PTH-008 Portal hypertensive gastropathy in the non cirrhotic patient: are we investigating this endoscopic finding adequately?

Abstract

<h3>Introduction</h3> Portal hypertensive gastropathy (PHG) is characterised by an endoscopic gastric mucosal appearance of a mosaic or snake skin like pattern with or without cherry red spots. It occurs in up to 65% of patients with liver cirrhosis and portal hypertension.¹However, PHG can also occur in patients without cirrhosis. It can be associated with non cirrhotic portal hypertension, extrahepatic portal vein obstruction, Budd Chiari syndrome and Helicobacter pylori (H Pylori). The severity of portal hypertension has been linked to the severity of cirrhosis (being more common in Childs Pugh C patients) and the presence of H pylori. The aim of this study was to evaluate the investigation of patients with PHG noted on endoscopy in the absence of known liver cirrhosis. <h3>Method</h3> A database of all patients with the endoscopic finding of PHG, noted on gastroscopies performed between October 2012 and January 2014, in a large district general hospital in North London was obtained. The patients were identified using the Unisoft Endoscopy Reporting software and data on patient demographics, diagnosis and investigations obtained from electronic patient records. A retrospective analysis of information on the patients’ diagnosis, endoscopic findings and further investigations organised including radiology and H pylori testing was performed. <h3>Results</h3> 113 patients were noted to have PHG on endoscopy during the study period. 23/113 (20.4%) did not have a diagnosis of chronic liver disease or cirrhosis. 17/23 (73.9%) patients had either a CT scan or ultrasound abdomen with portal and hepatic vein dopplers as part of their workup following the incidental finding of PHG on endoscopy. 10/23 (43.5%) patients underwent testing for H pylori (either urease test or faecal antigen) and 2 were found to be positive. Only 6 patients ultimately were diagnosed with clinically relevant pathology that would account for PHG; 2 had non cirrhotic portal hypertension, 2 had a liver abscess with portal vein thrombosis and 2 had H pylori related gastritis. The aetiology of PHG remained unclear in the remainder of the 17 patients. <h3>Conclusion</h3> A fifth of patients with PHG noted on endoscopy did not have liver cirrhosis. Just over 25% of patients in this group did not undergo further investigations to elucidate the cause of PHG. In our study, only 43% of patients with PHG in the absence of liver cirrhosis were tested for H pylori. Given that H pylori is a recognised association with PHG, we would recommend that all patients with PHG be tested for this easily treatable condition prior to undergoing further investigations to elucidate the cause of PHG. <h3>Disclosure of interest</h3> None Declared. <h3>Reference</h3> Burak KW, Lee SS (2001) Portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) syndrome. Gut 49:866–872