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The etiology of chronic splanchnic vein thrombosis in adults: a two-center analysis
Esin Oguz Kozan1, Gizem Isguzar2, Enver Ucbilek3
1Department of Internal Medicine - Hematology, Mersin University Medical Faculty Mersin, Turkey.
Insights
Portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS) have diverse causes, including cirrhosis, surgery, and congenital factors. Early detection requires broad diagnostic strategies for at-risk patients.
Area of Science:
- Vascular Medicine
- Hepatology
- Gastroenterology
Background:
- Portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS) are rare vascular disorders.
- Etiologies for PVT and BCS range from well-recognized to less common causes.
Purpose of the Study:
- To investigate the diverse etiologies of PVT and BCS.
- To improve early detection and management strategies for these conditions.
Main Methods:
- Retrospective review of 73 patients (58 with PVT, 15 with BCS).
- Detailed clinical evaluation to identify underlying diseases and related conditions (e.g., surgery).
Main Results:
- Over 76% of patients had at least one underlying disease.
- Common etiologies included cirrhosis, myeloproliferative disease, malignancy, rheumatological conditions, congenital factors, gastrointestinal surgery, and homocysteinemia.
- Rare causes identified: paroxysmal nocturnal haemoglobinuria, Crohn's disease, nephrotic syndrome, drug therapies, pregnancy, JAK2 mutation, and elevated factor VIII or fibrinogen.
Conclusions:
- A wide range of frequent and infrequent etiologies contribute to splanchnic vein thrombosis.
- Implementation of appropriate diagnostic strategies is crucial for at-risk patients.
Abstract:
Portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS) are rare vascular disorders with both well-recognized and less commonly identified etiologies.
Objectives:
This study aims to investigate the etiologies of portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS), thereby enhancing improving early detection and management strategies for these conditions. A retrospective review was undertaken to identify the etiologies of PVT and BCS.
Methods:
A detailed clinical evaluation was performed and all underlying diseases, such as MPD, and related conditions (e.g. surgery) associated with thrombosis were recorded.
Results:
The study comprised a total of 73 patients, with 58 diagnosed with PVT and 15 with BCS. Of these patients, 56 (76.7%) had at least one underlying disease. The most prevalent underlying diseases in patients with PVT were cirrhosis (32/58, 55.2%), myeloproliferative disease (3/58, 5.2%), malignancy (4/58, 6.9%), and rheumatological conditions (4/58, 6.9%). For BCS, 11/15 patients (73.3%) had at least one predisposing condition, including cirrhosis in six cases. Congenital causes were identified in 16/58 cases of PVT (27.6%), in 7/15 cases of BCS (46.7%). Thirty-two patients had previously undergone gastrointestinal surgery (PVT 24/58, BCS 8/15); surgery was the sole etiology in 15/73 patients (20.5%). Homocysteinemia was common (PVT 20/58, BCS 5/15). A multitude of rare etiologies were identified, including paroxysmal nocturnal haemoglobinuria, Crohn's disease, nephrotic syndrome, drug therapies, pregnancy, JAK2 mutation, and elevated factor VIII or fibrinogen.
Conclusions:
The presence of a wide range of diverse frequent-infrequent etiologies of congenital or acquired splanchnic vein thrombosis in this cohort underscores the necessity for the implementation of appropriate diagnostic strategies in a broad spectrum of at-risk patients.
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