Gefitinib-induced interstitial lung disease-addition of intravenous cyclophosphamide to corticosteroids is a valuable treatment option: A case report

Goto, Yasushi; Hojo, Masayuki; Takeda, Yuichiro; Kobayashi, Nobuyuki; Kudo, Kohsuke

doi:10.1007/s12032-009-9280-2

Cited by 3 publications

(3 citation statements)

References 8 publications

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“…Previous reported cases of gefitinib-induced ILD have typically been treated with a high-dose of corticosteroids (intravenous injection of 1 g/day methylprednisolone for three consecutive days, followed by 50 or 60 mg/day oral prednisone, which is reduced by 10 mg/week) or with the cessation of gefitinib administration, which result in ILD recovery or mortality (9,11). Intravenous cyclophosphamide has also been reported as a valid treatment (10). In the present study, gefitinib was discontinued immediately following the onset of ILD, and a low-dose of corticosteroids were administered at an early stage.…”

Section: Case Reportmentioning

confidence: 99%

“…However, gefitinib treatment may result in a number of severe adverse effects, including the development of interstitial lung disease (ILD) (3)(4)(5)(6)(7). Although certain studies have been conducted on the safety of re-administering gefitinib to patients who were suspected of suffering from gefitinib-induced ILD, no precise management strategy has been established for such cases (8)(9)(10)(11). The present study reports the case of a patient with lung adenocarcinoma, initially responding to gefitinib treatment.…”

Section: Introductionmentioning

confidence: 98%

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Re-administration of gefitinib following diffuse interstitial lung disease in a patient with advanced lung adenocarcinoma: A case report and review of the literature

Zhang

Zhu

et al. 2015

Oncology Letters

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Abstract. Interstitial lung disease (ILD) is a severe adverse effect of gefitinib treatment. Re-administration of gefitinib to patients suspected of suffering from gefitinib-induced ILD requires cautious consideration. In the majority of cases, gefitinib is not re-administered to such patients. The present study reports a case of advanced lung adenocarcinoma, where the patient developed gefitinib-induced ILD and gefitinib was re-administered at 3.5 months after discontinuation of gefitinib treatment. Initially, the patient achieved partial clinical remission, but developed diffuse ILD following gefitinib administration for 5 months. Following the onset of ILD, gefitinib was discontinued immediately and low-dose corticosteroids were administered at the early stages of ILD. Subsequent to recovery from the lung injury, gefitinib was re-administered along with N-acetylcysteine. The patient presented with good lung adenocarcinoma control and did not experience a recurrence of ILD for >16 months. Thus, early discontinuation and gefitinib re-administration with N-acetylcysteine may be a potential novel treatment strategy for gefitinib-induced ILD.

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Section: Case Reportmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Re-administration of gefitinib following diffuse interstitial lung disease in a patient with advanced lung adenocarcinoma: A case report and review of the literature

Zhang

Zhu

et al. 2015

Oncology Letters

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“…Comedication with GCs as prophylaxes have been highly recommended for alleviation of severe side effects caused by chemotherapeutic drugs [11, 12]. In contrast to chemotherapy, systemic administration of GCs is not a standard practice for managing adverse reactions caused by gefitinib treatment in NSCLCs, with the exception of critical conditions such as interstitial lung disease [13–16]. However, we observed from the NHI claims database that more than a quarter of patients (26.5%) were co-medicated with oral form GCs, including dexamethasone, methylprednisolone and prednisolone, during the course of gefitinib treatment.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids may compromise the effect of gefitinib in non-small cell lung cancer

et al. 2016

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The epidermal growth factor receptor (EGFR)-targeting tyrosine kinase inhibitors (TKIs) have shown remarkable benefits in non-small cell lung cancer (NSCLC) patients with drug-sensitive mutations in the EGFR gene. Responsive patients are usually continuously prescribed with TKIs until disease progression. Glucocorticoids (GCs) are potent homeostasis maintaining drugs and are frequently used in cancer patients to alleviate discomforts caused by anti-cancer therapies. Several previous studies reported that concomitant use of GCs may compromise the efficacy of chemo-therapeutics in patients with solid tumors. Little is known in the concomitant use of target therapy with GCs in treating NSCLC. In this study, we hypothesized that concomitant use of GCs in EGFR-TKI therapy may be detrimental and addressed this issue using cell cultures and xenograft studies followed by a retrospective population study based on data from the Taiwan national health insurance system. In cell cultures and xenograft studies, GCs were shown to unequally compromise the anti-cancer efficacy of TKIs in both PC9 and NCI-H1975 NSCLC cells models. In the retrospective population study, patients with similar disease status that were co-medicated with GCs had a significantly higher risk of disease progression.

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Gefitinib-induced interstitial pneumonia: A case report and review of the literature

Luo¹,

Lv²,

Li³

et al. 2014

Experimental and Therapeutic Medicine

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The aim of this study was to explore the clinical characteristics of and treatment strategies for interstitial pneumonia induced by gefitinib in patients with advanced non-small cell lung cancer (NSCLC). The detailed clinical data of one patient with NSCLC and gefitinib-induced interstitial pneumonia were compiled and a review of relevant previous studies was performed. Based on this case report and the review, the clinical characteristics, mechanisms and treatment strategies of this rare disease were analyzed. The analyses showed that older, male patients with a long smoking history, high smoking index and adenocarcinoma (particularly bronchoalveolar carcinoma) were more likely to suffer from interstitial pneumonia while taking gefitinib. The onset time of interstitial pneumonia was 1–2 months subsequent to gefitinib administration. The clinical manifestations included chest tightness, shortness of breath, progressive dyspnea, severe hypoxemia and respiratory failure. Diffuse infiltration and alveolar interstitial shadows were observed on the chest tomography scan. In such circumstances, a timely judgment is required, in addition to the withdrawal of gefitinib treatment and the administration of high-dose glucocorticoids, as well as oxygen inhalation and anti-infective therapies, in order to relieve the symptoms. In conclusion, following the onset of gefitinib-induced interstitial pneumonia, the discontinuation of gefitinib is likely to alleviate the suffering of the majority of patients. Early interstitial pneumonia is not an absolute index for the permanent discontinuation of gefitinib treatment. It is necessary to comprehensively consider the benefits and hazards of gefitinib for the patients.

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Gefitinib-induced interstitial lung disease-addition of intravenous cyclophosphamide to corticosteroids is a valuable treatment option: A case report

Cited by 3 publications

References 8 publications

Re-administration of gefitinib following diffuse interstitial lung disease in a patient with advanced lung adenocarcinoma: A case report and review of the literature

Re-administration of gefitinib following diffuse interstitial lung disease in a patient with advanced lung adenocarcinoma: A case report and review of the literature

Glucocorticoids may compromise the effect of gefitinib in non-small cell lung cancer

Gefitinib-induced interstitial pneumonia: A case report and review of the literature

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