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血浆嗜铬粒蛋白A标志着与达卡巴嗪和氮芥相关的呕吐及5-羟色胺释放,但与基于环磷酰胺的化疗无关。

Plasma chromogranin A marks emesis and serotonin release associated with dacarbazine and nitrogen mustard but not with cyclophosphamide-based chemotherapies.

作者信息

Cubeddu L X, O'Connor D T, Hoffmann I, Parmer R J

机构信息

Department of Pharmacology, School of Pharmacy, Central University of Venezuela, Caracas.

出版信息

Br J Cancer. 1995 Oct;72(4):1033-8. doi: 10.1038/bjc.1995.457.

Abstract

Chromogranin A (CgA) is present in high concentrations in enterochromaffin cells, where it is co-localised with serotonin in the storage granules. Plasma CgA has been reported to mark emesis and serotonin release associated with cisplatin treatment. However, it is not known whether plasma CgA could be an indicator of emesis and of serotonin release in patients receiving non-cisplatin chemotherapies. Therefore, in this study we evaluated, in cancer patients, the temporal relationships between the increases in plasma CgA and urinary 5-hydroxyindoleacetic acid (5-HIAA) and the development of vomiting following dacarbazine, nitrogen mustard and cyclophosphamide treatments. Metoclopramide was used as antiemetic. With dacarbazine, nitrogen mustard and cyclophosphamide the median time to the onset of emesis was 2.3, 2.8 and 5.3 h and the duration of intense emesis was 3, 2 and 6 h respectively. Plasma CgA and urinary 5-HIAA increased after dacarbazine- and nitrogen mustard-based chemotherapies, with maximal increases between 4 and 6 h after initiation of drug infusion. The time course for the increases in plasma CgA paralleled that of urinary 5-HIAA and the period of intense emesis. A highly significant (P = 0.0009) positive correlation (r = 0.68) was found between the increases in plasma CgA and in urinary 5-HIAA. Cyclophosphamide treatment was not associated with increases in plasma CgA and in urinary 5-HIAA, despite inducing emesis; this indicates that the increases in CgA and 5-HIAA after dacarbazine and nitrogen mustard are not due to the act of vomiting per se. In summary, plasma CgA is a marker of serotonin release (most likely from enterochromaffin cells) after dacarbazine and nitrogen mustard-based chemotherapies, exocytosis being the most likely mechanism for the release of serotonin. Serotonin released from enterochromaffin cells seems to trigger the emetic response to dacarbazine and nitrogen mustard; however, cyclophosphamide may release serotonin from a different pool (enteric serotonin neurons and/or CNS serotonin?).

摘要

嗜铬粒蛋白A(CgA)在肠嗜铬细胞中浓度很高,在储存颗粒中它与5-羟色胺共定位。据报道,血浆CgA可标记与顺铂治疗相关的呕吐和5-羟色胺释放。然而,尚不清楚血浆CgA是否可作为接受非顺铂化疗患者呕吐和5-羟色胺释放的指标。因此,在本研究中,我们评估了癌症患者在接受达卡巴嗪、氮芥和环磷酰胺治疗后,血浆CgA和尿5-羟吲哚乙酸(5-HIAA)升高与呕吐发生之间的时间关系。甲氧氯普胺用作止吐药。使用达卡巴嗪、氮芥和环磷酰胺时,呕吐开始的中位时间分别为2.3、2.8和5.3小时,剧烈呕吐的持续时间分别为3、2和6小时。基于达卡巴嗪和氮芥的化疗后,血浆CgA和尿5-HIAA升高,在开始输注药物后4至6小时达到最大升高。血浆CgA升高的时间进程与尿5-HIAA和剧烈呕吐期的时间进程平行。血浆CgA升高与尿5-HIAA升高之间发现高度显著的正相关(P = 0.0009,r = 0.68)。尽管环磷酰胺会引起呕吐,但它与血浆CgA和尿5-HIAA升高无关;这表明达卡巴嗪和氮芥后CgA和5-HIAA的升高并非由于呕吐本身。总之,血浆CgA是基于达卡巴嗪和氮芥的化疗后5-羟色胺释放(很可能来自肠嗜铬细胞)的标志物,胞吐作用是5-羟色胺释放的最可能机制。从肠嗜铬细胞释放的5-羟色胺似乎触发了对达卡巴嗪和氮芥的呕吐反应;然而,环磷酰胺可能从不同的来源释放5-羟色胺(肠5-羟色胺神经元和/或中枢神经系统5-羟色胺?)

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