Abnormally high thromboxane biosynthesis in homozygous homocystinuria. Evidence for platelet involvement and probucol-sensitive mechanism.
Homocystinuria due to homozygous cystathionine beta-synthase deficiency is an inborn error of metabolism characterized by a high incidence of thrombosis and premature atherosclerosis. We evaluated TXA2 biosynthesis in vivo and several in vitro tests of platelet function in 11 homocystinuric patients...
Uloženo v:
| Vydáno v: | J Clin Invest |
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| Hlavní autoři: | , , , , , , , , , |
| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
American Society for Clinical Investigation
1993
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC288283/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/8376592/ https://ncbi.nlm.nih.govhttps://doi.org/10.1172/JCI116715 |
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