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American Journal of Clinical Nutrition, Vol. 69, No. 6, 1194-1201, June 1999
© 1999 American Society for Clinical Nutrition


Original Research Communications

Hypermetabolism in clinically stable patients with liver cirrhosis1,2,3

Manfred J Müller, Joachim Böttcher, Oliver Selberg, Stefanie Weselmann, Klaus HW Böker, Mechthild Schwarze, Alexander von zur Mühlen and Michael P Manns

Background: Hypermetabolism has a negative effect on prognosis in patients with liver cirrhosis. Its exact prevalence and associations with clinical data, the nutritional state, and ß-adrenergic activity are unclear.

Objective: We investigated resting energy expenditure (REE) in 473 patients with biopsy-proven liver cirrhosis.

Design: This was a cross-sectional study with a controlled intervention (ß-blockade) in a subgroup of patients.

Results: Mean REE was 7.12 ± 1.34 MJ/d and correlated closely with predicted values (r = 0.70, P < 0.0001). Hypermetabolism was seen in 160 patients with cirrhosis (33.8% of the study population). REE was >30% above the predicted value in 41% of the hypermetabolic patients with cirrhosis. Hypermetabolism had no association with clinical or biochemical data on liver function. REE correlated with total body potassium content (TBP; r = 0.49, P < 0.0001). Hypermetabolic patients had lower than normal body weight and TBP (P < 0.05). About 47% of the variance in REE could be explained by body composition whereas clinical state could maximally explain 3%. Plasma epinephrine and norepinephrine concentrations were elevated in hypermetabolic cirrhotic patients (by 56% and 41%, respectively; P < 0.001 and 0.01). Differences in REE from predicted values were positively correlated with epinephrine concentration (r = 0.462, P < 0.001). Propranolol infusion resulted in a decrease in energy expenditure (by 5 ± 3%; P < 0.05), heart rate (by 13 ± 4%; P < 0.01), and plasma lactate concentrations (by 32 ± 12%; P < 0.01); these effects were more pronounced in hypermetabolic patients (by 50%, 33%, and 68%, respectively; each P < 0.05).

Conclusions: Hypermetabolism has no association with clinical data and thus is an extrahepatic manifestation of liver disease. Increased ß-adrenergic activity may explain {approx}25% of hypermetabolism.

Key Words: Liver cirrhosis • energy metabolism • energy expenditure • ß-adrenergic activity • catecholamines • nutritional state • Child-Pugh score • humans • hypermetabolism • liver transplantation




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