Assessment of liver fibrosis with acoustic radiation force impulse imaging versus liver histology in patients with chronic hepatitis C: a pilot study.

BACKGROUND: Acoustic radiation force impulse imaging (ARFI) involves the mechanical excitation of tissues using short-duration acoustic pulses to generate localized displacements in tissue. The displacements results in shear-wave propagation, tracked by ultrasonography (US) correlation-based methods and recorded in meters per seconds. AIM: To compare (ARFI) integrated into a conventional US with the standard histological examination of liver biopsy specimens for the assessment of liver fibrosis. MATERIALS AND METHODS: Histological fibrosis staging with standard liver biopsy using the Metavir scoring system as well as fibrosis assessment using ARFI were performed to 80 patients with chronic hepatitis C over a 3-month period. RESULTS: ARFI findings were identical to the biopsy findings in 61 (76.25%) patients.Fifty-eight (67.5%) patients with an early fibrosis stage (F0, F1, and F2) by histology had identical fibrosis stages using ARFI.Only 20 out of 26 patients with an advanced fibrosis stage (F3 and F4) using ARFI had advanced fibrosis histologically. In the advanced fibrosis stages, the sensitivity of ARFI was 70% and specificity was 80%, with positive and negative predictive values of 53.8 and 88.9%, respectively. The accuracy of detection of advanced fibrosis by ARFI was 77.5%. CONCLUSION: ARFI imaging is a promising noninvasive US-based method for the assessment of liver fibrosis.

Khat-induced liver injuries: A report of two cases.

Khat is consumed for recreational purposes in many countries, including Yemen, where >50% of adults chew khat leaves regularly. A wide spectrum of khat-induced liver injuries has been reported in the literature. Herein, we report two patients with khat-induced liver injury. Both patients clinically presented with acute hepatitis, one of whom showed radiological evidence of hepatic outflow obstruction. Based on the histological tests, both patients had acute hepatitis, which indicated drug-induced liver injury (DILI) on a background of chronic hepatitis and portal fibrosis; of the two, one presented with symptoms of immune-mediated liver injury.

Impact of nitazoxanide on sustained virologic response in Egyptian patients with chronic hepatitis C genotype 4: a double-blind placebo-controlled trial.

BACKGROUND: Nitazoxanide, approved for the treatment of Cryptosporidium parvum and Giardia lamblia, was found to inhibit hepatitis C virus replication. AIM: The aim of this study was to assess the impact of nitazoxanide as an add-on therapy to pegylated interferon α-2a and ribavirin on sustained virologic response (SVR) in patients with chronic hepatitis C. PATIENTS AND METHODS: A total of 200 patients with chronic hepatitis C were enrolled in the study, assigned randomly in a 1 : 1 ratio to two groups: group A (placebo group) and group B (nitazoxanide group). Five patients withdrew from the study after they signed the consent form.A total of 195 patients were evaluated: 97 patients in group A versus 98 patients in group B at a dose of 500 mg twice daily. Placebo and nitazoxanide were administered as an add-on therapy to pegylated interferon α-2a plus ribavirin following a 12-week lead-in phase. SVR was evaluated. Statistical analysis was carried out using the SPSS software. RESULTS: The mean age of the patients in group A was 46.5 versus 45.7 years in group B. In group A, 85 out of 97 (87.6%) patients were men and in group B, 84 out of 98 (85.7%) patients were men.In group A, 59 out of 97 (60.82%) patients achieved an SVR versus 57 out of 98 (58.16%) patients in group B (P=0.70); this difference was not significant. CONCLUSION: Our data did not show any significant impact of nitazoxanide on SVR.

Portal and splanchnic hemodynamics after partial splenic embolization in cirrhotic patients with hypersplenism.

To assess the acute effects of partial splenic embolization (PSE) on portal and splanchnic hemodynamics in patients with cirrhosis. Ninety-five patients with hypersplenism were included in the study. Duplex examinations were performed before and 3 and 7 days after PSE. Portal and splanchnic hemodynamics including vessel cross-sectional area (CSA), mean flow velocities (cm/s), blood flows (mL/min), Doppler indices as portal congestion index (CI), liver vascular index, hepatic artery and superior mesenteric artery (SMA) pulsatility and resistive indices (PI and RI), were performed before and after PSE. In our study, 69 of 95 patients were males (72.6%) and 26 females (27.3%). Chronic hepatitis C virus infection was the main cause of cirrhosis (81.1%). PSE failed technically in six patients (6.3%). After PSE, both CSA and CI significantly decreased (p < 0.05 and <0.01). The portal vein velocity significantly increased (p < 0.01). The portal flow volume (892.4 ± 151 mL/min) did not show significant changes. The hepatic artery RI and PI showed a steady increase that became significant 7 days post-PSE (p < 0.05). The RI and PI of SMA increased significantly after 7 days of PSE (p < 0.05). PSE has an immediate portal decompression effect in patients with portal hypertension without reduction in portal flow. This effect on portal pressure should be investigated in future studies as a potential tool for management of acute variceal bleeding when other medical procedures fail.

Predictors of hepatic decompensation after TACE for hepatocellular carcinoma.

AIM: To study predictive factors for hepatic decompensation after transarterial chemoembolisation (TACE) for hepatocellular carcinoma (HCC). METHODS: Between November 2009 and August 2010, of 254 patients with HCC who presented to our multidisciplinary HCC clinic for evaluation, 102 (40%) were amenable for TACE. In this prospective study, there were 102 patients with compensated cirrhosis with HCC and Child-Pugh Class A cirrhosis who underwent TACE at the National Liver Institute, Menoufiya University, Egypt. We excluded all patients with prior locoregional therapy, systemic therapy and/or surgical intervention. At baseline and at 1 month postprocedure, laboratory criteria, tumour criteria (size, number) and Child-Pugh score were recorded. Patients were classified into group 1 (no Child-Pugh point increase after TACE) and group 2 (one or more added Child-Pugh points after TACE, defining hepatic decompensation). Univariate and multivariate analyses were performed to identify factors predictive of hepatic decompensation. RESULTS: Patients were mostly males (82.4%) of mean age 58.4±8.1 years. The only significant changes in laboratory findings at 1 month after TACE were increased international normalised ratio, serum total bilirubin, alanine transaminase and aspartate transaminase and decreased serum albumin and α-fetoprotein (AFP). The statistically significant predictive factors for hepatic decompensation using univariate analysis were found to be baseline lower serum albumin, higher serum α-fetoprotein, more advanced Barcelona Clinic Liver Cancer (BCLC) stage, larger tumour size and a greater number of tumour nodules; with logistic regression, multivariate analysis found that at baseline larger tumour size (p=0.004 at 95% CI), higher serum AFP (p=0.046 at 95% CI) and lower serum albumin (p=0.033 at 95% CI) predicted decompensation; BCLC stage, number of tumour nodules and pre-TACE bilirubin did not predict changes in liver function. CONCLUSIONS: Lower serum albumin and increased tumour burden (larger tumour size/more nodules and higher α-fetoprotein) at baseline may help predict post-TACE decompensation.