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J. Carlos Teran, MD
Address
Department of Gastroenterology, Cleveland Clinic Florida,
3000 West Cypress Creek Road, Fort Lauderdale, FL 33309, USA.
Current Gastroenterology Reports 1999, 1:335340
Current Science Inc. ISSN 1522-8037
Copyright 1999 by Current Science Inc.
Introduction
Nutritional deficiencies and proteinenergy malnutrition
(PEM) are often present in chronic liver diseases but are
also seen in acute liver diseases, especially in cases of
hepatic failure. Most information in this field comes from
studies of end-stage cirrhotic patients whose diseases
followed various etiologies. Some information is also
available regarding nutritional therapy for acute alcoholic
hepatitis or fulminant hepatic failure. Less is known about
nutrition in noncirrhotic chronic liver diseases such as
chronic hepatitis, chronic cholestasis, or hepatic steatosis.
In this review, current knowledge of the pathogenesis of
and therapy for nutritional problems in liver diseases is
discussed, with emphasis on end-stage liver disease and
hepatic encephalopathy.
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Nutrition
Pathogenesis of proteinenergy
malnutrition in cirrhosis
The pathogenesis of malnutrition in cirrhosis is thought to
be multifactorial (Table 1). A majority of cirrhotic patients
suffer from gastrointestinal symptoms such as anorexia,
taste dysfunction, nausea, and vomiting, which affect their
nutrient intake [9]. Taste abnormalities have been associated with zinc and magnesium deficiencies [10]. Also, 40%
of cirrhotic patients have steatorrhea caused by cholestasis
or chronic pancreatitis. A survey on the food intake of hospitalized patients with cirrhosis showed a decrease in calor i e s a n d p r o t e i n i n g e s t i o n ave r a g i n g 50 % o f t h e
recommended dietary allowance [11]; however, a recent
controlled study showed that hospitalized cirrhotics have
similar intake to that of other hospitalized patients with
different conditions [12].
Perhaps the most interesting and important aspect of
the pathogenesis of PEM in cirrhosis is the presence of
serious metabolic abnormalities that mimic a state of
catabolism similar to sepsis or trauma [3]. Measurements
of the basal energy expenditure in cirrhotics have not
shown a statistically significant difference from measurements in healthy control subjects when energy expenditure
is expressed in calories per kilogram of body weight [13].
Prediction of resting energy expenditure based on HarrisBenedict equations is either too low or too high in 50% of
cirrhotics. When resting energy expenditure is expressed in
calories per kilogram of lean body mass, a significant
increase is seen in patients with cirrhosis compared to
healthy control subjects [14]. The presence of ascites
increases the resting energy expenditure. This means that
cirrhotic patients are spending more energy per unit of
metabolically active tissue, but their overall energy expenditure tends to be equal to that of healthy control subjects
because the cirrhotic patients body cell mass is decreased.
These patients tend to have respiratory quotients (RQ) that
are significantly lower than those of healthy control subjects after an overnight fast. The amount of fuel cirrhotic
patients utilize after an overnight fast is similar to that used
by healthy control subjects after 72 hours of starvation
[15]. In other words, the metabolism of cirrhotics mimics
that of starving control subjects even at early phases of
fasting. However, as opposed to a chronically starving
patient in whom the energy expenditure decreases over
time, cirrhotics continue to have increased energy expenditure that leads to progressive loss of muscle and fat mass,
which results in PEM.
Studies on carbohydrate metabolism in cirrhosis have
shown that these patients have a high prevalence of
glucose intolerance [17]. The pathogenesis of this abnormality is not well-defined, but it seems to be caused by a
postreceptor intracellular abnormality in both liver and
muscle. This is probably associated with the increase in
circulating catabolic hormones such as glucagon, cortisol,
and catecholamines. Associated with this insulin resistance
is a decreased storage of glycogen in the liver and muscle,
337
has been identified and treated. Branched-chain aminoacid formulas are thought to be beneficial for cirrhotic
patients with encephalopathy; randomized clinical trials
have not shown a significant advantage for branched-chain
amino-acid formulas over standard protein solutions
[25,26]. While branched-chain amino-acid formulas have
proven more effective than placebo and shown similar
results to lactulose or neomycin in the treatment of hepatic
encephalopathy, they are not better than standard protein
formulas, and they are more costly [23]. For these reasons, branched-chain amino-acid formulas are rarely recommended. In our practice we use them only occasionally
in cirrhotic patients with refractory encephalopathy or profound hepatic coma. In noncritically ill patients with
hepatic encephalopathy, other means of dietary manipulation can be attempted, such as supplementation of fiber or
vegetarian diets [23]. These regimens have proven beneficial mainly because soluble fiber ferments in the colon by
the same mechanism as lactulose.
The preservation of the skeletal muscle mass seems to
be beneficial in preventing recurrent encephalopathy. This
may be true because of the role of skeletal muscle in
ammonia elimination. Given the metabolic abnormalities
described in cirrhosis, which result in increased catabolism
during fasting, frequent small meals and a bedtime snack
are recommended to patients. Frequent meals have also
been shown to promote a positive nitrogen balance in
cirrhotic patients [27]. If ascites and hyponatremia are
present, water restriction is indicated. In cholestatic types
of cirrhosis such as primary sclerosing cholangitis and
primary biliary cirrhosis, supplementation of lipid soluble
vitamins (A, D, E, and K) and calcium may be necessary if
steatorrhea is present. Zinc deficiency is common in
cirrhotic patients from a decrease in hepatic storage
capacity. Vitamin A deficiency may arise due to decreased
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Nutrition
release from the liver. Zinc supplements should be considered for patients whose plasma levels are low or in those
with dysgeusia or night blindness. There is no evidence,
however, that zinc improves encephalopathy [23].
Conclusions
Nutritional problems in liver diseases are very prevalent.
They are brought about by a combination of factors including metabolic abnormalities, poor oral intake, and
malabsorption. Although nutritional assessment is difficult in liver disease, results from most studies indicate that
poor nutritional status based on anthropometric parameters correlates with a bad prognosis. Decompensated
cirrhosis and severe acute hepatitis should be considered
catabolic states similar to sepsis or trauma. Efforts to
improve the nutritional status of patients with cirrhosis,
alcoholic hepatitis, and fulminant hepatic failure are warranted, preferably through enteral nutrition or, when
needed, by parenteral nutrition. Branched-chain aminoacid formulas offer no advantages over standard amino
acids in the treatment of hepatic encephalopathy. Protein
restriction is not necessary except in cases of refractory
chronic encephalopathy or fulminant hepatic failure. Most
patients with cirrhosis tolerate a diet with normal amounts
of protein. Unnecessary protein restriction may cause iatrogenic malnutrition. For patients with noncirrhotic chronic
liver disease, a normal diet is recommended, and vitamin
and mineral supplements may also be needed. Dietary
manipulation and correction of the specific cause are recommended for the management of patients with fatty liver.
Patients receiving long-term parenteral nutrition may benefit from precise assessment of their energy requirements by
indirect calorimetry as well as choline supplementation.
Of importance
Of major importance
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An excellent review on the subject of malnutrition in cirrhosis.
Includes data on prevalence and pathogenesis of malnutrition and
the differences between alcoholic and nonalcoholic cirrhosis.
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