ABSTRACT
<p><b>OBJECTIVE</b>To use the European Nutritional Risk Screening (NRS)-2002 survey tool to investigate nutritional risk associated to different degrees of liver disease and to assess its ability to identify the nutritional risk of hospitalized patients with chronic liver disease.</p><p><b>METHODS</b>A total of 366 hospitalized patients were assessed with the NRS-2002 on the day of admission. Patients who meet the criteria for malnourishment (NRS-2002 score of more than 3 points (severely impaired nutritional status with body mass index (BMI) less than 18.5 kg/m2) were selected for further study to determine liver function. Patients were classified according to liver dysfunction-related features, including cirrhosis status, Child-Pugh classification, and underlying disease causes (e.g.alcohol, hepatitis virus infection). Chi square test was used in statistical analysis of inter-group difference.</p><p><b>RESULTS</b>The incidence of patients surveyed who were at nutritional risk was 41.0%, and the incidence of malnutrition was 7.6%. The patients with liver failure showed the highest rate of nutritional risk (72.8%). Moreover, among the 97 patients with liver cirrhosis, significantly more had Child-Pugh grade B than grade A (88.6% vs.33.1%; x2=24.019, P=0.000). The cause of liver failure with the highest incidence of nutritional risk was alcohol-related liver disease (66.7%). The overall malnutrition rate among the total 156 patients classified by the NRS-2002 as being at nutritional risk was 76.2%.</p><p><b>CONCLUSION</b>The NRS-2002 is a suitable screening tool for use in Chinese patients with mild early liver disease, but it must be interpreted carefully as its findings alone may promote a false positive rate. The NRS-2002 is less accurate in patients with end-stage liver disease.</p>
Subject(s)
Humans , Body Mass Index , Chronic Disease , Incidence , Liver Diseases , Nutrition Assessment , Nutrition Surveys , Nutritional Status , Risk AssessmentABSTRACT
<p><b>OBJECTIVE</b>To determine the differential protein and mRNA expressions of mitochondria fusion protein-2 (Mfn2) in hepatic tissues in conditions of cirrhosis and acute on chronic liver failure using rat model systems,and to determine the correlative effects on production of adenosine triphosphate (ATP) and reactive oxygen species (ROS).</p><p><b>METHODS</b>A liver cirrhotic rat model (LC rats) was established by intraperitoneal injection of carbon tetrachloride (CCl4,in vegetable oil),and these mice were subsequently used (10 weeks later) to establish the acute on chronic liver failure rat model (LF rats) by injecting lipopolysaccharide and D-amino-galactose.Control groups (normal controls,NC rats) were established for each model by intraperitoneal injection of vegetable oil only.Protein expression of Mfn2 in liver was quantified by western blotting with fluorescence densitometry and immunofluorescence staining,and mRNA expression was measured by real-time fluorescence quantitative PCR.ROS levels in liver were measured by fluorescence spectrophotometry,and ATP content was measured by bioluminescence assay.Significance of inter-group differences was assessed by one-way ANOVA,and correlations were determined using bivariate statistical modeling.</p><p><b>RESULTS</b>Mfn2 protein expression was significantly lower in the liver tissues from modeled rats than that from the control rats (LC:0.051+/-0.004 and LF:0.037+/-0.007 vs.NC:0.254+/-0.008;F=444.98,P less than 0.05).The mRNA expression followed the same trend of lower expression (LC:21.21+/-0.93 and LF:24.35+/-0.85 vs.NC:19.09+/-0.69; F=66.941,P less than 0.05).The ATP content in liver tissues was also significantly lower in the modeled rats (LC:2.07+/-0.05 mol/L and LF:1.81+/-0.11 mol/L vs.NC:3.24+/-0.08 mol/L; F =574.21,P less than 0.05).Lower Mfn2 expression was correlated with lower ATP content (r =0.982) and higher ROS content (r =0.803).</p><p><b>CONCLUSION</b>Reduced Mfn2 expression in liver tissue may cause a decrease in ATP synthesis and increase in ROS generation,thereby disrupting metabolism and increasing oxidative stress in the liver under conditions of cirrhosis and liver failure.</p>