Are patients with liver cirrhosis hypermetabolic?

Abstract

Hypermetabolism is not a constant feature of liver cirrhosis. It may occur in up to 18% of cirrhotics. Most of the deviations are due to increases in resting energy expenditure (REE). Dietary induced thermogenesis (DIT) is normal or slightly increased whilst the thermic effect of exercise TEE is of minor importance in cirrhosis. The increase in REE which reflects a systemic manifestation of liver disease cannot be identified by the clinical and biochemical measures of liver function. An increased REE is frequently seen in malnourished patients and this is mainly due to disproportional loss in muscle mass. Some cirrhotic patients cannot reduce REE in response to weight loss. This problem is not specific for liver cirrhosis but is also seen in other cachectic groups of patients. Adjustment of REE per kg fat free mass (FFM) may lead to erroneous conclusions (i) because of the non linearity of REE over the range of FFM and (ii) the different contributions of muscle mass and non-muscle body cell mass (BCM) to FFM over the range of FFM. There is circumstantial evidence that the metabolic rate per kg BCM is increased in malnourished cirrhotics. More specifically, cirrhosis increases in REE are associated with a deterioration in hepatic circulation. Increased sympathetic nervous system activity is frequently seen in cirrhosis and may provide a link between between reduced nutritive portal flow and increased whole body oxygen consumption. Increased REE is also associated with weight loss, a poorer liver function and a higher mortality after liver transplantation and thus may have prognostic value. Taken together, REE is variable in patients with cirrhosis. Hypermetabolism is seen in malnourished patients and those with impaired splanchnic hemodynamics. Hypermetabolism is associated with a poorer outcome after liver transplantation.