Increased production of platelet-derived thromboxane in patients with lupus anticoagulant.
The in vivo production of thromboxane A2 and prostacyclin was assessed in 31 samples from 25 patients with lupus anticoagulant and in 32 controls. The urinary excretion of 11-dehydro-thromboxane B2 (a major thromboxane metabolite of platelet origin) was very significantly increased (p less than 0.0003) in the patients contrasting with a lesser increase of urinary 2,3-dinor-6-keto-prostaglandin F1 alpha reflecting the vascular production of prostacyclin (p less than 0.02). Our study shows that in patients with lupus anticoagulant, platelet activation may occur without a compensatory increment in the vascular biosynthesis of prostacyclin suggesting an increased risk for thrombosis.
Maclouf
J
J
U150 INSERM, Hôpital Lariboisière, Paris, France.
Lellouche
F
F
Martinuzzo
M
M
Said
P
P
Carreras
L O
LO
D000328:Adult; D001792:Blood Platelets / Q000378:metabolism*; D002855:Chromatography, Thin Layer; D015232:Dinoprostone / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000502:physiology*; D013931:Thromboxanes / Q000096:biosynthesis* / Q000097:blood
D016682:Lupus Coagulation Inhibitor; D013931:Thromboxanes; D015232:Dinoprostone