title: Hypermetabolism in clinically stable patients with liver cirrhosis.
abstract: 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 beta-adrenergic activity are unclear.
  
  
  OBJECTIVE
  We investigated resting energy expenditure (REE) in 473 patients with biopsy-proven liver cirrhosis.
  
  
  METHODS
  This was a cross-sectional study with a controlled intervention (beta-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 beta-adrenergic activity may explain approximately 25% of hypermetabolism.
authors.affiliation: Medizinische Hochschule Hannover, Germany. mmueller@nutrfoodsc.uni-kiel.de
authors.forename: M J
authors.initials: MJ
authors.lastname: Müller
authors.forename: J
authors.initials: J
authors.lastname: Böttcher
authors.forename: O
authors.initials: O
authors.lastname: Selberg
authors.forename: S
authors.initials: S
authors.lastname: Weselmann
authors.forename: K H
authors.initials: KH
authors.lastname: Böker
authors.forename: M
authors.initials: M
authors.lastname: Schwarze
authors.forename: A
authors.initials: A
authors.lastname: von zur Mühlen
authors.forename: M P
authors.initials: MP
authors.lastname: Manns
mesh_terms: D000328:Adult; D001481:Basal Metabolism; D003430:Cross-Sectional Studies; D004734:Energy Metabolism; D004837:Epinephrine / Q000097:blood; D005260:Female; D005858:Germany / Q000453:epidemiology; D006801:Humans; D007773:Lactates / Q000097:blood; D008103:Liver Cirrhosis / Q000378:metabolism*; D008297:Male; D008659:Metabolic Diseases / Q000145:classification / Q000453:epidemiology / Q000209:etiology; D009638:Norepinephrine / Q000097:blood; D009752:Nutritional Status; D011188:Potassium / Q000097:blood; D015995:Prevalence; D012044:Regression Analysis
chemical_list: D007773:Lactates; D011188:Potassium; D009638:Norepinephrine; D004837:Epinephrine