Review article: a multidisciplinary approach to the diagnosis and management of Budd-Chiari syndrome.


Journal

Alimentary pharmacology & therapeutics
ISSN: 1365-2036
Titre abrégé: Aliment Pharmacol Ther
Pays: England
ID NLM: 8707234

Informations de publication

Date de publication:
04 2019
Historique:
received: 17 10 2018
revised: 06 11 2019
accepted: 29 12 2018
pubmed: 5 3 2019
medline: 24 3 2020
entrez: 5 3 2019
Statut: ppublish

Résumé

Budd-Chiari syndrome (BCS) is a rare but fatal disease caused by obstruction in the hepatic venous outflow tract. To provide an update of the pathophysiology, aetiology, diagnosis, management and follow-up of BCS. Analysis of recent literature by using Medline, PubMed and EMBASE databases. Primary BCS is usually caused by thrombosis and is further classified into "classical BCS" type where obstruction occurs within the hepatic vein and "hepatic vena cava BCS" which involves thrombosis of the intra/suprahepatic portion of the inferior vena cava (IVC). BCS patients often have a combination of prothrombotic risk factors. Aetiology and presentation differ between Western and certain Asian countries. Myeloproliferative neoplasms are present in 35%-50% of European patients and are usually associated with the JAK2-V617F mutation. Clinical presentation is diverse and BCS should be excluded in any patient with acute or chronic liver disease. Non-invasive imaging (Doppler ultrasound, computed tomography, or magnetic resonance imaging) usually provides the diagnosis. Liver biopsy should be obtained if small vessel BCS is suspected. Stepwise management strategy includes anticoagulation, treatment of identified prothrombotic risk factors, percutaneous revascularisation and transjugular intrahepatic portosystemic stent shunt to re-establish hepatic venous drainage, and liver transplantation in unresponsive patients. This strategy provides a 5-year survival rate of nearly 90%. Long-term outcome is influenced by any underlying haematological condition and development of hepatocellular carcinoma. With the advent of newer treatment strategies and improved understanding of BCS, outcomes in this rare disease have improved over the last three decades. An underlying haematological disorder can be the major determinant of outcome.

Sections du résumé

BACKGROUND
Budd-Chiari syndrome (BCS) is a rare but fatal disease caused by obstruction in the hepatic venous outflow tract.
AIM
To provide an update of the pathophysiology, aetiology, diagnosis, management and follow-up of BCS.
METHODS
Analysis of recent literature by using Medline, PubMed and EMBASE databases.
RESULTS
Primary BCS is usually caused by thrombosis and is further classified into "classical BCS" type where obstruction occurs within the hepatic vein and "hepatic vena cava BCS" which involves thrombosis of the intra/suprahepatic portion of the inferior vena cava (IVC). BCS patients often have a combination of prothrombotic risk factors. Aetiology and presentation differ between Western and certain Asian countries. Myeloproliferative neoplasms are present in 35%-50% of European patients and are usually associated with the JAK2-V617F mutation. Clinical presentation is diverse and BCS should be excluded in any patient with acute or chronic liver disease. Non-invasive imaging (Doppler ultrasound, computed tomography, or magnetic resonance imaging) usually provides the diagnosis. Liver biopsy should be obtained if small vessel BCS is suspected. Stepwise management strategy includes anticoagulation, treatment of identified prothrombotic risk factors, percutaneous revascularisation and transjugular intrahepatic portosystemic stent shunt to re-establish hepatic venous drainage, and liver transplantation in unresponsive patients. This strategy provides a 5-year survival rate of nearly 90%. Long-term outcome is influenced by any underlying haematological condition and development of hepatocellular carcinoma.
CONCLUSIONS
With the advent of newer treatment strategies and improved understanding of BCS, outcomes in this rare disease have improved over the last three decades. An underlying haematological disorder can be the major determinant of outcome.

Identifiants

pubmed: 30828850
doi: 10.1111/apt.15149
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

840-863

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Auteurs

Faisal Khan (F)

Liver Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Matthew J Armstrong (MJ)

Liver Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS Foundation Trust and University of Birmingham, Birmingham, UK.
Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.

Homoyon Mehrzad (H)

Imaging and Interventional Radiology Department, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Frederick Chen (F)

NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS Foundation Trust and University of Birmingham, Birmingham, UK.
Department of Clinical Haematology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Desley Neil (D)

Department of Cellular Pathology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Rachel Brown (R)

Department of Cellular Pathology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Owen Cain (O)

Department of Cellular Pathology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Dhiraj Tripathi (D)

Liver Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS Foundation Trust and University of Birmingham, Birmingham, UK.
Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.

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