Liver in Specific Hepatobiliary Disorders Hepatocellular Diseases

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Alcoholic liver disease The term 'alcoholic liver disease' refers to a spectrum of types of hepatic injury associated with continuous alcohol ingestion, ranging from alcoholic fatty liver to alcoholic stea-tohepatitis, fibrosis, and cirrhosis. Nutritional disturbances in alcoholics are an important cause of morbidity and mortality; all classes of nutrients are affected. Anorexia leads to decreased food intake and subsequent protein-calorie malnutrition. Maldigestion and malabsorption can occur secondary to chronic alcohol injury to small intestinal mucosa. Alcohol consumption is often associated with chronic pancreatic insufficiency, which results in steatorrhea and decreased absorption of dietary protein, fat, and fat-soluble vitamins. Chronic alcohol ingestion also results in impaired hepatic amino acid uptake and protein synthesis.

In alcoholics, utilization of lipids and carbohydrates is markedly compromised due to an excess of reductive equivalents and impaired oxidation of triglycerides. Alcoholics are often resistant to insulin and exhibit impaired uptake of glucose into muscle cells. Insulin-dependent diabetes is common. Heavy alcohol consumption is frequently associated with deficiencies of a wide variety of micronutrients, including the fat- and water-soluble vitamins, particularly folate, pyridoxal-5'-phosphate, thiamine, and vitamin A.

Table 1 summarizes the five published controlled trials of the effect of oral or enteral nutritional supplements on patients with alcoholic hepatitis. In most, nitrogen balance and/or protein synthesis improved, although no effect on mortality was shown, perhaps because of the small number of patients studied and/or the duration of follow-up. In the largest study, at 1-year follow-up, the experimental group had a significantly better survival: 2/24 (8%) died compared to 10/27 (37%) of the controls. In general, the effects of parenteral nutrition in alcoholic liver disease are similar to those noted the studies of enteral nutritional supplements.

Many studies have examined the effect of oral or enteral nutritional supplementation in patients with alcoholic cirrhosis. Results are summarized in Table 2. Many studies are small and of short duration, so it is not surprising that results are inconclusive. Most studies demonstrated an improvement in nitrogen balance and protein synthesis; only one showed increased survival in the treated group. Taken together, these studies suggest that there are benefits to nutritional supplementation in this population.

A variety of international associations have made nutritional recommendations for patients with various types of alcoholic liver disease. The primary recommendation is of course abstinence, which may be all that is needed in patients with fatty liver. Patients with alcoholic hepatitis should take 40kcal/kg, 1.5-2.0 g protein/kg, 4-5g/kg of carbohydrates, and 1-2g/kg of lipids per day. Those with cirrhosis without malnutrition should take 35kcal/kg, 1.3-1.5 g protein/kg, and carbohydrates and lipids as recommended for patents with alcoholic hepatitis. Those with cirrhosis and malnutrition should take higher amounts of protein (1.5-2.0g/kg) and lipids (2.0-2.5g/kg) and lower amounts of carbohydrates (3-4 g/kg). Fluid should be restricted to 2-2.5 l/day and all eight B vitamins, including folate and thiamine, as well as vitamins C and K should be routinely supplemented. In addition, patients with cholestasis should take 50% of their dietary lipids as medium-chain triglycerides

Table 1 Studies on therapy of alcoholic hepatitis with oral or enteral nutritional supplements



Patients (No.)

Duration (days)

Experimental treatment (EXP)

Control treatment (CTR)


Secondary end points

Galambos et al.

Open label



Oral (standard hospital diet)


Not assessed

Nitrogen balance + albumin


or intravenous supplement (51.6-77.4 g protein)

improved in EXP, CTR not assessed Improvement of albumin, transferrin, RBP

Mendenhall et al.




Standard hospital diet

Standard hospital diet


Positive nitrogen balance in



(2500 kcal/day) + 2200 kcal / day BCAA

EXP, delayed hypersensitivity improved

Calvey et al.




Standard diet (~2000 kcal/day) +

Standard diet,


Positive nitrogen balance in



65 g standard AA or BCAA

80 g protein/day

EXP, delayed hypersensitivty improved

Soberon et al.




Nasoduodenal tube, 35 kcal/

3 days standard hospital

0/6 controls

Nitrogen balance improved


kg/day, fat/carbohydrate/ protein 45/40/15%

diet (35 kcal/kg/day)

3/8 treatment

five-fold at 2 weeks

Cabre et al.




Nasogastric tube, 2000 kcal/day,

Standard diet

11/35 TEN 9/36

No dropouts in PRED,



72 g protein/day, 31 % BCAA

(1 g protein/kg) + 40 mg/day prednisolone


NS FU: 2/24 TEN 10/27 (P = 0.04)

8 dropouts in TEN; equal improvements of albumin, Child score, Maddrey score; equal rate of infections

aGalambos JT, Hersh T, Fulenwider JT et al. (1979) Hyperalimentation in alcoholic hepatitis. American Journal of Gastroenterology 72: 535-541.

^Mendenhall CL, Bongiovanni G, Goldberg S et al. (1985) VA cooperative study on alcoholic hepatitis. Ill: Changes in protein-calorie malnutrition associated with 30 days of hospitalization with and without enteral nutritional therapy. Journal of Parenteral and Enteral Nutrition 9: 590-596.

cCalvey H, Davis M, and Williams R (1985) Controlled trial of nutritional supplementation, with and without branched chain amino acids enrichment, in treatment of acute alcoholic hepatitis. Journal of HepatologyV. 141-151.

dSoberon S, Pauley MP, Duplantier R et al. (1987) Metabolic effects of enteral formula feeding in alcoholic hepatitis. Hepatology 7: 1204-1209.

"Cabré E, Rodriguez-lglesias P, Caballería J et al. (2000) Short-term and long-term outcome of severe alcohol-induced hepatitis treated with steroids or enteral nutrition: A multicenter randomized trial. Hepatology 32: 36-42.

AA, amino acids; BCAA, branched-chain amino acid; FU, follow-up; NS, not significant; PRED, prednisolone group; TEN, total enteral nutrition group.

From Stickel F, Hoehn B, Schuppan D, and Seitz HK (2003) Review article: Nutritional therapy in alcoholic liver disease. Alimentary Pharmacology & Therapeutics 18: 357-373.

Table 2 Studies on treating alcoholic cirrhosis with oral and enteral nutritional therapy®



Patients Duration Experimental treatment (No.) (days) (EXP)

Smith et ai.


Keohane et ai.

McGhee et al. (1983)c

Christie et al. (1985)d

Okita et al.

(1985)e Bunout et al.

(1989)f Cabre et al.

Hirsch et al. (1993/

Open label

Open label

Randomized, double-blind, crossover Randomized, double-blind, crossover Open label

Randomized, controlled Randomized, controlled Randomized


Randomized, controlled

Open label



10 4

36 28

64 90

12 (months)

Three different formulae: Oral 76-143 g protein, 2000-3716 kcal/day Oral BCAA formula: 80g protein/day through nasogastric tube 20 g casein + 30 g BCAA formula

BCAA (50%) formula

40g protein + 40 g BCAA

formula/day 50kcal/kg, 1.5 g protein/ day

2115 kcal/day including

71 g BCAA formula Standard diet + BCAA supplement (0.24 g/kg)

Casein supplement (1.5 g protein/day, 40 kcal/day/kg/day) Standard diet + casein supplement (1000 kcal/ day, 34 g protein/day) Increasing amounts of protein via standard diet (1.0-1.8 g/kg/day)

Control treatment Mortality (CTR)

Secondary end points



None Positive nitrogen balance, improved albumin, transferrin, creatinine/ height, midarm muscle, fat areas 1 death (HRF) Positive nitrogen balance, improved albumin

50 g casein/day


EXP equal to CTR, positive nitrogen balance

Standard diet (18% BCAA)

1 death (infection)

EXP equal to CTR, positive nitrogen balance

2100 kcal/day

80 g protein/day Standard diet

Standard diet

Standard diet + casein supplement Standard diet


EXP 2/17


EXP equal to CTR, positive nitrogen balance No differences

Child score improved, albumin improved Nitrogen balance improved in both, BCAA better than standard diet

Both groups improved nitrogen balance and albumin

Standard diet



Fewer hospitalizations, improved albumin and visceral protein

Increased protein retention through gradual or protein intake

Table 2 Continued



Patients Duration Experimental treatment (No.) (days) (EXP)

Control treatment Mortality (CTR)

Secondary end points

Campillo et ai. Open label (1995)'

Hirsch et ai. Open label


6 (months) Standard diet + casein None supplement (1000 kcal/ day, 34 g protein/day)

Standard diet


6 deaths/31


Anthropometric ratios improved

Increased albumin, improved cellular immunity aSmith J, Horowitz J, Henderson JM et ai. (1982) Enteral hyperalimentation in undernoursished patients with cirrhosis and ascites. American Journal of Clinical Nutrition 2: 1209-1218. ^Keohane PP, Attrill H, Brimble G et ai. (1983) Enteral nutrition in malnourished patients with hepatic cirrhosis and acute encephalopathy. Journal of Parenteral and Enteral Nutrition 7: 34-50. cMcGhee A, Henderson JM, Millikan WJ et ai. (1983) Comparison of the effects of hepatic-aid and casein modular diet on encephalopathy, plasma amino acids, and nitrogen balance in cirrhotic patients. Annals of Surgery\97\ 288-293.

^Christie ML, Sack DM, Pomposelli J et ai. (1985) Enriched branched-chain amino acid formula versus a casein-based supplement in the treatment of cirrhosis. Journal of Parenteral and Enteral Nutrition 9: 671-678.

"Okita M, Watanabe A, and Nagashima H (1985) Nutritional treatment of liver cirrhosis by branched-chain amino acid-enriched nutrient mixture. Journal of Nutritional Science and Vitaminology 31: 291-303.

fBunout D, Alcardi V, Hirsch S et ai. (1989) Nutritional support in hospitalized patients with alcoholic liver disease. European Journal of Clinical Nutrition 43: 615-621.

®Cabre E, Gonzalez-Huix F, Abad-Lacruz A et ai. (1990) Effect of total enteral nutrition on the short-term outcome of severely malnourished cirrhotics. A randomized controlled trial.

Gastroenterology 98: 715-720.

hMarchesini G, Dioguardi FS, Bianchi GP et ai. (1990) Long term oral branched-chain amino acid treatment in chronic hepatic encephalopathy. A randomized double-blind casein-controlled trial. The Italian Multicenter Study Group. Journal of Hepatoiogy 11: 92-101.

'Kearns PJ, Young H, Garcia G et ai. (1992) Accelerated improvement of alcoholic liver disease with enteral nutrition. Gastroenteroiogy\02\ 200-205.

;Hirsch S, Bunout D, De la Maza MP et ai. (1993) Controlled trial on nutritional supplementation in outpatients with symptomatic alcoholic cirrhosis. Journal of Parenteral and Enteral Nutrition 17: 119-124.

''Nielsen K, Kondrup J, Martinsen I et ai. (1995) Long-term oral refeeding of patients with cirrhosis of the liver. British Journal of Nutrition 74: 557-567.

'Campillo B, Bories PN, Leluan M et ai. (1995) Short-term changes in energy metabolism after 1 month of a regular oral diet in severely malnourished cirrhotic patients. Metabolism 44: 765-770.

mHirsch S, de la Maza MP, Gattas V et ai. (1999) Nutritional support in alcoholic cirrhotic patients improves host defenses. Journal of the American College of Nutrition 18: 434-414. BCAA, branched-chain amino acid; HRF, hepatorenal failure; NS, not significant.

From Stickel F, Hoehn B, Schuppan D, Seitz HK (2003). Review article: Nutritional therapy in alcoholic liver disease. Alimentary Pharmacology & Therapeutics 18: 357-373.

and should be supplemented with the fat-soluble vitamins—A, D, E, and K. The major strategy in the management of alcoholic cirrhotics with ascites and edema is to restrict fluids to 1-1.5 l/day and to restrict sodium as well.

Autoimmune liver disease The two major categories of autoimmune liver disease are primary biliary cirrhosis (PBC), a disease generally presenting in young female adults, and autoimmune hepatitis, which also most frequently presents in adults but can affect both sexes and present at any time from young childhood to mid-adulthood. PBC results in steatorrhea and malabsorption of the fat-soluble vitamins. Osteoporosis and osteopenia are common.

The nutritional consequences of autoimmune hepatitis, which can evolve into cirrhosis, are similar to those of alcoholic hepatitis and cirrhosis secondary to alcoholic liver disease, and thus the management is similar as well. Occasionally, autoimmune hepatitis can be accompanied by intestinal diseases such as inflammatory bowel disease or celiac disease, and the nutritional management should take both organ systems into account. Although mild liver function abnormalities are common in celiac disease, there are reports of celiac disease in patients with severe liver disease, all of whom demonstrated an improvement in their liver disease with introduction of a gluten-free diet.

Neonatal cholestasis The major differential diagnosis of conjugated hyperbilirubinemia in the first 30 days of life is extrahepatic biliary atresia and the neonatal hepatitis syndrome, for which a large number of specific genetic disorders have been identified. These include a-1 antitrypsin deficiency, inborn errors of bile salt synthesis or transport, cystic fibro-sis/liver disease, Alagille syndrome, hypothyroidism, and panhypopituitarism. The nutritional consequences are similar for all: steatorrhea and malabsorption of the fat-soluble vitamins and failure to thrive. Nutritional management is also similar for all: use of an elemental formula rich in medium-chain triglycerides (MCTs) and supplementation with vitamins A, D, E, and K. Water-miscible vitamin E is poorly absorbed; administration of vitamin E solubilized in polyethylene glycol succinate is a more effective way to administer vitamin E to chole-static infants.

Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) have become very important causes of liver disease in both children and adults, particularly because obesity is being diagnosed in epidemic proportions in both age groups and both liver disorders are most commonly associated with obesity. Children with NAFLD may present before their fifth birthday. The disorder is more common in males. Hepatic fibrosis is common and may even evolve into cirrhosis during childhood. Treatment consists of weight reduction and aerobic exercise. Vitamin E may be beneficial.

In adults, NASH and NAFLD have been recognized for at least 25 years as chronic liver diseases associated with obesity (with or without non-insulin-dependent diabetes mellitus and with or without hyperlipidemia). NAFLD may account for as much as 80% of cases of elevated liver enzymes in the United States. Most adults with the disorders are 110-130% above ideal body weight. The prognosis of NAFLD is good if weight reduction is achieved. NASH is usually slowly progressive but can lead to cirrhosis and the need for liver transplantation in the minority of individuals affected.

In many patients, NAFLD is a component of the insulin-resistance syndrome known as the 'metabolic syndrome,' which is characterized by central obesity, hypertension, hypertriglyceridemia, low levels of high-density lipoprotein-cholesterol, and hyperglyce-mia. In patients with this syndrome, it is hypothesized that there is greater insulin resistance in muscles and adipose tissue than in liver. As shown in Figure 1, in adult patients with NAFLD, the body mass index class >30kg/m2 is associated with an increased prevalence of each of the five components of the metabolic syndrome.

As shown in Table 3, compared to controls, patients with NASH exhibited a higher intake of

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