Nutritional Support in Chronic Liver Disease

Anne S Henkel; Alan L Buchman

Disclosures

Nat Clin Pract Gastroenterol Hepatol. 2006;3(4):202-209. 

In This Article

Treatment

The goals of nutritional therapy are to improve PCM and correct nutrient deficiencies. This can be accomplished via oral, enteral, or parenteral methods, or a combination of these modalities.

Intervention in the early stages of malnutrition can improve outcome. Hirsch et al. studied the effects of nutritional supplementation in patients with alcoholic cirrhosis.[47] They found that patients receiving a daily supplement of 1,000 kcal and 34 g of protein (given as a casein-based enteral nutrition product) had better outcomes compared with those in the control group; the number of hospitalizations was significantly fewer in the treated group, and additional parameters, including midarm circumference, serum albumin concentration, and hand-grip strength, also improved earlier in the treated group than in the control group. Mendenhall et al. studied the effects of oral nutritional support in patients with alcoholic hepatitis. In patients with severe malnutrition, inadequate caloric intake was associated with 51% mortality compared with 19% mortality in patients who received adequate oral nutrition (greater than 2,500 kcal/day).[48] One randomized, controlled trial demonstrated that providing nutritional supplementation to pretransplant candidates did not increase overall dietary energy or protein intake, and did not significantly improve post-transplant outcome. It is thought that the patients who received a nutritional supplement might have compensated for taking the supplement by decreasing their intake of food. This study concluded that regular dietary counseling is as effective in increasing energy intake as providing a nutritional supplement.[49]

Enteral Nutrition

As a general guideline, oral intake should be encouraged; if patients are unable to maintain adequate intake orally, a nasogastric tube should be inserted for enteral feeding. Cabre et al. found that, in severely malnourished patients with cirrhosis, enteral feeding improved serum albumin levels and Child-Turcotte-Pugh scores, and decreased in-hospital mortality rates, compared with the standard oral diet.[50] Hasse et al. demonstrated the benefit of early initiation of enteral feeding after transplantation.[51] Patients who received enteral feeds had an improved nitrogen balance and fewer viral infections after transplantation. Kearns et al. showed that aggressive nutritional intervention with enteral feeding accelerated improvement in alcoholic liver disease; patients who received enteral feeds demonstrated a more rapid decrease in bilirubin levels and improvement in hepatic encephalopathy compared with control participants.[52]

Parenteral Nutrition

Parenteral nutrition is a less desirable option than enteral nutrition and should be reserved for patients in whom enteral feeding cannot be achieved.[53] Wicks et al. showed that enteral feeding is as effective as parenteral feeding for maintaining nutritional status after liver transplantation, and has the benefit of decreasing complications and cost.[54] There is some evidence to suggest that parenteral feeding might be superior to enteral feeding in patients with portosystemic shunting, because enteral feeding might worsen hyperammonemia in this specific patient population.[55]

Guidelines for Meeting Nutritional Goals. In 1997, the European Society for Clinical Nutrition and Metabolism created guidelines for meeting nutritional goals in patients with end-stage liver disease.[53] They recommend initiation of enteral feeding when oral intake is inadequate. In patients with compensated cirrhosis, the guidelines recommend that patients consume 25-35 kcal/kg body weight per day of nonprotein energy and 1-1.2 g/kg body weight per day of protein or amino acids. In patients with complicated cirrhosis associated with malnutrition, nonprotein energy should be increased to 35-40 kcal/kg body weight per day and protein intake should increase to 1.5 g/kg body weight per day. According to the guidelines, protein intake should decrease to 0.5-1.5 g/kg body weight/day if stage I or II encephalopathy is present, and to 0.5 g/kg body weight/day if stage III or IV encephalopathy is present. More recent evidence suggests that protein restriction should not be recommended, even in the setting of episodic hepatic encephalopathy.[56]

Distribution of Calorie Intake

The distribution of calorie intake throughout the day has also been studied. It has been proposed that eating a late evening snack could alleviate the shift towards lipid oxidation by reducing the length of time a patient fasts overnight. Indeed, a late evening meal has been shown to improve the nitrogen balance[57] and raise the nonprotein respiratory quotient.[58] A typical recommendation for patients with advanced liver disease is to consume four to five small meals per day, as well as a late evening snack.

Supplementation with branched-chain amino acids.The usefulness of branched-chain amino acid (BCAA) supplementation in patients with cirrhosis has long been debated. It was proposed that depletion of BCAAs, as seen in many patients with advanced liver disease, might promote the development of hepatic encephalopathy by enhancing the passage of aromatic amino acids across the blood-brain barrier, resulting in the synthesis of false neurotransmitters. For this reason, it was hypothesized that BCAA supplementation might improve hepatic encephalopathy. Early investigations, therefore, focused on BCAAs as a potential treatment for hepatic encephalopathy. Although some controlled trials showed no benefit of BCAAs with respect to mental function,[59] several trials showed a significant improvement in hepatic encephalopathy with BCAA treatment.[60,61] A 2003 review of 11 randomized trials concluded that BCAAs improve hepatic encephalopathy, particularly when administered enterally to patients with chronic encephalopathy.[62]

Although there are conflicting data, there is more evidence of the beneficial effects of BCAAs to support their use in the treatment of malnutrition in patients with advanced cirrhosis. Marchesini et al. performed a multicenter, randomized trial examining the role of oral BCAA supplementation in patients with advanced liver disease.[63] The trial consisted of 174 patients with advanced cirrhosis who received 1 year of nutritional supplementation with BCAAs, lactoalbumin, or maltodextrins. BCAA administration was advantageous with regard to rates of mortality, progression of liver failure, and hospital admission. The most significant limitation that the investigators found was poor compliance with the BCAA-enriched diet; in the BCAA group, 15% of patients did not complete the treatment course. Poor compliance was attributed to poor palatability of the BCAA supplement. A recent multicenter, randomized, nutrient-intake-controlled trial demonstrated that oral supplementation with BCAAs for 2 years improved survival, serum albumin concentration, and quality of life in patients with decompensated cirrhosis.[64]

Recent studies advocate the use of nocturnal BCAA administration.[65] It is believed that BCAAs that are consumed during the day are primarily used as a source of energy for physical exercise, whereas when administered at night, BCAAs might be preferentially used for protein synthesis.

Correcting Nutrient Deficiencies. Nutritional therapy in patients with chronic liver disease should not only focus on treatment of PCM, but should also aim to correct specific nutrient deficiencies. Patients with advanced liver disease commonly develop micronutrient deficiencies. For example, patients with alcoholic liver disease who continue to consume alcohol are particularly at risk for deficiency of thiamine, folate, and magnesium.[66] Most patients with advanced liver disease, but particularly those with cholestatic liver disease, develop a deficiency of fat-soluble vitamins.[67]

Decreased serum vitamin A levels result from fat malabsorption, as well as defective mobilization of vitamin A from the liver.[68] One of the common complications of vitamin A deficiency is night blindness, which has been shown to improve with vitamin A supplementation, generally at a dose of 25,000 units/day for 4-12 weeks.[69] Persistent problems with dark adaptation, despite adequate supplementation, might result from concomitant zinc deficiency.[70] Vitamin A deficiency typically resolves within 2 weeks of liver transplantation.[69] Vitamin A toxicity is a potential risk of vitamin A supplementation. Vitamin A toxicity typically causes elevated transaminase levels and can eventually lead to cirrhosis, chronic hepatitis, or portal hypertension.[70] Although it was traditionally thought that the development of vitamin A toxicity requires doses well in excess of the recommended range, data now suggest that cirrhosis can develop at therapeutic doses of vitamin A (e.g. 25,000 IU/day for 6 years).[71] Liver disease resulting from vitamin A toxicity can persist for up to 1 year after discontinuation of the supplement.

Vitamin D deficiency is another complication of chronic liver disease, resulting primarily from malabsorption; decreased UV light exposure and inadequate dietary intake might also be contributing factors to vitamin D deficiency. Impaired hepatic 25-hydroxylation of vitamin D is also seen in patients with alcoholic cirrhosis.[72] Calcium deficiency, and eventually osteomalacia or osteoporosis, results from decreased intestinal calcium absorption. Up to 43% of patients undergoing transplant evaluation have osteoporosis.[73] There are conflicting data on whether vitamin D supplementation improves osteoporosis in patients with advanced liver disease. It has been suggested that osteoporosis does not respond to vitamin D supplementation in patients with primary biliary cirrhosis,[62] but it can improve in patients with alcoholic liver disease when 25-hydroxyvitamin D supplementation (25-50 mg/day) is taken.[74] A proposed guideline is to supplement all patients who have chronic liver disease with calcium (1 g/day) and vitamin D3 (800 IU/day).[75,76]

Zinc deficiency commonly occurs in patients with cirrhosis and has been implicated in the pathogenesis of hepatic encephalopathy.[77] Zinc supplementation at doses of 600 mg/day for 3 months has been shown to improve mental functioning in patients with hepatic encephalopathy,[78] although other studies show conflicting findings, and the role of zinc in treating hepatic encephalopathy remains controversial.

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