S1913 Portal Hypertensive Enteropathy Before and After Variceal Obliteration: An Endoscopic, Histopathologic and Immunohistochemical Study

Khayat, H.R. El; Khattib, Ahmed A. El; Nosseir, M. H.; Fouad, Yasser; Abouelezz, Mohamed; Amin, Hussein El

doi:10.1016/s0016-5085(10)63759-6

Cited by 11 publications

(11 citation statements)

References 18 publications

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“…Interestingly, in a study of PHE before and after EVs obliteration, the authors found that PHE increased significantly from 6.6% before obliteration to 46.7% after variceal obliteration [ 32 ]. This is similar to the results of another study [ 33 ] in which the authors found higher vascular endothelial growth factor (VEGF) tissue expression in the small bowel biopsies after variceal obliteration.…”

Section: Risk Factors Associated With Phementioning

confidence: 99%

Capsule Endoscopy for Portal Hypertensive Enteropathy

Jeon

Kim

2016

Gastroenterology Research and Practice

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Portal hypertensive enteropathy (PHE) is a mucosal abnormality of the small bowel that is observed in patients with portal hypertension (PH) and can lead to gastrointestinal bleeding and anemia. The pathogenesis is still not completely understood. The introduction of new endoscopic methods, including capsule endoscopy (CE) or balloon-assisted enteroscopy, has increased the detection of these abnormalities. CE can also serve as a road map for deciding subsequent interventions and evaluating the treatment effect. The prevalence of PHE is reportedly 40–70% in patients with PH. Endoscopic findings can be roughly divided into vascular and nonvascular lesions such as inflammatory-like lesions. Traditionally, PHE-associated factors include large esophageal varices, portal hypertensive gastropathy or colopathy, Child-Turcotte-Pugh class B or C, a history of variceal treatment, and acute gastrointestinal bleeding. More recently, on using scoring systems, a high computed tomography or transient elastography score was reportedly PHE-related factors. However, the prevalence of PHE and its related associated factors remain controversial. The management of PHE has not yet been standardized. It should be individualized according to each patient's situation, the availability of therapy, and each institutional expertise.

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Section: Risk Factors Associated With Phementioning

confidence: 99%

Capsule Endoscopy for Portal Hypertensive Enteropathy

Jeon

Kim

2016

Gastroenterology Research and Practice

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“…But a 2010 work from Egypt represents the most detailed and specifically designed prospective study that examined this puzzling question [19]. The results were in the affirmative as the paper showed that PHE changes (PHD included) increased in frequency and severity after esophageal variceal obliteration.…”

Section: Discussionmentioning

confidence: 95%

Portal Hypertensive Duodenopathy Manifesting as “Kissing” Duodenal Ulcers in a Nigerian with Alcoholic Cirrhosis: A Case Report and Brief Review of the Literature

Oluyemi¹,

Amole²

2012

Case Reports in Medicine

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Multiple duodenal ulcers are an uncommon finding in portal hypertensive duodenopathy (PHD). They represent a potential source of clinically significant bleeding from the upper gastrointestinal system in patients with cirrhosis. As this particular ulcer entity in relation to PHD has no distinguishing symptoms aside from those relating to the consequent bleeding, most of them are found either on routine endoscopic screening for cirrhotics or on endoscopic examination for cause(s) of bleeding in this patient population. The case documented below highlights many of the aspects of pathogenesis, associations, and consequences of this unique endoscopic finding in cirrhotic patients.

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“…The association of PHD in patients with prior variceal band ligation is very significant, and this relationship is well documented [ 2 , 11 ]. One such study showed an increase in the number of patients with PHD from 6.6% to 46.7% after variceal band ligation (p < 0.001) [ 12 ]. This study linked the development of PHD with an increase in VEGF expression in gastric and intestinal cells after variceal obliteration [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…One such study showed an increase in the number of patients with PHD from 6.6% to 46.7% after variceal band ligation (p < 0.001) [ 12 ]. This study linked the development of PHD with an increase in VEGF expression in gastric and intestinal cells after variceal obliteration [ 12 ]. Our patient had other evidence of portal hypertension prior to development of PHD, but the history of prior endoscopic band ligation was significant in his development of PHD.…”

Section: Discussionmentioning

confidence: 99%

Gastrointestinal Bleeding Secondary to Portal Hypertensive Duodenopathy in a Patient with Decompensated Liver Cirrhosis

Krishna

Igbinedion

Diaz

et al. 2018

Case Reports in Gastrointestinal Medicine

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With alcoholic cirrhosis and nonalcoholic fatty liver disease continuously on the rise in the United States, there is also a corresponding rise in portal hypertension. Portal hypertensive duodenopathy (PHD) is a complication of portal hypertension not commonly seen in cirrhotic patients. We present a case of a 46-year-old man who presented with decompensated liver cirrhosis secondary to gastrointestinal bleed. The patient underwent esophagogastroduodenoscopy (EGD) with findings indicative of PHD. Patient subsequently underwent transjugular intrahepatic portosystemic shunt (TIPS) with resolution of gastrointestinal bleed. We highlight TIPS as a management strategy in patients with PHD for whom less invasive measures are not effective.

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S1913 Portal Hypertensive Enteropathy Before and After Variceal Obliteration: An Endoscopic, Histopathologic and Immunohistochemical Study

Cited by 11 publications

References 18 publications

Capsule Endoscopy for Portal Hypertensive Enteropathy

Capsule Endoscopy for Portal Hypertensive Enteropathy

Portal Hypertensive Duodenopathy Manifesting as “Kissing” Duodenal Ulcers in a Nigerian with Alcoholic Cirrhosis: A Case Report and Brief Review of the Literature

Gastrointestinal Bleeding Secondary to Portal Hypertensive Duodenopathy in a Patient with Decompensated Liver Cirrhosis

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