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Effect Of Reducing Portal Pressure On Intestinal Barrier Function Of Patients With Decompensated Cirrhosis

Posted on:2014-01-10Degree:MasterType:Thesis
Country:ChinaCandidate:Z Q XiongFull Text:PDF
GTID:2254330401970715Subject:Digestive medicine
Abstract/Summary:PDF Full Text Request
Objective:To investigate the effect of lower portal pressure on intestine mucosal barrierfunction of patients with decompensated cirrhosis by observing the changes of plasmaendotoxin, diamine oxidase, D-lactic acid, liver function and portal vein width afterpropranolol plus conventional hepatoprotective symptomatic support.Methods:Sixty-four patients with decompensated cirrhosis in the Gastroenterology deptand Liver Diseases Branch of our hospital, diagnosed according to diagnosis complywith cirrhosis diagnostic criteria developed by the Conference of the National ViralHepatitis in2000and alcoholic liver disease diagnostic criteria developed by thehepatology Institute of Chinese Medical Association on October2001(draft), wereselected and randomly assigned to treatment group (31patients) or control group (33patients). Patients in treatment group were treated with oral propranololhydrochloride tablets (Inderal) and routine methods. Propranolol was started with10mg/d and increased with10mg everyday until the resting heart rate of patientsreduced to about75%of their basal heart rate or their heart rate was less than50beats/min (hepatic venous pressure gradient reduced to less than12mm Hg orbaseline level reduced more than20%). Patients in control group were just treatedwith routine methods. The treatment time was two weeks. The portal vein width ofpatients was measured before and after treatment by color Doppler ultrasound. Liverfunction (ALT, AST, TBIL, ALB), plasma levels of endotoxin and D-lactate, anddiamine oxidase (DAO) activity were also detected before and after treatment.Results:There was no statistically difference in liver function (ALT, AST, ALB, TBIL)between the two groups before treatment (P>0.05). After treatment, the liver function (ALT, AST, TBIL, ALB) of both groups was improved (P<0.05). No significantdifference was observed in (ALT, AST, TBIL, ALB) between control and treatmentgroup (P>0.05). There was no significant difference in portal vein width betweencontrol and treatment groups before treatment (P>0.05); The portal vein width wasimproved in treatment group (P <0.05), while no improvement was noted in controlgroup (P>0.05) after treatment. There was no statistically difference in plasmaendotoxin concentration, diamine oxidase activity (DAO) and D-lactic acid contentbefore treatment. The plasma endotoxin concentration, diamine oxidase activity(DAO) and D-lactic acid content in both control and treatment group weresignificantly decreased after treatment (P<0.05), and a more apparent decrease wasobserved in treatment group than in control group (P<0.05).Conclution:The present experiment observed the changes of plasma endotoxin concentration,diamine oxidase activity, D-lactic acid content, liver function and portal vein width ofpatients with decompensated cirrhosis after propranolol plus conventionalhepatoprotective symptomatic support. The results showed that plasma endotoxinconcentration, diamine oxidase activity and D-lactic acid content were significantlyreduced, liver function was improved and portal vein width was reduced aftertreatment. These findings indicate that propranolol could reduce the portal veinpressure of patients with decompensated cirrhosis and is helpful for intestinal mucosarepair and intestinal permeability reduction. The improvement of intestinal barrierfunction is beneficial to the treatment and prognosis improvement of patients withdecompensated cirrhosis...
Keywords/Search Tags:Liver cirrhosis, Portal hypertension, Intestinal mucosal barrier, Plasma Endotoxin(ETX), Propranolol
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