In:
Lupus, SAGE Publications, Vol. 16, No. 12 ( 2007-12), p. 981-986
Abstract:
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 (TXB 2 ) and 2,3-dinor 6-ketoPGF 1α (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, TXB 2 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, TXB 2 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 TXB 2 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. Lupus (2007) 16, 981—986.
Type of Medium:
Online Resource
ISSN:
0961-2033
,
1477-0962
DOI:
10.1177/0961203307083313
Language:
English
Publisher:
SAGE Publications
Publication Date:
2007
detail.hit.zdb_id:
2008035-9
