Exacerbation of Portal Hypertensive Enteropathy after Endoscopic Injection Sclerotherapy for Esophageal Varices.


Journal

Digestion
ISSN: 1421-9867
Titre abrégé: Digestion
Pays: Switzerland
ID NLM: 0150472

Informations de publication

Date de publication:
2021
Historique:
received: 18 06 2019
accepted: 02 09 2019
pubmed: 2 10 2019
medline: 19 8 2021
entrez: 2 10 2019
Statut: ppublish

Résumé

Portal hypertensive enteropathy (PHE) is a well-known small-bowel lesion that occurs with liver cirrhosis (LC) and is associated with increased hepatic venous pressure. However, it is unclear how esophageal varices (EV) treatment actually affects PHE. We aimed to analyze the effects of EV treatment on PHE. Among LC patients who underwent capsule endoscopy (CE) more than twice to confirm PHE at our hospital from February 2009 to September 2018, we targeted those with no change in the Child-Pugh classification after EV treatment for the prevention of bleeding. Patients were assigned to groups based on the EV treatment method (endoscopic injection sclerotherapy [EIS] group or endoscopic variceal ligation [EVL] group). We analyzed the PHE findings before and after treatment, and we investigated changes in the collateral vein using computed tomography imaging. We analyzed 42 LC patients (27 men; mean age, 65.3 years); 20 were in the EIS group and 22 were in the EVL group. Exacerbation of PHE was significantly prevalent in the EIS group (90%) compared to that in the EVL group (50%). CE of PHE showed significantly prevalent exacerbation of villous edema in the EIS group (65%) compared to that in the EVL group (23%). Stenosis or disappearance of the feeding vessel (55%) and exacerbation of the hepatofugal collateral vein (35%) were significantly prevalent in the EIS group. EIS exacerbates PHE, especially villous edema, in LC patients with changes in collateral circulation.

Identifiants

pubmed: 31574519
pii: 000503060
doi: 10.1159/000503060
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

188-196

Informations de copyright

© 2019 S. Karger AG, Basel.

Auteurs

Ichiro Otani (I)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Shiro Oka (S)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan, oka4683@hiroshima-u.ac.jp.

Hiroshi Aikata (H)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Sumio Iio (S)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Akiyoshi Tsuboi (A)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Sayoko Kunihara (S)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Yuko Nagaoki (Y)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Shinji Tanaka (S)

Department of Endoscopy, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

Kazuaki Chayama (K)

Department of Gastroenterology and Metabolism, Hiroshima University Hospital, Minami-ku, Hiroshima, Japan.

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