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'Nipped in the Budd': hepatic venous outflow obstruction in evolution
Haris Karageorgiou1, Rajeshwar P Mookerjee, Neill R Patani
1Gastroenterology & Hepatology Unit, Department of Gastroenterology, University College London Hospitals, London, UK.
European Journal of Gastroenterology & Hepatology
|January 14, 2005
Summary
Budd-Chiari syndrome (BCS) can develop from inflammation and thrombocytosis in individuals with genetic and lifestyle risk factors. This case shows complete thrombus regression with anticoagulation, questioning long-term treatment necessity.
Area of Science:
- Hepatology
- Vascular Medicine
- Thrombosis Research
Background:
- Budd-Chiari syndrome (BCS) is a rare hepatic venous thrombosis with high morbidity and mortality.
- Predisposing factors include genetic mutations (e.g., MTHFR C677T), oral contraceptive use, and inflammatory conditions.
- Inflammatory foci, such as perforated duodenal ulcers, can precipitate BCS in susceptible individuals.
Observation:
- A 39-year-old woman with a perforated duodenal ulcer developed asymptomatic BCS during hospitalization.
- She possessed multiple pro-thrombotic risk factors: oral contraceptive use and homozygous MTHFR C677T mutation leading to hyperhomocysteinemia.
- Laparoscopic surgery further increased thrombotic risk, leading to inferior vena cava thrombus and hepatic infarction.
Findings:
- The patient experienced complete radiological regression of the hepatic thrombus and parenchymal changes.
- Resolution occurred after the inflammatory focus resolved and platelet count normalized.
- Oral anticoagulation was the sole treatment, as systemic thrombolysis was declined.
Implications:
- This case demonstrates the potential for spontaneous resolution of evolving BCS under specific conditions.
- It raises questions about the optimal duration of oral anticoagulation for BCS.
- A conservative management approach may be viable for some evolving BCS cases, warranting further investigation.