TITLE

URINARY 11-DEHYDRO-THROMBOXANE B2 AS A MARKER OF THE ANTI-PLATELET EFFECTS OF CLOPIDOGREL OR ASPIRIN THERAPY IN HEALTHY MALE VOLUNTEERS

AUTHOR(S)
Armstrong, P. C. J.; Dhanji, A. A.; Tucker, A. T.; Mitchell, J. A.; Warner., T. D.
PUB. DATE
November 2009
SOURCE
Heart;Nov2009, Vol. 95 Issue 22, p1
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Activated platelets release large amounts of the cyclooxygenase-dependent product, thromboxane A2 (TxA2), and increased urinary levels of the TxA2 metabolite 11-dehydro-thromboxane B2 (Tx-M) appear positively associated with atherosclerotic disease (1,2). Anti-thrombotic doses of aspirin significantly lower these levels, and such measurements have been linked to risk determination of stroke, myocardial infarction and cardiovascular death (2). Consequently, Tx-M is considered a marker of both platelet activation and aspirin anti-platelet effectiveness. Clopidogrel is another important anti-platelet therapy, but no study has been conducted to determine its effects upon Tx-M levels. A small non-blinded trial of 16 healthy male volunteers assigned to seven days of standard anti-thrombotic aspirin (75?mg/day) or clopidogrel (75?mg/day) therapy. Blood and urine was collected before and on day 7 of treatment. Platelets were incubated with arachidonic acid (AA) (1?mM) to stimulate the acute production of TxA2 and serum TxB2 levels determined by radioimmunoassay. Urinary 11-dehydro-TxA2 metabolites were measured using a commercial ELISA. Aspirin abolished AA-induced serum TxB2 production (n?=?8, P?=?<0.05) and caused a significant reduction in Tx-M levels (58?±?9%, n?=?8, P?=?<0.05). Clopidogrel inhibited AA-induced TxB2 production by 45?±?9% (n?=?8, P?=?<0.05) and urinary Tx-M levels by 59?±?11% (n?=?8, P?=?
ACCESSION #
47362773

 

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