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降钙素原讲稿.ppt

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感染早期 (- 6-12 小时后重复检测!) 亚急性心内膜炎 局部感染 YES! 是否可能存在细菌感染而PCT不升高的情况? 对PCT结果的解读必须结合临床! Important! 结合每个患者的临床情况 考虑到影响 PCT 水平的因素 想到疾病的 动态过程 ( PCT水平的变化) 局部感染 必须采用更敏感的方法和 更低的界限值! 解读PCT结果时的注意事项 降钙素原(PCT) 感染后出现早而快,控制后快速下降 高度特异性和灵敏度 升高水平与病情严重程度正相关 检测简便, 体内和体外都很稳定 必须结合临床解释结果 小结:Procalcitonin降钙素原 谢谢大家 * * 所以,临床需要面对的问题: 如何在紧急情况下快速确诊,赢得“Golden Hours”? 如何在复杂而连续变化的过程中正确判断疾病的发展预后? 如何提高治疗成功率,及降低死亡率? 如何更有效利用有限的医疗资源? * Site of synthesis for PCT in healthy persons are the C-cells of the thyroid. Expression of CT-mRNA takes place only in the neuroendocrine cells. Release occurs in the form of the posttranslational processed hormone Calcitonin enclosed in Golgi vesicles. This hormone plays an important role in the pathway and regulation of calcium and phosphate in the bone metabolism. * In contrast to the role of PCT in the framework of the endocrine processes there are alternative possibilities of synthesis in connection with microbial infections. Inductors for the synthesis are inflammatory cytokines like IL-1β and TNF-αbut also elements of membranes or cell wall of the microbes like LPS or peptidoglycanes. This pathway was first described by Müller et al. 2001. After induction of sepsis it was possible to detect mRNA for PCT in all investigated tissues. * 解释:细菌作为抗原刺激单核细胞释放细胞因子,单核细胞与薄壁细胞(脂肪细胞)黏附才会使高尔基体合成释放PCT。 Linscheid et al. 2004 described the mechanism of the biochemical pathway and site of synthesis of PCT after bacterial infection. They investigated which factors affected the synthesis. Results show that in case of bacterial infection two mechanisms of synthesis are at work. At first cytokine-stimulated adherent monocytes release PCT in low quantities (2h). This synthesis is limited. But it plays an important role in the initiation of PCT synthesis in storage tissues of humans. This PCT burst is initiated in all storage tissues (18h). Parenchymal tissue is the most common type of tissue in the human organism. This explains why extreme

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