Fasting Serum Gastrin Level in Patients with Portal Hypertensive Gastropathy

Abstract

P ortal hypertension is defined as the pathological elevation in portal venous pressure, in which the pressure in the portal venous system is at least 5 mm Hg higher than the pressure in the inferior vena cava. Portal hypertension becomes clinically significant when the portal venous pressure gradient exceeds a threshold value of 10 mmHg. Portal hypertension may result into many vascular decompensation complications which may be serious such as variceal bleeding and clinical decompensation such as hepatic encephalopathy (HE) and ascites. Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in patients with portal hypertension. These changes in the mucosa include friability of the mucosa and the presence of ecstatic blood vessels at the surface. Patients with portal hypertensive gastropathy may experience bleeding from the stomach, which may uncommonly manifest itself in vomiting blood or melena. The mechanisms involved in the pathogenesis of PHG have not been fully elucidated. However, regulation of gastric nitric oxide, prostaglandins, tumor necrosis factor α (TNF-α), and epidermal growth factor (EGF) production may be involved.