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Homocystinuria is a metabolic disorder characterized by serious vascular thromboses and elevated plasma levels of Homocysteine and Homocysteic Acid. The etiology of the thromboses is unknown. Platelets produce proaggregatory and prothrombotic Thromboxane A2 (TXA2) while vascular endothelium produces antiaggregatory and antithrombotic PGI2. An imbalance in production of TXA2 and/or PGI2 can lead to bleeding or thrombosis. We investigated production of platelet TXB2 (the stable end product of TXA2) and vascular 6- Keto-PGF1α (the end product of PGI2) in platelets and vascular endothelium exposed in vitro to Homocysteine and Homocysteic Acid, 0.4 to 2.0 mM. Conversion of 14C arachidonic acid (AA) to platelet TXB2 was increased in the presence of Homocysteine or Homocysteic Acid. In 8 paired experiments, mean platelet TXB2 increased to 19.4±3.5% (1SE) in the presence of Homocysteic Acid, compared to control values of 14.6±3.6% (p&lt;0.01). Similarly, in 4 paired experiments platelet TXB2 was increased (18.7±2.3%) in the presence of Homocysteine, when compared to a mean value of 7.8±1.1% (p&lt;0.05) in the control platelets. No differences in vascular 6-Keto-PGF1α production were observed in 6 paired experiments when vessels were incubated with either buffer, Homocysteine or Homocysteic Acid (0.73 ± .07; 0.7 ± .05; 0.76 ±.07%). These studies demonstrate that Homocysteine and Homocysteic Acid alter platelet and vascular AA metabolism by increasing production of prothrombotic platelet TXA2 without a compensatory increase in anththrombotic vascular PGI2. Such an imbalance may explain the marked thrombotic tendency seen in patients with homocystinuria. It also provides evidence for the use of thromboxane synthetase inhibitors in this disorder.

An Imbalance In Platelet-Vascular Prostaglandin Synthesis Induced By Homocysteine And Homocysteic Acid