Randomized controlled trial of scleroligation versus band ligation alone for eradication of gastroesophageal varices.

BACKGROUND AND AIMS: Gastric varices develop in 5% to 33% of patients with portal hypertension. Their most common form is concomitant gastroesophageal varices. Scleroligation (combined sclerotherapy and band ligation) has been used successfully in management of esophageal varices but has not been evaluated previously in the management of gastroesophageal varices. The aim of this work was evaluation of a new scleroligation technique for management of bleeding gastroesophageal varices regarding efficacy, adverse events, variceal recurrence, and survival. METHODS: This study was conducted on 120 cirrhotic patients with bleeding gastroesophageal varices, whom we divided randomly into 2 groups of 60 patients each-a band ligation group and a scleroligation group. RESULTS: The mean number of sessions was lower in the scleroligation group than in the band ligation group (2.22 ± 0.92 and 3.43 ± 0.67, respectively) (P < .001), as were the duration of treatment and total number of bands used. Cost and survival were comparable in the 2 groups. There was no significant difference between the 2 maneuvers regarding adverse events, recurrence rates, or rebleeding rates after obliteration. Recurrence was significantly higher in patients with larger varices, ulceration, and postprocedure pyrexia. Rebleeding was significantly higher among those who experienced postprocedure pyrexia and developed or had worsening of gastric antral vascular ectasia. CONCLUSIONS: Scleroligation appears to achieve a faster rate of eradication with fewer treatment sessions and total number of bands deployed to achieve variceal obliteration than band ligation and is comparable in cost and in adverse event and recurrence rates. (Clinical trial registration number: NCT02646202.).

Apoptotic and anti-apoptotic seromarkers for assessment of disease severity of non-alcoholic steatohepatitis.

BACKGROUND AND STUDY AIMS: This study aimed to find out non-invasive markers for the assessment of severity of non-alcoholic steatohepatitis (NASH) in an attempt to decrease the need for liver biopsy. It also aimed to evaluate the key role of apoptosis in the pathogenesis of the disease and the suggested role of anti-apoptotic factors in therapeutic modalities and disease prognosis. PATIENTS AND METHODS: The serum levels of soluble Fas (s. Fas), s. Fas ligand, cytokeratin 18 (CK-18) fragment and Bcl-2 were measured in 80 patients and 15 non-hepatic subjects as control. The patients were divided based on histological examination of liver biopsy into three groups. Group I included 40 patients with NASH, group II had 40 patients with non-alcoholic fatty liver disease (NAFLD) non-NASH and group III had 15 non-hepatic subjects as control. Apoptosis of hepatocytes was assessed by morphological examination using a light microscope and expressed as number per square millimetre. RESULTS: There was a significant increase in the serum levels of s. Fas, s. Fas ligand and CK-18 fragments in the NASH group. The anti-apoptotic protein Bcl-2 showed significantly low levels in NASH patients. Apoptosis of hepatocytes was significantly higher in the NASH group. The degree of apoptosis was inversely correlated with the level of Bcl-2. A significant correlation between both s. Fas and CK-18 fragment with liver histology with regard to lobular inflammation and ballooning was found. CONCLUSIONS: Increased serum levels of s. Fas and CK-18 fragment in the NASH group and its correlation with the severity of disease suggested the key role of apoptosis in NASH pathogenesis which can be used for the assessment of the severity of NASH. A high level of anti-apoptotic Bcl-2 in NAFLD suggests its protective role in disease progress.

The role of hepatic expression of STAT1, SOCS3 and PIAS1 in the response of chronic hepatitis C patients to therapy.

BACKGROUND: The underlying mechanisms of hepatitis C virus (HCV) resistance to treatment are unknown. Signal transducers and activators of transcription (STAT) proteins play a critical role in antiviral defense. OBJECTIVE: To explore some of the mechanisms of HCV resistance to interferon, the expression of STAT1 and its negative regulators, protein inhibitor of activated STAT (PIAS1) and suppressor of cytokine signalling (SOCS3), in liver tissues of both inteferon responders and nonresponders in chronic HCV patients. METHODS: Sixty patients were divided into the following groups: group 1a comprised 38 treatment-responder chronic HCV patients; group 1b consisted of 22 treatment-nonresponder chronic HCV patients; and group 2 consisted of six control subjects. Liver biopsies were examined for histological scoring; STAT1, SOCS3 and PIAS1 expression was analyzed using Western blotting methods. RESULTS: STAT1 expression in the liver tissue of patients in group 1 was significantly increased compared with group 2 patients (P=0.001), while no significant difference in expression was observed between group 1a and group 1b patients (P=0.747). However, phosphorylated STAT1 protein was expressed at a significantly higher level in liver tissue of patients in group 1a compared with patients in group 1b (P=0.001). Western blot analysis of PIAS1 and SOCS3 protein expression in liver tissues from groups 1 and 2 revealed significantly increased expression in group 1 compared with group 2 (P=0.001). In addition, PIAS1 and SOCS3 protein expression was significantly higher in the liver tissues of patients in group 1b compared with patients in group 1a. CONCLUSION: Levels of STAT1 and/or the protein expression of its negative regulators, PIAS1 and SOCS3, may be a good predictor of response to therapy. These could be used as biomarkers that are easily detected by Western blotting or immunostaining during standard histopathological liver biopsy analysis.