Factors Associated With Protein-energy Malnutrition in Chronic Liver Disease

We aimed to elucidate the incidence of protein–energy malnutrition (PEM) in patients with chronic liver disease and to identify factors linked to the presence of PEM. A total of 432 patients with chronic liver disease were analyzed in the current analysis. We defined patients with serum albumin level of 3.5 g/dL and nonprotein respiratory quotient (npRQ) value using indirect calorimetry less than 0.85 as those with PEM. We compared between patients with PEM and those witho ut PEM in baseline characteristics and examined factors linked to the presence of PEM using univariate and multivariate analyses. There are 216 patients with chronic hepatitis, 123 with Child–Pugh A, 80 with Child–Pugh B, and 13 with Child–Pugh C. Six patients (2.8%) had PEM in patients with chronic hepatitis, 17 (13.8%) in patients with Child–Pugh A, 42 (52.5%) in patients with Child–Pugh B, and 10 (76.9%) in patients with Child–Pugh C (P< 0.001). Multivariate analysis revealed that Child–Pugh classification (P< 0.001), age 64 years (P1⁄4 0.0428), aspartate aminotransferase (AST) 40 IU/ L (P1⁄4 0.0023), and branched-chain amino acid to tyrosine ratio (BTR) 5.2 (P1⁄4 0.0328) were independent predictors linked to the presence of PEM. On the basis of numbers of above risk factors (age, AST, and BTR), the proportions of patients with PEM were well stratified especially in patients with early chronic hepatitis or Child–Pugh A (n1⁄4 339, P< 0.0001), while the proportions of patients with PEM tended to be well stratified in patients with Child–Pugh B or C , PhD, Tomoyuki , PhD, , and Shuhei Nishiguchi, MD, PhD (Medicine 95(2):e2442) Abbreviations: %C = substrate oxidation of carbohydrate, %F = substrate oxidation rates of fat, %P = substrate oxidation of protein, ALT = alanine aminotransferase, AST = aspartate aminotransferase, BMI = body mass index, BTR = branchedchain amino acid (BCAA) to tyrosine ratio, HOMA-IR = homeostasis model assessment-insulin resistance, LC = liver cirrhosis, npRQ = non-protein respiratory quotient, PEM = protein-energy malnutrition, REE = rest energy expenditure, UN = urinary excretion of nitrogen, VCO2 = carbon dioxide production per minute, VO2 = oxygen consumption per minute. INTRODUCTION T he liver plays a unique role in carbohydrate metabolism by maintaining glucose concentration levels in the normal range and it is also an essential organ for the metabolism of three major nutrients: protein, fat, and carbohydrate. Liver cirrhosis (LC), which develops over a long period of time due to chronic inflammation, is often complicated with protein– energy malnutrition (PEM). PEM is one of the most common complications in LC patients. PEM is associated with an increased risk of complications, including ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome, and thus, it is linked to high morbidity and mortality for LC patients. Predicting the presence of PEM and appropriate nutritional support is therefore essential for improving prognosis in chronic liver disease patients with PEM. Protein malnutrition can be assessed using serum albumin value. It has been demonstrated that, in metabolic disorders of protein, the degradation and synthesis rates of albumin decreased and the half-life of serum albumin became longer. In general, patients with serum albumin value of 3.5 g/dL are considered to have protein malnutrition and it is easily tested in clinical practice, although a previous study reported that conventional definition of hypoalbuminemia as a serum albumin level of 3.5 g/dL should be reconsidered. On the contrary, measurement of nonprotein respiratory quotient (npRQ) using indirect calorimetry for assessing the degree of energy malnutrition is highly limited in daily clinical practice due to the high cost for indirect calorimetry. Thus, other alternative markers will be needed for predicting the presence of PEM. Particularly, in early stages of chronic liver disease such as hild–Pugh A, the presence of PEM tends ng to the delay of initiation of nutritional PEM is linked to sarcopenia, which is www.md-journal.com | 1 characterized by the depletion of skeletal muscle mass and negatively effect on survival and quality of life in patients with LC and has thus recently attracted attention for clinicians. On the basis of these backgrounds, in the current study, we aimed to elucidate the incidence of PEM in patients with chronic liver disease and to identify factors linked to the presence of PEM. PATIENTS AND METHODS