儿童白血病/淋巴瘤患者尿6-酮- pgf1 α水平的研究这可能是血管损伤的迹象

Yoshihito Morioka, Kentaro Tsunamoto, Shinsaku Imashuku
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引用次数: 0

摘要

为了确定抗肿瘤化疗对白血病/淋巴瘤儿童血管系统的影响,采用放射免疫分析法(RIA)测定尿中6-酮- pgf1 α的排泄量。在接受治疗的4例患者中,6-酮- pgf1 α平均升高至148(范围;治疗期间la升高至126 ~ 170 %,3 ~ 5 d后恢复到治疗前水平。在18名完成治疗的长期幸存者中,6-酮- pgf1 α的平均值为275(范围;52-905) ng/g肌酐,健康对照儿童平均值为146(范围;71-348) ng/g肌酐。这些结果与我们的假设相反,即化疗可能导致PGI2(6-酮- pgf1 α的前体)的合成减少,并表明尿中6-酮- pgf1 α的增加反映了白血病/淋巴瘤儿童患者急性暴露于化疗药物的血管反应和长期强化化疗可能导致的血管损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Urinary 6-keto-PGF1α level in patients with childhood leukemia/lymphoma; A possible indicator of vascular damage

To determine the effect of anti-neoplastic chemotherapy on the vascular system(s) of children with leukemia/lymphoma, urinary excretion of 6-keto-PGF was measured by radioimmunoassay (RIA).

In 4 patients receiving therapy, 6-keto-PGF increased to a mean of 148 (range; 126–170)% during therapy, la increased returned to pre-treatment level 3–5 days later. In 18 long-term survivors who had completedtherapy, 6-keto-PGF was determined to be a meanof 275 (range; 52–905) ng/g creatinine, and in the healthy control children the mean was 146 (range; 71–348) ng/g creatinine. These results were contrary to our hypothesis that chemotherapy might cause a decreased synthesis of PGI2, a precursor of 6-keto-PGF, and suggest that increased urinary 6-keto-PGF reflects a vascular response to acute exposure to chemotherapeutic drugs and possible vascular damage due to long-term intensive chemotherapy in pediatric patients with leukemia/lymphoma.

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