Activated platelets as a possible early marker to predict clinical efficacy of leukocytapheresis in severe ulcerative colitis patients
Activated platelets as a possible early marker to predict clinical efficacy of leukocytapheresis in severe ulcerative colitis patients
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DOI：
10.1007/s00535-006-1789-y
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发表时间：
2006-06-01
影响因子：
6.3
通讯作者：
Matsumoto, Takayuki
中科院分区：
文献类型：
--
作者：
Fukunaga, Ken;Fukuda, Yoshihiro;Matsumoto, Takayuki
背景白细胞分离术（LCAP）是治疗活动期溃疡性结肠炎（UC）的有效辅助手段。由于LCAP可能具有去除和调节白细胞以及血小板的潜力，因此我们评估了活化血小板与LCAP治疗反应之间的相关性。方法. 14例重度UC患者每周接受LCAP治疗，连续5周。他们的平均临床活动指数（CAI）和内镜指数（EI）分别为9.6 +/- 3.4和10.9 +/- 1.0。在每次LCAP之前和之后采集他们的外周血，并在流式细胞术之前用血小板活化依赖性表面抗原（CD 63、CD 62-P）的荧光抗体染色。在最后一次LCAP后进行内镜评价。结果5周后50%（7/14）的患者出现临床缓解（CAI < 4），缓解组（RG）与无缓解组（NG）的临床背景差异无统计学意义。RG组第1次LCAP后CD 63+（P < 0.03）和CD 62-P+（P < 0.05）血小板数明显减少，且随LCAP次数增加，减少率逐渐降低。RG组的EI评分（尤其是粘膜损伤）显着改善（P < 0.04），但NG组则无改善。结论.这些结果表明，对LCAP的治疗反应反映在群体和/或血小板功能的调节中，特别是在第一次治疗后。在第一次LCAP后立即减少这种活化的血小板可能是预测重度UC患者反应的早期标志物。
Background. Leukocytapheresis (LCAP) is an effective adjunct for patients with active ulcerative colitis (UC). Because LCAP may have the potential to remove and modulate not only leukocytes but also platelets, we evaluated the correlation between activated platelets and the therapeutic response to LCAP. Methods. Fourteen patients with severe UC received weekly LCAP for 5 consecutive weeks. Their average clinical activity index (CAI) and endoscopic index (EI) were 9.6 +/- 3.4 and 10.9 +/- 1.0, respectively. Their peripheral blood was sampled before and after every LCAP and stained with fluorescent antibodies to the activation-dependent surface antigens of platelets (CD63, CD62-P) prior to flow cytometry. Endoscopic evaluations were performed after the last LCAP. Results. Clinical remission (CAI < 4) was induced in 50% of the patients (7/14) after 5 weeks, and there were no significant differences observed in clinical background between the responder group (RG) and the nonresponder group (NG). In the RG, the populations of CD63(+) (P < 0.03) and CD62-P+ (P < 0.05) platelets were significantly decreased after the first LCAP, and their reduction ratio decreased gradually with repeated LCAP. A significant improvement of the EI score, especially mucosal damage, was achieved in RG (P < 0.04) but not in NG. Conclusions. These results indicate that the therapeutic responses to LCAP were reflected in modulations of population and/or platelet functions, especially after the first session. The decrease of such activated platelets immediately after the first LCAP may be an early marker for predicting the response in patients with severe UC.