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Endothelial dysfunction during acute methionine load in hyperhomocysteinaemic patients
J Constans1, A D Blann, F Resplandy
1Service de Médecine Interne et Pathologie Vasculaire, Hôpital Saint-André, 33075, Bordeaux, France. joel.constans@chu-aquitaine.fr
Atherosclerosis
|November 24, 1999
Summary
Elevated homocysteine levels may impair blood vessel function. A methionine load increased von Willebrand factor, indicating endothelial dysfunction in patients with occlusive vascular disease.
Area of Science:
- Cardiovascular Science
- Hematology
- Metabolic Research
Background:
- Hyperhomocysteinemia is linked to arterial and venous thrombosis.
- Endothelial damage is a potential mechanism for thrombosis in hyperhomocysteinemia.
Purpose of the Study:
- To investigate if a methionine load, increasing plasma homocysteine, also elevates markers of endothelial or platelet dysfunction.
- To assess endothelial and platelet function in patients with arterial or venous occlusive disease after methionine loading.
Main Methods:
- Two patient groups (hyperhomocysteinemic and non-hyperhomocysteinemic) with occlusive vascular disease were studied.
- Plasma levels of soluble thrombomodulin, von Willebrand factor, P-selectin, and tissue factor plasma inhibitor were measured.
- Measurements were taken before and 6 hours after an oral methionine load (100 mg/kg).
Main Results:
- A methionine load significantly increased von Willebrand factor in both patient groups (P<0.02).
- This suggests that endothelial dysfunction occurs following the methionine load.
Conclusions:
- Oral methionine loading can induce endothelial dysfunction.
- This finding supports the hypothesis that homocysteine may contribute to vascular disease through endothelial damage.