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עמוד בית
Thu, 21.11.24

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May 2016
Dan Meir Livovsky MD, Orit Pappo MD, Galina Skarzhinsky PhD, Asaf Peretz MD AGAF, Elliot Turvall MSc and Zvi Ackerman MD

Background: Recently we observed patients with chronic liver disease (CLD) or chronic reflux symptoms (CRS) who developed gastric polyps (GPs) while undergoing surveillance gastroscopies for the detection of either esophageal varices or Barrett's esophagus, respectively.

Objectives: To identify risk factors for GP growth and estimate the gastric polyp growth rate (GPGR).

Methods: GPGR was defined as the number of days since the first gastroscopy (without polyps) in the surveillance program, until the gastroscopy when a GP was discovered.

Results: Gastric polyp growth rates in CLD and CRS patients were similar. However, hyperplastic gastric polyps (HGPs) were detected more often (87.5% vs. 60.5%, P = 0.051) and at a higher number (2.57 ± 1.33 vs. 1.65 ± 0.93, P = 0.021) in the CLD patients. Subgroup analysis revealed the following findings only in CLD patients with HGPs: (i) a positive correlation between the GPGR and the patient's age; the older the patient, the longer the GPGR (r = 0.7, P = 0.004). (ii) A negative correlation between the patient's age and the Ki-67 proliferation index value; the older the patient, the lower the Ki-67 value (r = -0.64, P = 0.02). No correlation was detected between Ki-67 values of HGPs in CLD patients and the presence of portal hypertension, infection with Helicobacter pylori, or proton pump inhibitor use.

Conclusions: In comparison with CRS patients, CLD patients developed HGPs more often and at a greater number. Young CLD patients may have a tendency to develop HGPs at a faster rate than elderly CLD patients.

February 2013
E. Ashkenazi, Y. Kovalev and E. Zuckerman
 Portal hypertension is the leading cause of morbidity and mortality in liver cirrhosis. Complications of portal hypertension in cirrhotic patients include esophageal and gastric varices, portal hypertensive gastropathy, ascites, hepatorenal syndrome, hepatopulmonary syndrome and portopulmonary hypertension. The hepatic venous pressure gradient should be at least 10 mmHg for esophageal varices to appear, and more than 12 mmHg for acute esophageal variceal bleeding. This article reviews the pathophysiology responsible for portal hypertension and its complications, and the treatments used for esophageal varices in the setting of primary and secondary prophylaxis and during active bleeding.

 

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