Budd-Chiari syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Pathogenesis

• Occlusion of at least two hepatic veins leads to Budd-Chiari syndrome. Single hepatic vein occlusion is usually silent.
• Obstruction in the venous drainage from liver results in venous congestion causing hepatomegaly.Patients develop postsinusoidal portal hypertension.
• Stasis of blood and congestion cause hypoxic damage of hepatocytes, affecting the liver function.This can result in centrilobular fibrosis, nodular regenerative hyperplasia and ultimately cirrhosis.
• Hepatocellular necrosis results from increased sinusoidal pressure.
• Budd-Chiari is commonly associated with atrophy of peripheral regions and enlargement of the caudate lobe because blood is directly shunted through it into the inferior vena cava.

Genetics

• Genes associated with increased expression in the pathogenesis of Budd-Chiari syndrome include:
  • Matrix metalloproteinase 7
  • Superior cervical ganglion 10 (SCG10)
  • Proliferating cell nuclear antigen gene
  • C-MYC oncogene
  • Tumor protein p53 gene
• Thrombospondin-1 gene expression is decreased in Budd-Chiari syndrome.