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Pulmonary toxicity induced by mitomycin C is highly responsive to glucocorticoids

โœ Scribed by Alex Yuang-Chi Chang; J. Philip Kuebler; Kishan J. Pandya; Robert H. Israel; Bruce C. Marshall; Douglass C. Tormey


Book ID
102671472
Publisher
John Wiley and Sons
Year
1986
Tongue
English
Weight
644 KB
Volume
57
Category
Article
ISSN
0008-543X

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โœฆ Synopsis


The authors have studied five cases of biopsy-proven pulmonary toxicity caused by the administration of mitomycin C (M), vincristine, and cisplatin in 64 patients with advanced non-small cell lung cancer. The clinical triad of progressive dyspnea, rales, and pulmonary infiltrates presented in all five cases. In addition, pulmonary function tests showed hypoxemia (four/five), reduced forced vital capacity (three/four), total lung capacity (two/three), and forced expiratory volume (FEVI) (three/four) and very profound reduction in diffusion capacity (three/three). Transbronchial biopsy for tissue examination was necessary to rule out other causes. Characteristics but nonspecific pathologic changes were documented in all five cases. All the patients responded quickly and dramatically to high-dose glucocorticoids with improvement of hypoxia, dyspnea, exercise tolerance, and sense of well being. In three patients the pulmonary infiltrates cleared. However, abrupt stopping or early withdrawal of steroid resulted in aggravation of dyspnea and pulmonary infiltrate in three cases who improved subsequently with escalation of steroid doses. The authors conclude that the treatment of choice for pulmonary toxicity induced by M or M-containing chemotherapy regimens is a high dose of glucocorticoid and discontinuation of M at once when suspicion is raised.


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