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Increased thromboxane formation in patients with antiphospholipid syndrome
Author(s) -
ÅRFORS L.,
VESTERQVIST O.,
JOHNSSON H.,
GRÉEN K.
Publication year - 1990
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1990.tb01908.x
Subject(s) - prostacyclin , platelet , thromboxane , antiphospholipid syndrome , chemistry , creatinine , medicine , platelet activation , aspirin , urine , thromboxane a2 , endocrinology , thromboxane b2 , pathophysiology , thrombosis
. Thirty‐one patients with IgG antibodies to cardiolipin (ACLA) were studied to determine their in vivo formation of the platelet aggregating and vasoconstricting substance thromboxane A 2 (TxA 2 ) and the platelet inhibiting and vasodilating substance prostacyclin (PGI 2 ). This was done by measurements in urine of their enzymatically formed metabolites 2,3‐dinor‐TxB 2 and 2,3‐dinor‐6‐keto‐PGF 1 x , respectively, using gas chromatography mass spectrometry. It is demonstrated that patients with IgG ACLA have a highly significant increase in the biosynthesis of TxA 2 compared with age‐matched healthy controls (807 pM 163 [SEM] vs. 230 pM 15 pg mg ‐1 creatinine, P = 0.5). A significant increment of the formation of PGI 2 was also found (189 pM 23 (SEM) vs. 125 pM 11 pg mg ‐1 creatinine, P = 0.03), although this was much less pronounced than that for TxA 2 . We conclude that the highly increased formation of TxA 2 , reflecting platelet activation, in patients with IgG ACLA is of pathophysiologic relevance for their tendency to arterial and venous thrombosis and hence that they should be considered for prophylactic treatment with inhibitors of TxA 2 formation, like aspirin.