Variceal recurrence 4 years post endoscopic band ligation in hepatitis C patients who achieved sustained virological response with oral direct-acting antiviral therapy.

Oral Direct-acting antivirals (DAAs) are safe, highly effective altering disease burden and prognosis in hepatitis C patients. Sustained virologic response (SVR) is achieved nowadays in more than 90% of the treated patients and related to the improvements in functions of the liver, fibrosis plus survival. Furthermore, portal hypertension is thought to be improved with achievement of virological response, parallel to the improvements in hepatic inflammation and fibrosis. We aimed to assess the recurrence rate of oesophageal varices by long-term follow-up in patients treated with different DAAs regimens who had achieved SVR. We studied 176 Child A cirrhotic HCV patients who achieved SVR after DAAs treatment and had a history of endoscopic oesophageal varices obliteration and were on maximum tolerated propranolol dose. They were subjected to follow-up upper gastrointestinal endoscopy repeated every 6 months for 4 years. Fifty-two patients (29.5%) had recurrence of oesophageal varices observed during the 4-years follow-up upper GIT endoscopy. On multivariate analysis, platelet count was the only significant variable, P-value = .007*. HbA1C, HOMA IR, BMI 1 and BMI 2 showed non-significant differences between the studied groups. By ROC analysis, we identified baseline platelet count of 96 000/µL with 100% sensitivity (95% confidence interval [CI] [91%-100%]) and 74% specificity (95% CI [65%-81%]). Spearman correlation showed a positive correlation between AFP, age, AST, Bilirubin, creatinine, INR. Patients who achieved SVR post DAAs showed a significant decrease in oesophageal varices recurrence post endoscopic obliteration. Baseline platelet count was found to be a strong independent predictor for oesophageal varices recurrence.

Evaluation of circulating zonulin as a potential marker in the pathogenesis of nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disorders ranging from simple hepatic steatosis up to nonalcoholic steatohepatitis (NASH) evolving to cirrhosis and hepatocellular carcinoma (HCC). Liver biopsy is still the gold standard modality for diagnosing and staging NAFLD. The linkage between intestinal microbiota and NAFLD, might suggest a potential role of serum zonulin in NAFLD diagnosis. To appraise the role of circulating zonulin in NAFLD pathogenesis, 56 subjects with proved NAFLD by ultrasonography and liver biopsy, as well as 20 healthy controls were tested. Liver function tests, serum glucose, fasting insulin, C peptide, lipid profile, homeostasis model assessment of insulin resistance (HOMA-IR), IL-6, and circulating zonulin were performed to all subjects. Aspartate transaminase (AST), alanine transaminase (ALT), gamma-glutamyl transferase (GGT), triglycerides, HDL-c, fasting insulin, C peptide, HOMA-IR, IL-6, and serum zonulin were higher in NAFLD group than in controls (p < 0.05), and in NASH patients than those with simple steatosis (p < 0.05). Zonulin was positively correlated with body mass index (BMI), ALT, triglycerides, fasting insulin, HOMA-IR, liver histopathology, and serum IL-6 (p < 0.05), with inverse correlation to HDL-C (p < 0.05). At cut off 8.3 pc/mL, serum zonulin was found to be of diagnostic value of NASH occurrence with 100% sensitivity and specificity (AUR = 1.000, p-value = <0.001). The increasing zonulin levels in NAFLD patients with steep rise in NASH group denotes a possible role in pathogenesis of NAFLD occurrence and progression. This could open a new avenue of implicating zonulin antagonists as targeted therapies in NAFLD prevention.