Portal hypertension and its complications are the leading causes of morbidity and mortality in patients with liver cirrhosis. Noninvasive assessment of liver stiffness had been an effective tool for assessment of fibrosis progression in chronic liver disease. It was intended to assess liver stiffness measurement (LSM), portal vein diameter (PVD), splenic bipolar diameter (SD), and the platelet count/spleen diameter (PC/SD) ratio in patients who test positive for the hepatitis C virus (HCV) and to study the impact of non-selective beta blockers (NSBB) on the grade of esophageal varices (EVs) and liver elasticity. Subjects were 80 patients with Child-Pugh grade A or B compensated cirrhosis who tested positive for HCV. All of the patients underwent a laboratory workup including AFP, HCV antibodies, HCV RNA, HBsAg, LSM according to real-time elastography, upper gastrointestinal endoscopy (UGIE) to detect and grade EVs, calculation of the PC/SD ratio, and measurement of the PVD and SD according to real-time abdominal ultrasonography. All patients were given the maximum tolerated dose of NSBB for three months, and UGIE, LSM, PC/SD, PVD, and SD were subsequently reassessed and reported. LSM and the PC/SD ratio were exceptional noninvasive tools for prediction of significant EVs (grade ≥ II, p < 0.001) with a sensitivity 82.4% and a specificity 82.6% at a cutoff point 18 kPa for LSM, and a sensitivity 94.1% and specificity 69.6% at a cutoff point 880 for the PC/SD ratio. LSM is highly correlated with PVD, the PC/SD ratio, SD, and the Child-Pugh score. NSBB significantly decreased PVD. The percent change in PVD significantly correlated with LSM, the grade of EVs, and SD. Findings indicated that LSM is a noninvasive, rapid, and reproducible tool with which to detect portal hypertension and EVs. NSBB therapy can effectively decrease PVD and may consequently improve the EV grade with no significant impact on LSM in patients with liver cirrhosis.
Background: Esophageal varices is one of the major complications of portal hypertension and one of the main causes of death in cirrhotic patients, so prophylaxis from esophageal varices bleeding can decrease the number of deaths in those patients. Aim of the work: To assess the effect of non-selective beta blockers on portal vein diameter and grades of esophageal varices. Subjects and methods: Our study was carried out at Gastroenterology and Hepatology unit, Internal Medicine department, Zagazig University hospital. Forty patients with HCV positive liver cirrhosis were enclosed in the study. All were Child Pugh grade A and B, diagnosed by clinical examination, laboratory investigations (hepatitis C virus antibody, hepatitis C virus RNA by polymerase chain reaction, hepatitis B virus surface antigen, liver and kidney functions, complete blood count, INR and alpha feto-protein) and pelvi-abdominal ultrasound findings. Upper gastrointestinal (GI) endoscopy was done at the beginning of the study for detection and grading of esophageal varices (EVs) and those without EVs were excluded, also portal vein diameter (PVD) was recorded by ultrasound. The maximum tolerated dose of Propranolol (decrease pulse rate by 25% but not below 60 beats per minute) was given to all patients for three months. EVs grading, by upper GI endoscopy, and PVD were reassessed at the end of the study. Results: Propranolol showed a significant reduction in heart rate and PVD for the pre and posttreatment results after three months of treatment (P<0.001 for both). The dose of Propranolol didn't show significant effect on reduction of small size EVs (P=0.07) while the percent of reduction of PVD correlated significantly with percent of reduction in EVs grade for the pre and post-treatment (P<0.05). A cut off point for detection of significant EVs (GII and III) was 12.5 mm with sensitivity 82.4%, specificity 47.8%, positive predictive value (PPV) 53.8% and negative predictive value (NPV) 78.6%. Conclusion: Non-selective beta blocker (Propranolol) caused significant reduction in portal vein diameter and the percentage of reduction of portal vein diameter significantly correlated with change in esophageal varices grades.
Background The presence of bacteremia as a complication of variceal bleeding in patients with liver cirrhosis had been investigated by many studies. The aim of this study was to assess the bacteremia as a risk factor for variceal upper gastrointestinal tract bleeding in cirrhotic patients. A cross-sectional study was conducted on 99 patients with chronic liver disease divided into three groups: group I included 35 patients presented with first attack of variceal bleeding, group II included 35 patients presented with recurrent attacks of variceal bleeding, and group III included 29 patients with no history of previous variceal bleeding as a control group. Routine laboratory tests were done, upper GI endoscopy, blood culture, and measurement of procalcitonin level in blood. Results Patients with recurrent variceal bleeding had statistically (p < 0.05) the highest percentage of positive blood culture followed by patients with first variceal bleeding and the control (60% vs 45.7% vs 24.1%) respectively. In addition to procalcitonin results, patients with recurrent variceal bleeding had statistically the highest values of PCT followed by patients with first variceal bleeding and the control (1.92 vs 0.325 vs 0.22 ng/ml) respectively. Multivariate regression analysis showed that procalcitonin and hemoglobin only was the significant predictors for variceal bleeding. Hemoglobin at cutoff value of ≤ 9.6 and procalcitonin (ng/dl) at cutoff value of > 1.76 is the most specific in predicting bleeding 86.21%, 86.21% (CI 95%) respectively. Conclusion Bacteremia and procalcitonin are risk factor for variceal bleeding in cirrhotic patients. Procalcitonin can be used as easily measurable and surrogate biomarker for bacteremia and variceal bleeding.
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