Energy expenditure and substrate oxidation in patients with cirrhosis: The impact of cause, clinical staging and nutritional state

• Published in: Hepatology (Baltimore, Md.) Md.), 1992-05, Vol.15 (5), p.782-794
• Main Authors: Müller, Manfred J., Lautz, Hans U., Plogmann, Birgit, Bürger, Mechthild, Körber, Jürgen, Schmidt, Friedrich W.
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Energy Metabolism; Female; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Liver Cirrhosis - complications; Liver Cirrhosis - etiology; Liver Cirrhosis - metabolism; Male; Medical sciences; Middle Aged; Nutritional Status; Oxidation-Reduction; Severity of Illness Index
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.1840150507

Many clinicians subjectively feel that cirrhotic patients frequently have clinical signs of hypermetabolism. However, it is unknown whether hypermetabolism is a constant feature of chronic liver disease, corresponds to liver destruction and repair or is of prognostic value. This article is about resting energy expenditure and substrate oxidation rates in 123 patients with biopsy‐proven cirrhosis differing with respect to cause, duration of the disease, biochemical parameters of parenchymal cell damage, cholestasis, liver function, number of complications, clinical staging and nutritional state. Resting energy expenditure varied between 1,090 and 2,300 kcal/day and differed from the predicted values in 70% of the patients. Resting energy expenditure was closely related to fat‐free mass, and 52% of the variability could be explained by fat‐free mass, age and sex. Of all the patients, 18% were hypermetabolic and 31% were hypometabolic. Hypermetabolism showed no strict association with the cause of cirrhosis, the duration of the disease, liver function, cholestasis, cell damage, clinical staging, blood hemoglobin, plasma thyroid hormone levels or human leukocyte antigens. An increased resting energy expenditure was associated with significant losses of muscle, body cell mass and extracellular mass at unchanged body fat, whereas fat and fat‐free mass were increased in hypometabolic patients when compared with normometabolic patients. Lipid oxidation was increased, but glucose oxidation was reduced in nearly all patients with cirrhosis. This was most pronounced at advanced stages of liver disease. Although similar with respect to liver function and clinical staging, 76.2% of hypermetabolic patients had transplants within the observation period, compared with only 16.7% and 8.1% in the normometabolic group and hypometabolic group, respectively. Posttransplantation mortality was independent of pretransplantation resting energy expenditure, but it increased significantly in patients with losses in body cell mass. In conclusion, hypermetabolism is not a constant feature of cirrhosis and results more from extrahepatic than from hepatic factors. It may cause malnutrition and contributes to the clinical outcome of patients with chronic liver disease. (HEPATOLOGY 1992;15:782–794).