Journal
LUPUS
Volume 16, Issue 12, Pages 981-986Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/0961203307083313
Keywords
systemic lupus erythematosus; asprin resistance; thromboxane; prostacyclin; oxidative stress
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Funding
- NCRR NIH HHS [5 M01 RR00095] Funding Source: Medline
- NHLBI NIH HHS [HL65082, HL04012] Funding Source: Medline
- NIDDK NIH HHS [DK48831] Funding Source: Medline
- NIEHS NIH HHS [ES13125] Funding Source: Medline
- NIGMS NIH HHS [GM15431] Funding Source: Medline
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Incomplete suppression of thromboxane biosynthesis during aspirin therapy is associated with increased cardiovascular risk. Since systemic lupus erythematosus (SLE) is associated with platelet activation and increased cardiovascular mortality, we compared thromboxane and prostacyclin biosynthesis in patients with SLE and control subjects, and measured inhibition of thromboxane excretion in aspirin-treated subjects. We measured the urinary excretion of 11-dehydro thromboxane B-2 (TXB2) and 2,3-dinor 6-ketoPGF(1 alpha) (PGI-M), the stable metabolites of thromboxane A(2) and prostacyclin, respectively, in 74 patients with SLE and 70 controls. In subjects who were not receiving aspirin, TXB2 excretion was higher in patients with SLE [0.40 ng/mg creatinine (0.26-0.64), median (interquartile range)] than controls [0.31 ng/mg creatinine (0.23-0.44)] (P = 0.04), and in these patients, TXB2 excretion correlated with disease activity (rho = 0.28, P = 0.03) and tumor necrosis factor alpha (rho = 0.48, P < 0.001). Aspirin therapy resulted in significantly lower TXB2 excretion in controls (P = 0.01), but not in patients with SLE (P = 0.10), compared with subjects not receiving aspirin. Prostacyclin biosynthesis did not differ among patients and controls, and was not affected by aspirin (P all >0.35). Thromboxane biosynthesis is increased in SLE and is associated with disease activity. Additionally, response to aspirin may be attenuated in some patients with SLE.
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