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• W2086360072 abstract "Dear Sir,Although immunosuppressive agents are indispensable in organ transplantation, at present fewer than ten agents are in clinical use. The need for new agents for clinical use is, therefore, very high. Following mizoribine, 15-deoxyspergualin (15-DSG) is the second immunosuppressive agent clinically applied in Japan. 15-DSG – an immunosuppressive agent that is a 15-deoxy analogue of spergualin – was isolated at Ohira-san, Tochigi Prefecture, Japan, in 1981 from the culture filtrate of Bacillus laterosporus [1]. It has become the focus of much attention with efforts being made to confirm its effectiveness. Its immunosuppressive action was first reported in 1985 [2]. Since that time it has been found to be effective in prophylaxis and treatment of rejection in kidney transplantation [3]. A synergy between 15-DSG and ciclosporin A (CS-A) has been shown by several authors [4, 5, 6]. An additive effect of these two drugs given in combination at low and full therapeutic doses has been shown [5, 6]. This is of interest, since CS-A treatment has been implicated in thrombotic risk in renal transplant recipients when compared with patients not treated with CS-A [7]. It is well known that platelet activation and endothelial, anatomical, and functional dysfunctions play a pivotal role in the pathogenesis of thrombosis. It has been reported that CS-A enhances in vitro platelet aggregation [8]and may damage the endothelium [9]. Considering the fact that no data are available on the effects of 15-DSG on platelet function, the purpose of this study was to determine whether these drugs alter platelet aggregation in whole blood and in platelet-rich plasma (PRP).Venous blood was obtained from healthy volunteers (control group, n = 12), kidney transplant recipients treated with CS-A, prednisone, and azathioprine (n = 7), and from uremic patients treated by means of chronic hemodialysis (HD, n = 7) and continuous ambulatory peritoneal dialysis (CAPD, n = 6) who denied taking any antiplatelet drugs for at least 2 weeks prior to sampling (except heparin before the onset of dialysis). All subjects gave their informed consent. Venous blood was collected into trisodium citrate (9:1 volume ratio). The platelet aggregation in the whole blood and in PRP was studied as reported earlier [10]. 15-DSG (Spanigin; Nippon Kayaku, Japan) was used at final concentrations of 10, 100, and 1,000 ng/ml. Samples were preincubated with 15-DSG at 37°C for 5 min prior to the addition of agonists: adenosine diphosphate (Chrono Log, USA), 10 µM in whole blood and 5 µM in PRP; collagen (Chrono Log), 2 µg/ml in whole blood and 0.5 µg/ml in PRP; arachidonic acid (Sigma, USA), 0.5 mM in whole blood and PRP; ristocetin (Chrono Log), 1.45 mg/ml in whole blood and 0.75 mg/ml in PRP, and serotonin (Sigma), 1 µM in PRP. Statistical analysis was performed by means of the Wilcoxon rank sum test with p < 0.05 considered significant. All results are summarized in tables 1 and 2. 15-DSG did not cause spontaneous platelet aggregation. Incubation with 15- DSG at any dose seemed to have no influence on platelet aggregation induced by ristocetin, adenosine diphosphate, and arachidonic acid in both whole blood and PRP and by serotonin in PRP in the control group and uremic (CAPD and HD) patients. Only collagen-induced platelet aggregation in the whole blood was found to be inhibited significantly by different concentrations of the drug used in hemodialyzed patients. In the control group, the highest concentration of 15-DSG used inhibited collagen-induced platelet aggregation in PRP. Incubation with 15-DSG at any dose did not alter the sensitivity of platelets obtained from kidney allograft recipients to any of the agonists used in both whole blood and PRP.So far, there have been no data considering in vivo and in vitro effects of DSG on platelet aggregation. Recently, we have shown an augmented platelet sensitivity following preincubation with CS-A upon stimulation with various agonists in both whole blood and PRP [11]as well as enhanced platelet aggregation in kidney transplant recipients treated with CS-A [12]. Conversion of patients from CS-A to azathioprine resulted in a tendency to reduced platelet aggregability [8], similar to findings reported by Vanrenterghem et al. [7]who found enhanced platelet aggregation in CS-A-treated patients when compared to subjects given to azathioprine. Previously, we also demonstrated that azathioprine inhibited collagen-induced aggregation of normal and uremic platelets in the whole blood, whereas both azathioprine and mizoribine significantly inhibited serotonin-induced aggregation of normal and uremic platelets [13]. Enhanced platelet aggregatory responses following preincubation with CS-A may have clinical implications not only with regard to the reported trend towards thromboembolic complications in kidney transplant recipients treated with CS-A. 15-DSG is devoid of some drawbacks of CS-A like erythrocytosis, thromboembolic complications, or hypertension. In humans the adverse reactions of 15-DSG have been shown to be relatively mild, with, in most cases, transient hematologic disorders [5], and they are dose dependent [14]. However, the mode of action of 15-DSG has been a subject of discussion for several years. It is of interest that CS-A and 15-DSG administered together at low doses potentiated each other without signs of toxicity in different animal models of allograft transplantation [4, 5, 14]. However, there was no synergy with FK 506 or azathioprine in the rat heart allograft model [14].Since available data concerning platelet function under 15-DSG treatment are lacking, further studies are needed to clarify the effects of this drug on platelet aggregation in transplanted patients. Because of probable synergy of 15-DSG with CS-A, 15-DSG deserves further exploration and precise determination of its clinical place." @default.
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• W2086360072 title "15-Deoxyspergualin and Platelet Aggregation in vitro" @default.
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