Resting Energy Expenditure in Patients with Alcoholic Hepatitis

Abstract

Patients with alcoholic hepatitis are typically malnourished. A hypermetabolic state would explain, at least in part, the muscle wasting observed in these patients. However, data on hypermetabolism in liver disease are limited and conflicting. In this study, we evaluated measured energy expenditure (MEE) vs predicted energy expenditure (PEE), and MEE in relation to urinary creatinine excretion in 20 patients with moderate and severe alcoholic hepatitis, and 20 controls. Patients with alcoholic hepatitis had depressed creatinine height index (moderate 66%, severe 78%) demonstrating muscle depletion. Patients with alcoholic hepatitis also had depressed mean serum albumin concentrations, the moderate group 2.6 g/dl and the severe group 2.0 g/dl. The mean values for measured energy expenditure in moderate alcoholic hepatitis patients, severe alcoholic hepatitis patients, and the control group were: 1556 kcal, 1878 kcal, and 1943 kcal, respectively. The mean measured energy expenditures per g of creatinine for the same groups were: 1520 kcal, 1813 kcal, and 1043 kcal, respectively. The mean measured energy expenditure/predicted energy expenditure ratio was not increased in alcoholic hepatitis patients compared to controls. However, when related to urinary creatinine excretion, the alcoholic hepatitis patients had a mean measured energy expenditure that was 55% higher than controls. In conclusion, whereas the measured energy expenditure to predicted energy expenditure ratio was not elevated in alcoholic hepatitis patients compared to controls, the measured energy expenditure per gram of creatinine was significantly increased in alcoholic hepatitis patients, supporting the concept of alcoholic hepatitis as a hypermetabolic state.

Resting energy expenditure should be measured in patients with cirrhosis, not predicted

“…24 However, underestimates of mean measured REE have been recorded in this patient group using these formulae with individual differences between predicted and measured values exceeding 20% in one third of patients. 17,18,[25][26][27][28][29][30][31][32][33] No information is, however, available on the relative accuracy of the predictions in various population subgroups. Similarly, little if any information is available on the accuracy of the estimates of REE obtained, in this patient population, using other prediction formulae.…”

“…They suggest, but do not advocate, that if the facilities for measurement are not available, then energy expenditure could be estimated by use of the Harris-Benedict prediction formulae. 24 However, it has been shown that these formulae may underestimate mean measured values of REE in patients with cirrhosis by up to 13%, 17,18,[25][26][27][28][29][30][31][32][33] though presently, it is unclear whether this discrepancy is equally evident in all population subgroups.A number of alternative prediction formulae are available, 34-39 but the accuracy of the REE estimates derived from these has not been studied systematically in patients with chronic liver disease. A prediction formula developed specifically for use in this patient population, which incorporated a measure of fat-free mass (FFM) derived using bioelectrical impedance analysis, has been proposed by Mü ller et al 40 but this has not been validated.…”

Detection and treatment of medical inpatients with or at-risk of malnutrition: Suggested procedures based on validated guidelines

“…We found eight studies among the guidelines assessing REE in groups of malnourished or at-risk medical inpatients with various acute illnesses (acute renal failure [26], cancer [27,28], ulcerative colitis [29], acute pancreatitis [30], alcoholic hepatitis [31,32], congestive heart failure [33]). Among them, we found six studies (four observational studies [27À30] and two non-randomized trials [31,32]), in which REE was measured by indirect calorimetry and compared to the value predicted by Harris-Benedict formula.…”

“…Among them, we found six studies (four observational studies [27À30] and two non-randomized trials [31,32]), in which REE was measured by indirect calorimetry and compared to the value predicted by Harris-Benedict formula. The formula failed to accurately predict REE in all studies.…”

Influence of the metabolic sequelae of liver cirrhosis on nutritional intake

“…The nutritional and metabolic consequences of cirrhosis have attracted considerable interest over the past decade (1)(2)(3)(4)(5); given the central role of the liver in metabolism, it is not surprising that undernutrition is common in chronic liver disease (6)(7)(8). In recent years, the focus of research in this area has been on the identification of clinical or biochemical markers associated with nutritional risk (9,10).…”