Rheumatology international · 2004
Platelet-activating factor and P-selectin activities in thrombotic and nonthrombotic Behçet's patients.
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Tunc S Ercan, Aksu Kenan, Keser Gokhan, Oksel Fahrettin, Doganavsargil Eker, Pirildar Timur, Turk Tufan, Terzioglu Ender, Huseyinov Afig
Аннотация
OBJECTIVE: The aim of this study was to compare plasma Platelet-activating factor (PAF) and P-selectin (CD62P) activities in Behçet's disease patients with and without thrombosis.
METHODS: In this cross-sectional and descriptive study, 30 consecutive Behçet's patients were included, 15 of them with venous thrombosis. All patients were also divided into two subgroups according to the presence or absence of clinical activity. Plasma PAF levels, basal and Ca++ ionophore (A23187)-induced leukocyte (cellular) PAF activities, and platelet-rich plasma DeltaCD62P activity (the mean fluorescent density difference between CD62P phycoerythrin-positive and -negative stains) were evaluated.
RESULTS: In the thrombotic group, plasma PAF (P=0.001), basal leukocyte PAF (P=0.017), induced leukocyte PAF (P=0.024), and DeltaCD62P (P=0.023) levels were significantly higher than in the nonthrombotic group. In the whole group of Behçet's patients, there was a positive correlation between plasma PAF and DeltaCD62P levels (r=0.533, P=0.002). When we compared clinically active and inactive patients with respect to the above parameters, there was no significant difference, irrespective of thrombosis. Plasma PAF (P=0.001), basal leukocyte PAF (P=0.004), and DeltaCD62P (P=0.038) levels were significantly higher in the presence of both clinical activity and thrombosis than of clinical activity alone.
CONCLUSION: Platelet-activating factor and CD62P may contribute to endothelial injury and thrombosis development in Behçet's disease. These two parameters seem related to the presence of thrombosis rather than clinical activity.
METHODS: In this cross-sectional and descriptive study, 30 consecutive Behçet's patients were included, 15 of them with venous thrombosis. All patients were also divided into two subgroups according to the presence or absence of clinical activity. Plasma PAF levels, basal and Ca++ ionophore (A23187)-induced leukocyte (cellular) PAF activities, and platelet-rich plasma DeltaCD62P activity (the mean fluorescent density difference between CD62P phycoerythrin-positive and -negative stains) were evaluated.
RESULTS: In the thrombotic group, plasma PAF (P=0.001), basal leukocyte PAF (P=0.017), induced leukocyte PAF (P=0.024), and DeltaCD62P (P=0.023) levels were significantly higher than in the nonthrombotic group. In the whole group of Behçet's patients, there was a positive correlation between plasma PAF and DeltaCD62P levels (r=0.533, P=0.002). When we compared clinically active and inactive patients with respect to the above parameters, there was no significant difference, irrespective of thrombosis. Plasma PAF (P=0.001), basal leukocyte PAF (P=0.004), and DeltaCD62P (P=0.038) levels were significantly higher in the presence of both clinical activity and thrombosis than of clinical activity alone.
CONCLUSION: Platelet-activating factor and CD62P may contribute to endothelial injury and thrombosis development in Behçet's disease. These two parameters seem related to the presence of thrombosis rather than clinical activity.