Evidence for an Association Between Intrahepatic Vascular Changes and the Development of Hepatopulmonary Syndrome.


Journal

Chest
ISSN: 1931-3543
Titre abrégé: Chest
Pays: United States
ID NLM: 0231335

Informations de publication

Date de publication:
01 2019
Historique:
received: 13 05 2018
revised: 21 08 2018
accepted: 05 09 2018
pubmed: 8 10 2018
medline: 12 10 2019
entrez: 8 10 2018
Statut: ppublish

Résumé

Hepatopulmonary syndrome (HPS) is characterized by an arterial oxygenation defect, defined by an increased alveolar-arterial oxygen gradient, induced by pulmonary vascular dilatations in the context of liver disease. The pathogenesis of HPS is poorly understood. Morphologic changes associated with HPS are unknown. This study aimed at describing imaging and pathology changes associated with HPS. We performed a case-control study in candidates for transplant with suspicion of cirrhosis. Each patient with HPS (Pao CT scans and Doppler ultrasounds from 21 patients with HPS were compared with those from 63 control subjects. HPS was associated with a two- to threefold higher prevalence of obstructed intrahepatic portal branches, of slowed or hepatofugal portal blood flow, and of large abdominal portosystemic shunts. Hepatic artery diameter was also larger in patients with HPS. Explanted livers from 19 patients with HPS were compared with those from 57 control subjects. HPS was associated with a fourfold higher prevalence of portal venule thrombosis and a ninefold higher prevalence of extensive vascular proliferation within fibrous septa. Obstruction of centrilobular venules, sinusoidal dilatation, and liver parenchymal extinction were also more common in patients with HPS. HPS is associated with intrahepatic vascular changes and with features suggesting severe portal hypertension. These results raise the hypothesis that intrahepatic vascular changes precipitate the development of HPS, opening new therapeutic perspectives for HPS.

Sections du résumé

BACKGROUND
Hepatopulmonary syndrome (HPS) is characterized by an arterial oxygenation defect, defined by an increased alveolar-arterial oxygen gradient, induced by pulmonary vascular dilatations in the context of liver disease. The pathogenesis of HPS is poorly understood. Morphologic changes associated with HPS are unknown. This study aimed at describing imaging and pathology changes associated with HPS.
METHODS
We performed a case-control study in candidates for transplant with suspicion of cirrhosis. Each patient with HPS (Pao
RESULTS
CT scans and Doppler ultrasounds from 21 patients with HPS were compared with those from 63 control subjects. HPS was associated with a two- to threefold higher prevalence of obstructed intrahepatic portal branches, of slowed or hepatofugal portal blood flow, and of large abdominal portosystemic shunts. Hepatic artery diameter was also larger in patients with HPS. Explanted livers from 19 patients with HPS were compared with those from 57 control subjects. HPS was associated with a fourfold higher prevalence of portal venule thrombosis and a ninefold higher prevalence of extensive vascular proliferation within fibrous septa. Obstruction of centrilobular venules, sinusoidal dilatation, and liver parenchymal extinction were also more common in patients with HPS.
CONCLUSIONS
HPS is associated with intrahepatic vascular changes and with features suggesting severe portal hypertension. These results raise the hypothesis that intrahepatic vascular changes precipitate the development of HPS, opening new therapeutic perspectives for HPS.

Identifiants

pubmed: 30292761
pii: S0012-3692(18)32500-5
doi: 10.1016/j.chest.2018.09.017
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

123-136

Informations de copyright

Copyright © 2018 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Auteurs

Clément Lejealle (C)

Service d'Hépatologie, DHU Unity, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France.

Valérie Paradis (V)

Service d'Anatomie Pathologique, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France.

Onorina Bruno (O)

Service d'Imagerie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France.

Emmanuelle de Raucourt (E)

Service d'Hématologie-Biologique, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France.

Claire Francoz (C)

Service d'Hépatologie, DHU Unity, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France.

Olivier Soubrane (O)

Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France; Service de Chirurgie Hépato-biliaire et Transplantation Hépatique, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France.

Didier Lebrec (D)

Service d'Hépatologie, DHU Unity, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France.

Pierre Bedossa (P)

Service d'Anatomie Pathologique, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France.

Dominique Valla (D)

Service d'Hépatologie, DHU Unity, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France.

Hervé Mal (H)

Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France; Service de Pneumologie B et Transplantation Pulmonaire, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France.

Valérie Vilgrain (V)

Service d'Imagerie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France.

François Durand (F)

Service d'Hépatologie, DHU Unity, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; INSERM, UMR-1149, Centre de Recherche sur l'Inflammation, Paris-Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France.

Pierre-Emmanuel Rautou (PE)

Service d'Hépatologie, DHU Unity, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France; Université Denis Diderot-Paris 7, Sorbonne Paris Cité, 75018 Paris, France; INSERM, UMR-970, Paris Cardiovascular Research Center-PARCC, Paris, France. University, Boston, MA. Electronic address: pierre-emmanuel.rautou@inserm.fr.

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