Hepatopulmonary syndrome.
ABG, arterial blood gas
AT2, alveolar type II
AV, arteriovenous
CBDL, common bile duct ligation
ET-1, endothelin-1
ETB, endothelin receptor B
FEV1, forced expiratory volume in the first second
FVC, forced vital capacity
HPS, hepatopulmonary syndrome
IPVDs, intrapulmonary vascular dilatations
LT, liver transplantation
MELD exceptions
NO, nitric oxide
P(A-a)O2, alveolar-arterial oxygenation gradient
PDGF, platelet-derived growth factor
PIGF, placental growth factor
PVL, portal vein ligation
PaO2, partial pressure of arterial oxygen
SE, standard exception
SP, surfactant protein
SaO2, oxygen saturation
TAA, thio-acetamide
TNFα, tumour necrosis factor alpha
Tc-MAA, 99mTechnetium-labeled macroaggregated albumin
UNOS, United Network for Organ Sharing
V/Q, ventilation-perfusion
VCAM1, vascular cellular adhesion molecule 1
VEGF, vascular endothelial growth factor
cirrhosis
portal hypertension
vWF, von Willebrand factor
Journal
JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237
Informations de publication
Date de publication:
Sep 2022
Sep 2022
Historique:
received:
08
05
2022
revised:
10
06
2022
accepted:
15
06
2022
entrez:
29
8
2022
pubmed:
30
8
2022
medline:
30
8
2022
Statut:
epublish
Résumé
Hepatopulmonary syndrome (HPS) is a pulmonary vascular complication of liver disease, which adversely affects prognosis. The disease is characterised by intrapulmonary vascular dilatations and shunts, resulting in impaired gas exchange. A complex interaction between the liver, the gut and the lungs, predominately impacting pulmonary endothelial cells, immune cells and respiratory epithelial cells, is responsible for the development of typical pulmonary alterations seen in HPS. Liver transplantation is the only therapeutic option and generally reverses HPS. Since the implementation of the model for end-stage liver disease (MELD) standard exception policy, outcomes in patients with HPS have been significantly better than they were in the pre-MELD era. This review summarises current knowledge and highlights what's new regarding the diagnosis and management of HPS, and our understanding of pathogenesis based on experimental models and translational studies.
Identifiants
pubmed: 36035361
doi: 10.1016/j.jhepr.2022.100527
pii: S2589-5559(22)00099-4
pmc: PMC9403489
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
100527Informations de copyright
© 2022 The Authors.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details.
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