IntroductionFor patients with liver cirrhosis (LC), increased intrahepatic vascular resistance and blood flow of the portal venous system cause portal hypertension. Jonas et al. reported that portal hypertension alters the gastrointestinal tract mucosa and increases susceptibility to injury. Impaired oxygenation of the mucosa is the probable mechanism for this increased susceptibility; decreased hemoglobin oxygen saturation has been documented in the duodenal mucosa of patients with LC. The GI tract of patients with LC is subject to various pathological lesions. Mucosal edema, erythema, angioectasia, and varices have been detected mainly in the stomach and colon of these patients.Recently, capsule endoscopy (CE) has improved the detectability of small‐bowel lesions and has become the gold standard non‐invasive technique. With the spread of CE, portal hypertension in the small bowel has been reported. Portal hypertensive enteropathy (PHE) is defined as inflammatory‐like lesions (edematous, erythematous, granular, and friable lesions) and/or vascular lesions (cherry red spots, telangiectasias, or angiodysplasia‐like lesions and varices). Akyuz et al. reported that PHE was found in 90.5% of patients with portal hypertension. We also reported that PHE was detected by CE in 67% of patients with LC.However, the clinical significance of PHE is unclear, and factors reported to be associated
Journal of Gastroenterology and Hepatology – Wiley
Published: Jan 1, 2018
Keywords: ; ; ;
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