首页> 美国卫生研究院文献>British Journal of Cancer >Pulmonary toxicity after granulocyte colony-stimulating factor-combined chemotherapy for non-Hodgkins lymphoma.
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Pulmonary toxicity after granulocyte colony-stimulating factor-combined chemotherapy for non-Hodgkins lymphoma.

机译:粒细胞集落刺激因子联合化疗对非霍奇金淋巴瘤的肺毒性。

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Sporadic cases have developed pulmonary toxicity after receiving chemotherapy and granulocyte colony-stimulating factor (G-CSF). However, because such cases received chemotherapy that alone frequently causes pulmonary toxicity, the role of G-CSF in this toxicity has been unclear. CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity. However, we observed a considerable incidence of this toxicity in non-Hodgkin's lymphoma subjects receiving CHOP therapy and G-CSF (6 out of 52 subjects, 11.5%). In this cohort, among various characteristics, including the dose and interval of CHOP therapy, only the mean peak leucocyte count (MPLC) with each therapy cycle was associated with development of this toxicity (MPLC > or = 23.0 x 10(9) l(-1), 6 out of 29 cases; MPLC < 23.0 x 10(9) l(-1), 0 out of 23 cases; P = 0.020). These findings suggest that the effect of G-CSF is the main determinant of the pulmonary toxicity in these cases. Because the toxicity was associated with a large MPLC and did not recur in cases readministered G-CSF, an idiosyncratic reaction to G-CSF is unlikely to be the pathogenesis of this toxicity. Thus, lowering the G-CSF dose seems to be useful in the prevention of this toxicity. In all six cases, the time course of manifestation of the toxicity was the same, and early application of high-dose corticosteroid led to cure. This knowledge will be helpful in the care of similar cases.
机译:零星病例在接受化疗和粒细胞集落刺激因子(G-CSF)后发展为肺毒性。但是,由于此类病例仅靠化学疗法治疗就经常引起肺部毒性,因此尚不清楚G-CSF在这种毒性中的作用。 CHOP治疗(环磷酰胺,阿霉素,长春新碱和泼尼松龙)仅轻微诱导肺毒性。但是,我们在接受CHOP治疗和G-CSF的非霍奇金淋巴瘤受试者中观察到这种毒性的发生率很高(52名受试者中有6名,占11.5%)。在该队列中,包括CHOP治疗的剂量和间隔在内的各种特征中,只有每个治疗周期的平均白细胞峰值(MPLC)与这种毒性的发生相关(MPLC>或= 23.0 x 10(9)l( -1),29例中的6例; MPLC <23.0 x 10(9)l(-1),23例中的0; P = 0.020)。这些发现表明,在这些情况下,G-CSF的作用是肺毒性的主要决定因素。因为毒性与大的MPLC有关,并且在重新施用G-CSF的情况下不会复发,所以对G-CSF的特异反应不太可能是这种毒性的发病机理。因此,降低G-CSF剂量似乎可用于预防这种毒性。在所有六个病例中,毒性表现的时间过程是相同的,并且大剂量皮质类固醇的早期应用导致治愈。这些知识将有助于类似情况的护理。

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