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Gefitinib‐induced interstitial lung disease showing improvement after cessation: Disassociation of serum markers
Author(s) -
KITAJIMA Hiroko,
TAKAHASHI Hiroki,
HARADA Kazutoki,
KANAI Akiko,
INOMATA ShinIchiro,
TANIGUCHI Haruko,
SAIKAI Toyohiro,
ABE Shosaku
Publication year - 2006
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2006.00835.x
Subject(s) - medicine , gefitinib , interstitial lung disease , lung , disease , pathology , lung cancer , oncology , epidermal growth factor receptor , cancer
Gefitinib (ZD1839), a small‐molecule epidermal growth factor receptor tyrosine kinase inhibitor, is an anticancer agent for patients with non‐small cell lung carcinoma. Recently, however, as a result of accumulating evidence, it has been recognized that gefitinib can give rise to lethal lung toxicity. The authors report a case of interstitial lung disease (ILD) induced by gefitinib, which improved promptly following cessation of the administration of the agent. Clinical signs suggesting a good prognosis were noted, namely, findings similar to acute eosinophilic pneumonia on CT and a disassociation in the elevation of specific serum markers of ILD. At the time of onset of ILD, serum concentrations of surfactant protein (SP)‐A and SP‐D were significantly increased, whereas that of KL‐6 was not increased. A previous study of three cases of lethal lung toxicity resulting from gefitinib administration revealed a significant and almost equal increase in KL‐6, SP‐A and SP‐D. These results suggest that SP‐A and SP‐D may be indicators of gefitinib‐induced ILD and that KL‐6 is a predictor of outcome. Using a combination of these markers may help to establish a differential prognosis in patients with gefitinib‐induced ILD.