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A Triple Hit Mechanism in Budd–Chiari Syndrome: Hormonal, Metabolic, and Vascular Synergy

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Budd–Chiari syndrome is a rare hepatic vascular disorder caused by obstruction of hepatic venous outflow, most often related to an underlying prothrombotic condition. We report the case of a 31-year-old woman with no significant past medical history who presented with 20 days of epigastric pain and asthenia. Clinical examination revealed hepatomegaly associated with ascites. Laboratory tests showed mild hepatic cytolysis, cholestasis, and early hepatic insufficiency. Abdominal CT angiography confirmed Budd–Chiari syndrome with hepatic venous outflow obstruction, hepatic dysmorphy, moderate ascites, and stenosis of the retrohepatic inferior vena cava. Etiological work-up revealed recent reintroduction of estrogen-containing oral contraceptives, elevated homocysteine levels associated with heterozygous MTHFR mutation, and no other major thrombophilic disorder. The patient was treated with oral anticoagulation with favorable clinical evolution. This case highlights the multifactorial nature of Budd–Chiari syndrome and the synergistic interaction between hormonal exposure, metabolic abnormalities, and anatomical venous obstruction.
Title: A Triple Hit Mechanism in Budd–Chiari Syndrome: Hormonal, Metabolic, and Vascular Synergy
Description:
Budd–Chiari syndrome is a rare hepatic vascular disorder caused by obstruction of hepatic venous outflow, most often related to an underlying prothrombotic condition.
We report the case of a 31-year-old woman with no significant past medical history who presented with 20 days of epigastric pain and asthenia.
Clinical examination revealed hepatomegaly associated with ascites.
Laboratory tests showed mild hepatic cytolysis, cholestasis, and early hepatic insufficiency.
Abdominal CT angiography confirmed Budd–Chiari syndrome with hepatic venous outflow obstruction, hepatic dysmorphy, moderate ascites, and stenosis of the retrohepatic inferior vena cava.
Etiological work-up revealed recent reintroduction of estrogen-containing oral contraceptives, elevated homocysteine levels associated with heterozygous MTHFR mutation, and no other major thrombophilic disorder.
The patient was treated with oral anticoagulation with favorable clinical evolution.
This case highlights the multifactorial nature of Budd–Chiari syndrome and the synergistic interaction between hormonal exposure, metabolic abnormalities, and anatomical venous obstruction.

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