AIM: In non-alcoholic steatohepatitis (NASH), fibrosis begins around the central veins, as also happens with alcoholic liver disease, so the symptoms of portal hypertension may be due to central vein occlusion. The aim of this study was to define the prevalence of esophagogastric varices and the clinical outcome after endoscopic treatment in NASH patients with severe fibrosis. METHODS: The subjects were 72 patients with clinicopathologically confirmed NASH who had bridging fibrosis (F3) or cirrhosis (F4) determined by the examination of liver biopsy specimens, and who underwent upper gastrointestinal endoscopy. The prevalence and pattern of endoscopically detected varices at the time of liver biopsy were evaluated. The results of NASH patients (n = 11) with endoscopically treated esophageal varices were compared to those with alcoholic (n = 67) and hepatitis C virus-associated cirrhosis (n = 152). RESULTS: Esophagogastric varices were detected in 34 out of the 72 (47.2%) patients; esophageal varices in 25 (34.7%) and gastric varices in nine (12.5%), while six of these patients had variceal bleeding. In NASH patients, the cumulative recurrence-free probability at 24 months after endoscopic treatment was 63.6%, the bleeding-free probability was 90.9%, and the 5-year survival was 100%. Only one out 11 patients died of liver failure at 70 months after treatment. CONCLUSION: About half of NASH patients with severe fibrosis had esophagogastric varices. The clinical status and course of the varices do not necessarily improve after endoscopic treatment. NASH patients with esophagogastric varices need to be followed up carefully, like patients with other chronic liver diseases.
AIM: In non-alcoholic steatohepatitis (NASH), fibrosis begins around the central veins, as also happens with alcoholic liver disease, so the symptoms of portal hypertension may be due to central vein occlusion. The aim of this study was to define the prevalence of esophagogastric varices and the clinical outcome after endoscopic treatment in NASH patients with severe fibrosis. METHODS: The subjects were 72 patients with clinicopathologically confirmed NASH who had bridging fibrosis (F3) or cirrhosis (F4) determined by the examination of liver biopsy specimens, and who underwent upper gastrointestinal endoscopy. The prevalence and pattern of endoscopically detected varices at the time of liver biopsy were evaluated. The results of NASH patients (n = 11) with endoscopically treated esophageal varices were compared to those with alcoholic (n = 67) and hepatitis C virus-associated cirrhosis (n = 152). RESULTS: Esophagogastric varices were detected in 34 out of the 72 (47.2%) patients; esophageal varices in 25 (34.7%) and gastric varices in nine (12.5%), while six of these patients had variceal bleeding. In NASH patients, the cumulative recurrence-free probability at 24 months after endoscopic treatment was 63.6%, the bleeding-free probability was 90.9%, and the 5-year survival was 100%. Only one out 11 patients died of liver failure at 70 months after treatment. CONCLUSION: About half of NASH patients with severe fibrosis had esophagogastric varices. The clinical status and course of the varices do not necessarily improve after endoscopic treatment. NASH patients with esophagogastric varices need to be followed up carefully, like patients with other chronic liver diseases.