O Karacan1, F O Eyüboglu, S Akçay, O Ozyilkan. 1. Department of Pulmonary Diseases, Başkent University Faculty of Medicine, Ankara, Turkey. ozgurkaracan@yahoo.com
Abstract
BACKGROUND: Acute pulmonary toxicity in cancer patients treated with docetaxel has been reported in previous phase II studies and case reports. Unlike transient pulmonary infiltrates, it is demonstrated that docetaxel-induced interstitial pneumopathy is a severe clinical condition that generally leads to respiratory failure. CASE REPORT: We report a patient with breast cancer who received 2 cycles of docetaxel in 3-week intervals and developed respiratory failure. The clinical, pathologic, and radiographic data supported pulmonary toxicity caused by a hypersensitivity reaction to docetaxel as the most likely etiology. The patient developed the same symptoms and radiological findings after 1 cycle of paclitaxel administration. Unlike other more severe examples in the literature, this patient's condition did not require mechanical ventilation, and she recovered after corticosteroid treatment. CONCLUSION: The present case raises the possibility that taxanes, as a group of chemotherapeutic agents, may cause the same type of adverse reaction in the pulmonary parenchyma. The authors recommend that any patient who develops a taxane-induced pulmonary toxic reaction, not be rechallenged or treated with another agent of the same class.
BACKGROUND: Acute pulmonary toxicity in cancerpatients treated with docetaxel has been reported in previous phase II studies and case reports. Unlike transient pulmonary infiltrates, it is demonstrated that docetaxel-induced interstitial pneumopathy is a severe clinical condition that generally leads to respiratory failure. CASE REPORT: We report a patient with breast cancer who received 2 cycles of docetaxel in 3-week intervals and developed respiratory failure. The clinical, pathologic, and radiographic data supported pulmonary toxicity caused by a hypersensitivity reaction to docetaxel as the most likely etiology. The patient developed the same symptoms and radiological findings after 1 cycle of paclitaxel administration. Unlike other more severe examples in the literature, this patient's condition did not require mechanical ventilation, and she recovered after corticosteroid treatment. CONCLUSION: The present case raises the possibility that taxanes, as a group of chemotherapeutic agents, may cause the same type of adverse reaction in the pulmonary parenchyma. The authors recommend that any patient who develops a taxane-induced pulmonary toxic reaction, not be rechallenged or treated with another agent of the same class.