Xylooligosaccharide decreases blood ammonia levels in patients with liver cirrhosis

Abstract

Purpose: Xylooligosaccharide (XOS) is one of the commercially available prebiotics (functional food ingredients). It has recently been demonstrated XOS can improve physical conditions by changing the intestinal environment. We have previously reported that XOS improved hyperammonaemia produced by high-protein diet in rats, while it lowered blood nitrogen levels and increased faecal nitrogen excretion. The purpose of this study was to evaluate the effects of XOS on blood ammonia levels and intestinal flora in patients with liver cirrhosis. Methods: Fourteen cirrhotic patients (HBV: 3; HCV: 7; others: 4) with clinically stable and mild hyperammonaemia but without apparent hepatic encephalopathy, were given 3.0 g of XOS per os daily for two weeks. The levels of blood ammonia, along with other laboratory values such as serum AST, ALT, bilirubin and albumin, were assessed at the beginning and the end of trial. After faecal samples were collected at the beginning and the end of study, the diluted suspensions were anaerobically incubated, and changes in the proportion of faecal bacteria were assessed. No modification on food intake or medication, considered to be influential on intestinal microflora, was made during the study. Results: Two-week oral administration of XOS resulted in reduced blood ammonia levels in patients with liver cirrhosis (the beginning and the end: 85.5 31.7 mol/l and 62.1 22.1, respectively), while other laboratory values were unaffected (AST, ALT, bilirubin and albumin at the beginning: 75.0 49.4 IU/l, 47.3 39.5 IU/l, 1.16 0.89 mg/dl, 3.16 0.59 g/dl, respectively; those at the end: 58.2 29.1, 34.9 16.5, 1.35 0.82, 3.12 0.60, respectively). Furthermore, XOS promoted the growth of intestinal Bifidobacteria, while suppressing that of Bacteroides. No diarrhoea , flatulence or other complications were complained. Conclusions: XOS effectively improved mild hyperammonaemia in cir-rhotic patients. Though the exact mechanism is not yet clear, the results of our study implicate that XOS can exert its effect by inhibiting enteric colonisation of ammonia-producing anaerobes such as Bacteroides. XOS could be a new promising alternative for treatment of hepatic encephalop-athy, because of its dose being considerably low and side effects less. Further clinical randomised-controlled studies examining a large number of cirrhotic patients should be necessary. Purpose: Recent reports from Japan suggest higher prevalence of Hepatitis C virus (HCV) antibody in patients with Hypertrophic Cardiomyopathy (HCM) compared to a control population of blood donors (15.7% vs 2.4% p 0.001). In half the patients with coexisting HCV and HCM, the virus was isolated from the myocardium, including negative strands, indicating active replication and a possible pathogenic role. The aim was to study the prevalence of left ventricular hypertrophy in a group of patients with chronic hepatitis C, compared to patients with liver diseases of other causes. Methods: We compared the 2D and M-mode echocardiographic parameters of left ventricular hypertrophy and left ventricular mass index in a group of HCV patients (N 26), to that of patients with non-HCV related liver diseases (N 22). Patients with evidence of valvular heart disease or pericardial effusion were excluded. All the patients had advanced liver disease with Child Pugh score of 8 or higher, at the time of cardiac evaluation. The left ventricular wall thickness and dimension were measured in diastole. Relative wall thickness was calculated as a ratio of total wall thickness (septal wall posterior wall) to left ventricular dimension in diastole. P values were obtained using the two-sided, two-sample t test. Results: Echocardiographic dimensions for patients with HCV did not differ significantly from non-HCV patients. For LVMI, the difference between groups was significantly less than 21 g/m2 (which is less than 21% of the non-HCV mean). For SWT, PWT, LVDD and RWT, the differences were significantly less than 1.8 mm (17%), 1.6 mm (15%), 4.0 mm (8%) and 0.10 (24%) respectively. Conclusions: There is an increase in the left ventricular mass index in all groups of liver patients, compared to normal control population. Absence of a significant difference in the left ventricular measurements between the two groups of liver patients, does not support a pathogenic role for HCV, in hypertrophic heart disease. Variable HCV (N 26) Mean (SD) Non HCV (N 22) Mean (SD) P 95% CI for difference* Normal values in adults** Lt. Ventricular mass index g/m2 104 (31) N 24 102 (35) 0.91 18 to21 92 16 Septal wall thickness (mm) 11.1 (1.8) 10.5 (2.2) 0.27 0.5 to 1.8 6 to 11 Posterior wall thickness (mm) 11.0 (1.8) 10.5 (1.8) 0.30 0.5 to 1.6 6 to 11 LV Dimension in Diastole (mm) 49.2 (6.7) 48.9 (6.2) 0.90 3.5 to 4.0 35 to 57 Relative wall thickness 0.46 (0.11) 0.42 (0.07) 0.20 0.02to 0.10 0.45