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Cerebral vein thrombosis and mild hyperhomocysteinemia: three new cases
A Rigamonti1, M R Carriero, G Boncoraglio
1Carlo Besta Neurological Institute, Via Celoria 11, I-20133 Milan, Italy.
Insights
Mild hyperhomocysteinemia, a known risk factor for deep vein thrombosis, may also contribute to cerebral vein thrombosis (CVT). Routine homocysteine level checks and treatment in idiopathic CVT patients are suggested to mitigate risks.
Area of Science:
- Neurology
- Genetics
- Clinical Medicine
Background:
- Deep vein thrombosis (DVT) is linked to mild hyperhomocysteinemia.
- Cerebral vein thrombosis (CVT) is a rare but serious condition with various risk factors.
Observation:
- Three patients with CVT were identified with elevated homocysteine levels.
- These patients also possessed the C677T polymorphism in both alleles of the methylene tetrahydrofolate reductase (MTHFR) gene.
- No other risk factors for CVT were identified in these cases.
Findings:
- Hyperhomocysteinemia, particularly with the MTHFR C677T homozygous genotype, is proposed as a potential risk factor for CVT.
- Elevated homocysteine levels may play a role in the pathogenesis of cerebral venous sinus thrombosis.
Implications:
- Routine screening for elevated homocysteine levels is recommended for patients diagnosed with idiopathic CVT.
- Pharmacological correction of hyperhomocysteinemia may reduce the risk of CVT recurrence or development.
- This finding could lead to new preventative strategies for CVT.
Abstract:
Mild hyperhomocysteinemia is an established risk factor for deep vein thrombosis. We report three patients with cerebral vein thrombosis (CVT) in which the only risk factor we were able to identify was increased blood homocysteine levels and the C677T polymorphism in both alleles of the methylene tetrahydrofolate reductase MTHFR gene. We suggest that hyperhomocysteinemia should also be a risk factor for CVT. Since this condition can be effectively and safely corrected by drugs, we suggest that homocysteine levels should be routinely determined in patients with idiopatic CVT, and even mildly increased levels corrected pharmacologically, in the hope of reducing the risks associated with this condition.