidelines by the European Association for the Study of the Liver and the American Association for the Study of Liver Diseases. J. Hepatol. 2014;61:642-659.