Lung cancer remains the leading cause of malignancy-related mortality worldwide, with over one million cases diagnosed yearly (1). Non-small-cell lung cancer (NSCLC) accounts for >80% of all lung cancers. Because it is typically diagnosed at an advanced stage, chemotherapy (CT) remains the cornerstone of treatment, however, conventional treatment of NSCLC has apparently reached a plateau of effectiveness in improving survival of patients. For better toxicity profile than conventional CT, molecular targeted therapies for cancer become a new therapeutic areas in recent years. Gefitinib (Iressa) is an Epidermal Growth Factor Receptor Type 1/tyrosine kinase (HER1/EGFR) inhibitor and block the signal transduction pathway implicated in the proliferation and survival of cancer cells (2,3). The development of gefitinib in the treatment of advanced non-small-cell-lung cancer (NSCLC) raised a great enthusiasm among physicians. Gefitinib is well tolerated and less toxic compared to conventional cytotoxic drugs, but gefitinibrelated interstitial lung disease (ILD) has been reported as a serious adverse effect (4). Here, we reported a case of acute lung injury induced by gefitinib that was detected in the early phase with high-resolution (HR) CT, and successfully treated with corticosteroid and BIPAP assisted ventilation therapy.

A 63-year-old man presented with cough and dyspnoea on exertion. He had been previously healthy until adenocarcinoma in the left upper lung with ipsilateral malignant pleural effusion and left pulmonary HLN (hilar lymph node) and left supraclavicular lymph node and mediastinal lymph nodes metastasis (T1N3M1a, stage IV) was diagnosed in May 2010. He received combined chemotherapy with bevacizumab (Avastin) 400 mg d0/3 weeks and gemcitabine 1,600 mg d1, 8/3 weeks and carboplatin 500 mg d1/3weeks for 6 courses. At the same time, left-sided intrathoracic instillation of OK-432 was given. Disease progression on chest CT scan was recognized in December 2010. Daily treatment with oral gefitinib (250 mg/ day) was commenced. At this time his CT scan showed no lung tissue abnormality in the right upper lobe (Figure 1). The patient then received gefitinib (250 mg/day) on December 20, 2010. However, aggravated dyspnea on exertion with a dry cough developed after 7 days of gefitinib treatment. Hypoxemia and a 75% of oxyhemoglobin saturation at rest were measured by pulse oximetry. The body temperature was 37.0 ℃; pulse rate was 100 beats/min and the blood pressure was 135/85 mmHg. Arterial blood gas analysis at rest (FiO₂ =0.29) were illustrated in Table 1 (Values 1). Leucocyte cell count was 1.0×10⁴/mm³ with 77% neutrophils. All cultures and stains for infectious etiologies including common bacteria, fungi, pneumocystis, legionella, nocardia, viruses were negative. Chest CT revealed ground glass opacity (GGO) in the right upper lobe (Figure 2), which suggesting an acute interstitial pneumonia. He was admitted under the impression of gefitinib-related interstitial pneumonitis. After admission, gefitinib was discontinued immediately and methylprednisolone 80 mg/day was started. At the same time, BIPAP assisted ventilation was used. The Ventilator parameters were: IPAP 12 cmH₂O, EPAP 4 cmH₂O, FiO₂ 75%, R 18 bpm. Dyspnoea and cough were resolved 7 days after commencement of treatment with methylprednisolone and BIPAP assisted ventilation, and a chest CT taken 10 days after the start of treatments demonstrated a scar-like lesion without GGO in the right upper lobe (Figure 3). Arterial blood gas analysis in room air (FiO₂ =0.29) were illustrated in Table 1 (Values 2). The daily dosage of prednisolone was decreased by 20 mg per day depending on the patient’s response. The patient was followed up for 2 months after the start of treatment with corticosteroids and remained well.

Disclosure: The authors declare no conflict of interest.