Portal hypertension (PH) has many complications, some life-threatening. Historically, esophageal (EV) and gastric varices (GV), portal hypertensive gastropathy (PHG), and ascites were associated with PH [1]. Until just over a decade ago, the endoscopic examination of the small intestine was limited by its length. At the dawn of the millennium, deep enteroscopy (wireless or device-assisted) has been advanced by the advent of double-balloon technique and wireless capsule endoscopy (CE) [2, 3]. Since then, deep enteroscopy has identified portal hypertensive enteropathy (PHE) as a potentially significant complication of PH [4]. Due to its inherent advantages, CE has the latter has become the preferred method for PHE detection, particularly in the West [2]. Patients with advanced liver disease run an increased risk of gastrointestinal (GI) bleeding. In cirrhotic patients with chronic GI blood loss, with no obvious bleeding source visualized with bidirectional digestive endoscopy, PHE should be considered [5]. Nevertheless, whether it is necessary to routinely perform pan-enteroscopy in patients with PH with no evidence of obscure gastrointestinal bleeding (OGIB) is still a matter of continuing clinical research [6]. Documentation of PHE with small bowel CE is becoming more frequent [4, 5]. A consensus has emerged with regard to the type and distribution of small intestine mucosal abnormalities that constitute PHE [4, 5, 7]. The characteristic lesions of PHE include red spots indicative of arteriovenous malformations, patchy mucosal erythema, diffuse mucosal edema (so-called ‘herring-roe’ appearance), varices, and spontaneous mucosal bleeding [8, 9]. However, the prevalence of PHE ranges between 20 and 90 % [4, 5]. Furthermore, only a few studies have considered other clinical factors associated with the presence of PHE with conflicting results. In 2005, De Palma et al. were one of the first groups to use CE to study the type and prevalence of PH-related small intestinal lesions in a group of patients with liver cirrhosis of different etiologies, complicated by PH and anemia. In comparison with a control population diagnosed with irritable bowel syndrome, they essentially redefined PHE in the era of CE, reporting that large esophageal varices, PHG, portal hypertensive colopathy (PHC), and severe liver disease (Child–Pugh class C) are associated with the presence of PHE [7]. Conversely, the etiology of liver cirrhosis, patient gender, and history of EV hemorrhage were not associated with the presence of PHE. More recently, another landmark study by Abdelaal et al. [10] reported that CE findings consistent with PHE were present in 67.7 % of patients with liver cirrhosis. They were more common in patients with high liver stiffness as measured by FibroScan, higher Child–Pugh score, large EVs, PHG, and a history of endoscopic EV sclerotherapy or band ligation. Furthermore, they refined the currently used classification of PHE CE findings into four main types: (1) red spots; (2) angiectasia; (3) small intestinal varices; and (4) inflammatory-like lesions [4, 8–10]. More importantly, however, Abdelaal et al. introduced the concept of combining auxiliary data such as transient elastography with more conventional clinical data in an attempt to select a patient population in risk for PHE. Takahashi et al. [11] reported that in CE, mucosal edema, unlike red spots and angiectasia, correlated well with the hepatic venous pressure gradient (HVPG). The latter had no significant K. J. Dabos ! A. Koulaouzidis (&) Endoscopy Unit, Centre for Liver and Digestive Disorders, The Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh, UK e-mail: akoulaouzidis@hotmail.com
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