Effect of Colchicine on Platelet-Platelet and Platelet-Leukocyte Interactions: a Pilot Study in Healthy Subjects

被引:0
|
作者
Binita Shah
Nicole Allen
Bhisham Harchandani
Michael Pillinger
Stuart Katz
Steven P. Sedlis
Christina Echagarruga
Svetlana Krasnokutsky Samuels
Pajazit Morina
Prabhjot Singh
Liza Karotkin
Jeffrey S. Berger
机构
[1] New York University School of Medicine,Department of Medicine, Division of Cardiology
[2] Department of Medicine,Department of Medicine, Division of Rheumatology
[3] Section of Cardiology,Department of Medicine, Divisions of Cardiology and Hematology
[4] Veterans Affairs New York Harbor Health Care System,undefined
[5] New York University School of Medicine,undefined
[6] New York University School of Medicine,undefined
来源
Inflammation | 2016年 / 39卷
关键词
colchicine; platelet aggregation; neutrophil; monocyte; tissue adhesion;
D O I
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学科分类号
摘要
The cardioprotective mechanisms of colchicine in patients with stable ischemic heart disease remain uncertain. We tested varying concentrations of colchicine on platelet activity in vitro and a clinically relevant 1.8-mg oral loading dose administered over 1 h in 10 healthy subjects. Data are shown as median [interquartile range]. Colchicine addition in vitro decreased light transmission platelet aggregation only at supratherapeutic concentrations but decreased monocyte- (MPA) and neutrophil-platelet aggregation (NPA) at therapeutic concentrations. Administration of 1.8 mg colchicine to healthy subjects had no significant effect on light transmission platelet aggregation but decreased the extent of MPA (28 % [22–57] to 22 % [19–31], p = 0.05) and NPA (19 % [16–59] to 15 % [11–30], p = 0.01), platelet surface expression of PAC-1 (370 mean fluorescence intensity (MFI) [328–555] to 333 MFI [232–407], p = 0.02) and P-selectin (351 MFI [269–492] to 279 [226–364], p = 0.03), and platelet adhesion to collagen (10.2 % [2.5–32.6] to 2.0 % [0.2–9.5], p = 0.09) 2 h post-administration. Thus, in clinically relevant concentrations, colchicine decreases expression of surface markers of platelet activity and inhibits leukocyte-platelet aggregation but does not inhibit homotypic platelet aggregation.
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页码:182 / 189
页数:7
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