Nutrition Therapy in Liver Disease

The following is an excellent review by Drs Patton and Aranda-Michel regarding the etiology and nutrition therapy of liver disease. As the authors clearly point out, malnutrition is a significant problem in end-stage liver disease, resulting in increased morbidity and mortality. Unfortunately, there are few data to suggest that aggressive nutritional supplementation (ie, oral, enteral, or parenteral) improves clinical outcome in those patients with end-stage cirrhosis. It has been my clinical observation that clinical improvement in terms of function and quality of life is marginal at least. I suspect this may be the result of a sick liver not being able to appropriately process nutrients. It is fascinating to observe that usually within 4 months after hepatic transplantation, these patients begin to regain muscle mass and function and exhibit an improved quality of life. I therefore believe that the treatment of choice of the malnutrition in this group of patients is hepatic transplantation and not prolonged enteral or parenteral support. In regards to the causes of malnutrition, the authors mention that early satiety and subsequent decreased food intake may be the result of gastroparesis or delayed gastric emptying secondary to the ascites. We have recently reported that gastric emptying is unchanged after large-volume paracentesis in cirrhotics. I suspect the problem of early satiety experienced by cirrhotics with ascites is the result of reduced gastric accommodation or relaxation and not necessarily delayed gastric emptying. Studies evaluating gastric accommodation in cirrhotics with ascites are currently underway. In terms of enteral access for feeding, I would agree with the authors that a soft small-bore feeding tube (8 to 10 French) is usually well tolerated for a short period, ie, 4 to 8 weeks. I would also caution against the use of a gastrostomy tube because the risk of leakage and peritonitis is significantly increased in cirrhotics with ascites. I would agree with the authors that the use of total parenteral nutrition (TPN) should be limited because of the increased incidence of catheter infection. If TPN is given and the patient has cholestatic liver disease, ie, elevated bilirubin, copper and manganese should be held because these are excreted through the hepatic circulation. In terms of dietary changes or supplements, I would point out that supplying protein from a vegetable source may be better than an animal source because fewer aromatic amino acids are produced from vegetable sources. Careful attention should also be given to excess vitamin A intake because high hepatic levels of vitamin A may worsen hepatic function. We have recently reported that serum vitamin A levels may not correlate with hepatic tissue levels. Therefore, caution should be given for vitamin A replacement based on serum vitamin A levels alone. I agree with the authors that future randomized studies are needed to evaluate clinical outcome of aggressive nutrition support in end-stage cirrhotics, specifically, those on the waiting list for hepatic transplantation. These studies will be limited by lack of specific markers of nutritional response and duration of therapy required.