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Published on: December 9, 2022
Patients with Cushing's syndrome suffer from provoked venous thromboembolism and are anticoagulated in various
Agata Hanna Bryk-Wiązania1,2, Mari Minasyan2, Alicja Hubalewska-Dydejczyk1,2
1Chair and Department of Endocrinology, Jagiellonian University Medical College, Krakow, Poland.
Insights
Cushing's syndrome patients experiencing venous thromboembolism (VTE) had provoked episodes mainly due to transient factors. Anticoagulant regimens varied, highlighting the need for validated risk scores and treatment guidelines.
Area of Science:
- Endocrinology
- Hematology
- Clinical Medicine
Background:
- Cushing's syndrome (CS) significantly increases venous thromboembolism (VTE) risk (18-fold).
- Identifying VTE triggers and optimal anticoagulation in CS patients is crucial for management.
Purpose of the Study:
- To identify factors provoking VTE in patients with CS and VTE.
- To describe the anticoagulant regimens used in these cases.
Main Methods:
- Retrospective observational study of patients in the European Registry on CS (ERCUSYN).
- VTE provocation factors assessed using International Society of Thrombosis and Hemostasis (ISTH) guidance, Padua score, and CS-VTE score.
- Anticoagulant treatments and durations were recorded.
Main Results:
- Nine patients experienced ten VTE episodes over a median of 4.3 years (7.8% prevalence).
- All VTEs were provoked, primarily by transient major (50%) and minor (20%) factors.
- Anticoagulation primarily involved vitamin K antagonists (4/8), direct oral anticoagulants (3/8), and low-molecular-weight heparin (1/8); median duration was 2.75 years.
Conclusions:
- Further multicenter studies are needed.
- Development of a validated thrombotic risk score and treatment guidelines for VTE in CS patients is recommended.
Objective:
Cushing's syndrome (CS) is associated with an 18-fold greater risk of venous thromboembolism (VTE). We aimed to identify factors which provoke VTE among patients with CS and VTE and to describe the anticoagulant regimen used in these cases.
Methods:
In this retrospective observational study, patients included in the European Registry on CS (ERCUSYN) in Krakow center, Poland, were followed for the occurrence of VTE and anticoagulant treatment. We identified factors provoking VTE according to the International Society of Thrombosis and Hemostasis (ISTH), along with factors included in the Padua score and CS-VTE score.
Results:
Of the 128 patients followed for a median of 4.3 years, there were nine patients who experienced ten VTE episodes (prevalence of 7.8% and incidence of 13.4 per 1000 patient-years). All VTEs were classified as provoked according to the ISTH guidance, predominantly due to the transient major and minor (50% and 20%, respectively) factors, while they were less commonly due to persistent (30%) factors. In 2/9 patients, we could not identify any risk factor for VTE according to the Padua score, while in 2/6 patients according to the CS-VTE score. Patients were mostly anticoagulated with vitamin K antagonists (4/8 patients), followed by direct oral anticoagulants (3/8) and low-molecular-weight heparin (1/8). The median duration of anticoagulation was 2.75 years and exceeded beyond the primary treatment in 28% of episodes provoked by transient factors.
Conclusion:
Further, multicenter studies are required to create a validated thrombotic risk score and guidelines regarding VTE treatment in CS patients.
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