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Enoxaparin Failure in Patient With Cerebral Venous Sinus Thrombosis and Prothrombin G20210A Mutation: Case Report
Adithya Polavarapu1, Anita Bhushan2, Walter Duarte-Celada3,4
1Bhaskar Medical College (BMC), Hyderabad, Telangana, India.
Insights
Patients with cerebral venous sinus thrombosis (CVST) and prothrombin gene mutations may resist low-molecular-weight heparin (LMWH). Unfractionated heparin may be a more effective treatment option for these individuals.
Area of Science:
- Neurology
- Hematology
- Pharmacology
Background:
- Cerebral venous sinus thrombosis (CVST) is a rare cerebrovascular disease.
- The prothrombin G20210A mutation is a known risk factor for CVST.
- Optimal anticoagulation for CVST remains debated.
Purpose of the Study:
- To report a case of CVST with a prothrombin G20210A mutation resistant to LMWH.
- To highlight the potential for LMWH resistance in this patient population.
Main Methods:
- Case report of a young woman with CVST.
- Initial treatment with LMWH showed no therapeutic effect.
- Switched to unfractionated heparin, resulting in rapid clinical improvement and sinus recanalization.
- Genetic testing confirmed a heterozygous prothrombin G20210A mutation.
Main Results:
- The patient with CVST and prothrombin G20210A mutation exhibited resistance to LMWH.
- Unfractionated heparin led to significant clinical improvement and recanalization.
- Coagulation studies did not show therapeutic anticoagulation with LMWH despite compliance.
Conclusions:
- This case suggests potential LMWH resistance in CVST patients with prothrombin gene mutations.
- Close monitoring of coagulation parameters and clinical response is crucial for CVST patients on LMWH.
Introduction:
Cerebral venous sinus thrombosis (CVST) is a rare, serious, and complex cerebrovascular disease. The prothrombin G20210A mutation is the second most common inherited thrombophilia and is considered to be one of the etiologies of CVST. The optimal heparinoid medication for treatment remains a topic of debate.
Case Report:
This case report describes a young woman with CVST who did not respond to low-molecular-weight heparin (LMWH). The patient was initially treated with LMWH; however, her symptoms and clot burden in the sagittal sinus worsened, and coagulation studies showed no evidence of therapeutic anticoagulation despite good compliance. Unfractionated heparin was then initiated, and the patient's symptoms improved dramatically within 24 hours, along with the recanalization of the cerebral venous sinuses. Genetic testing revealed a heterozygous mutation in the prothrombin gene (G20210A). This mutation is a known risk factor for CVST. However, it is unclear why the patient did not respond to LMWH but responded appropriately to unfractionated heparin.
Conclusion:
This case report highlights the potential for LMWH resistance in patients with CVST and prothrombin gene mutations. These findings also emphasize the importance of close monitoring of coagulation parameters and clinical response in patients with CVST receiving LMWH.
