Enhanced platelet sensitivity to prostacyclin in patients in an active stage of Takayasu arteritis

Citation
T. Watanabe et al., Enhanced platelet sensitivity to prostacyclin in patients in an active stage of Takayasu arteritis, THROMB RES, 104(2), 2001, pp. 77-83
Citations number
24
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS RESEARCH
ISSN journal
0049-3848 → ACNP
Volume
104
Issue
2
Year of publication
2001
Pages
77 - 83
Database
ISI
SICI code
0049-3848(20011015)104:2<77:EPSTPI>2.0.ZU;2-9
Abstract
Patients in an active stage of Takayasu arteritis are often complicated wit h thrombosis in the affected vessels. We investigated whether alteration of platelet sensitivity to prostacyclin is involved in platelet function in t hese patients. Twelve female patients in an active stage (48.3 +/- 11.8 yea rs, mean +/-S.D.), diagnosed clinically by a persistently elevated erythroc yte sedimentation rate (> 40 mm/h) with typical symptoms, along with 10 gen der- and age-matched patients in an inactive stage and 12 control subjects were enrolled. Half-maximal concentration (EC50) for platelet aggregation t o collagen was determined in the presence and absence of 1 nM iloprost, a s table prostacyclin analog. Sensitivity of platelets to prostacyclin was qua ntified by the ratio of EC50 (R) in the presence of iloprost to that in its absence. Patients in an active stage exhibited enhanced platelet aggregati on, as demonstrated by significantly lower EC50 to collagen and increased p lasma thromboxane B-2 concentration. However, R values in these patients we re significantly higher (4.00 +/-1.05; P < .001) than those in the inactive patients or controls (2.58 +/- 0.62 and 2.43 +/- 0.68, respectively), sugg esting enhanced sensitivity to prostacyclin in patients with active disease . Plasma 6-keto-PGF1 alpha levels were lower in the active patients than th ose in other groups of subjects. We conclude that platelets in an active st age of TA may be sensitive not only to collagen but also to prostacyclin. T he increase in sensitivity of the platelets to prostacyclin could be a comp ensatory mechanism against a decrease in the prostanoid production, presuma bly associated with endothelial dysfunction. (C) 2001 Elsevier Science Ltd. All rights reserved.