Impact of non-selective beta blockers on portal hypertension and hepatic elasticity in hepatitis C virus-related liver cirrhosis.

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.

Evaluation of different therapeutic approaches for spontaneous bacterial peritonitis.

BACKGROUND AND STUDY AIMS: Spontaneous bacterial peritonitis (SBP) is a significant cause of mortality in cirrhosis. Reducing toxic burden of infected ascitic fluid through paracentesis needs further studies as adjunctive therapy of SBP. We aimed to evaluate different therapies for SBP. PATIENTS AND METHODS: Thirty-six cirrhotic ascitic patients with SBP were examined and classified according to treatment modality (5-7 days) into: Group A received cefotaxime, group B received cefotaxime and albumin 1.5 g/kg body weight within 6h of SBP being diagnosed and 1g/kg body weight on day 3, group C received cefotaxime and paracentesis with volume dependent albumin infusion. Control group of 12 cirrhotic ascitic patients free from SBP were included. Routine laboratory tests, ascitic fluid analysis for leucocytes and culture were done, inflammatory mediators such as nitric oxide and tumour necrosis factor alpha were measured in serum and ascitic fluid. Duplex-Doppler assessment of portal flow volume and renal resistive index, Echocardiography to measure end diastolic and end systolic volumes, stroke volume and cardiac output were done. Tests were carried out before and after therapy. RESULTS: Treatment response was assessed by, cardiac haemodynamics, portal and renal flow and NO and TNF. All studied parameters; laboratory, cardiac, Doppler exhibited a significant improvement in group B in contrast to the other groups as demonstrated by post therapy reduction of (blood and ascitic fluid WBCs & PNLS, serum and ascitic NO & TNF and renal resistive index), elevation of (serum albumin and portal flow volume) and improvement of cardiac haemodynamic. CONCLUSION: Treatment of spontaneous bacterial peritonitis by cefotaxime and body weight based albumin infusion gave most favourable results compared to other regimens. Postulation of removing toxic burden through paracentesis has not been confirmed.