A 59-year-old man with history of nonalcoholic steatohepatitis (NASH) cirrhosis and portal hypertension with previous esophageal variceal ligation presented with 2 days of melena and fatigue. He was taking 20 mg of propranolol 3 times per day. Hemoglobin was 7 g/dL and platelets were 59,000/L. Esophagogogastroduodenostomy (EGD) performed 1 year earlier revealed large distal esophageal varices requiring ligation with 5 bands and gastritis located in the antrum. EGD during this admission revealed small distal esophageal varices, as well as 3 large polyps and many small polyps in the distal body and antrum (Figures 1 and 2). The large polyps were resected via hot snare polypectomy (Figure 3). Two hemoclips were applied to 1 polypectomy site and argon plasma coagulation ablation was performed for the base of the largest polyp. Histopathologic examination of the polyps revealed hyperplastic-like gastric polyps with marked foveolar hyperplasia with cystic dilations, edematous and fibrotic stroma, a prominent capillary proliferation in the lamina propria, and scattered telangiectactic vessels, consistent with portal hypertensive polyposis (PHP).
Figure 1
Endoscopic view of multiple, large portal hypertensive polyps in the antrum.
Figure 2
Endoscopic view of two large portal hypertensive polyps in the antrum.
Figure 3
View of the antrum following hot snare removal of the largest polyps.
Endoscopic view of multiple, large portal hypertensive polyps in the antrum.Endoscopic view of two large portal hypertensive polyps in the antrum.View of the antrum following hot snare removal of the largest polyps.PHP is a rare entity documented in patients with history of cirrhosis and portal hypertension.[1] The histopathological examination of portal hypertensive polyps reveals mucosal hyperplasia and vascular proliferation with significantly higher vessel diameter of >50 μm and increased vascular density as compared to non-portal hypertensive polyps.[2] Of note, our patient did not have the finding of PHP prior to esophageal variceal ligation. It is possible that altered hemodynamics in the portal pressure gradient following esophageal variceal ligation may have contributed to the formation of PHP. Previous studies have documented more frequent development and worsening of portal hypertensive gastropathy in patients following esophageal variceal ligation.[3]
Disclosures
Author contributions: K. Kolkhorst wrote the manuscript and is the article guarantor. P. Kulkarni revised the manuscript.Financial disclosure: None to report.Informed consent was obtained for this case report.
Authors: Susanne W Carmack; Robert M Genta; Christopher M Schuler; M Hossein Saboorian Journal: Am J Gastroenterol Date: 2009-04-28 Impact factor: 10.864