Crizotinib Associated with Ground-Glass Opacity Predominant Pattern Interstitial Lung Disease: A Retrospective Observational Cohort Study with a Systematic Literature Review

Créquit, Perrine; Wislez, Marie; Feith, Jocelyne Fleury; Rozensztajn, N.; Jabot, L.; Friard, S.; Lavolé, A.; Gounant, V.; Fillon, Julie; Antoine, Martine; Cadranel, Jacques

doi:10.1097/jto.0000000000000577

Cited by 49 publications

(43 citation statements)

References 31 publications

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“…Consequently, we anticipate that, due to the large diffusion of these treatments, most clinicians will have to deal with this side-effect. ICI-ILD appears to be more frequent than is observed with other drugs used to treat NSCLC, such as pemetrexed, erlotinib, gefitinib, docetaxel, gemcitabine or crizotinib [21][22][23][24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Immune-checkpoint inhibitors associated with interstitial lung disease in cancer patients

et al. 2017

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Immunotherapy is becoming a standard of care for many cancers. Immune-checkpoint inhibitors (ICI) can generate immune-related adverse events. Interstitial lung disease (ILD) has been identified as a rare but potentially severe event.Between December 2015 and April 2016, we conducted a retrospective study in centres experienced in ICI use. We report the main features of ICI-ILD with a focus on clinical presentation, radiological patterns and therapeutic strategies.We identified 64 (3.5%) out of 1826 cancer patients with ICI-ILD. Patients mainly received programmed cell death-1 inhibitors. ILD usually occurred in males, and former or current smokers, with a median age of 59 years. We observed 65.6% grade 2/3 severity, 9.4% grade 4 severity and 9.4% fatal ILD. The median (range) time from initiation of immunotherapy to ILD was 2.3 (0.2−27.4) months. Onset tended to occur earlier in lung cancer versus melanoma: median 2.1 and 5.2 months, respectively ( p=0.02). Ground-glass opacities (81.3%) were the predominant lesions, followed by consolidations (53.1%). Organising pneumonia (23.4%) and hypersensitivity pneumonitis (15.6%) were the most common patterns. Overall survival at 6 months was 58.1% (95% CI 37.7-73.8%).ICI-ILD often occurs early and displays suggestive radiological features. As there is no clearly identified risk factor, oncologists need to diagnose and adequately treat this adverse event.This article has supplementary material available from

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Section: Discussionmentioning

confidence: 99%

Immune-checkpoint inhibitors associated with interstitial lung disease in cancer patients

et al. 2017

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“…Chest CT shows a predominant GGO pattern, which is localized and faint. Some cases of successful crizotinib retreatment after crizotinib-induced ILD have been reported, but they all had the non-DAD pattern (6,7). Retreatment with crizotinib should be avoided in patients with the DAD pattern, as the mortality rate of such patients is very high.…”

Section: Discussionmentioning

confidence: 99%

Alectinib as a treatment option following recovery from crizotinib-induced interstitial lung disease in patients with anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer

Nukaga

Naoki

Kamo

et al. 2016

Molecular and Clinical Oncology

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Abstract.Crizotinib is a tyrosine kinase inhibitor that displays antitumor activity against anaplastic lymphoma kinase (ALK)-positive advanced non-small-cell lung cancer. However, crizotinib-associated interstitial lung disease (ILD) has been reported as an infrequent, but potentially fatal complication. We herein describe the case of a 63-year-old male patient with ALK-rearranged advanced lung adenocarcinoma. Chest computed tomography (CT) revealed extensive bilateral ground-glass opacity and airspace consolidation with traction bronchiectasis on day 27 of crizotinib therapy. No signs of infection or left heart failure were identified and we considered the lesions to be consistent with crizotinib-induced ILD. Following corticosteroid treatment and discontinuation of crizotinib, CT revealed improvement of ILD, but also showed regrowth of the tumor. Alectinib, a novel alternative ALK inhibitor, was initiated, and has been successfully continued, with neither disease progression nor recurrence of ILD. The present case indicates that alectinib may be considered as an alternative agent in cases of crizotinib-induced ILD, irrespective of the pattern of ILD, i.e., a diffuse alveolar damage (DAD) or non-DAD pattern, with careful observation. IntroductionCrizotinib is a tyrosine kinase inhibitor that has antitumor activity against anaplastic lymphoma kinase (ALK)-positive advanced non-small-cell lung cancer (NSCLC) (1). However, crizotinib-associated interstitial lung disease (ILD) has been reported as an infrequent but potentially fatal complication (2,3).Alectinib is a novel oral ALK inhibitor with high potency and selectivity for ALK, which displays promising antitumor activity in NSCLC. Alectinib has shown promising activity in patients with crizotinib-resistant disease and has been generally well-tolerated in clinical trials (4,5). The safety of alectinib for patients who develop crizotinib-induced ILD has not been determined. We herein describe a case of ALK-positive NSCLC successfully treated with alectinib after developing crizotinib-induced ILD. Case reportA 63-year-old Japanese man with a 25 pack-year smoking history presented with a 4-month history of cough. The patient was diagnosed with advanced lung adenocarcinoma (cT4N3M1b), with bone, brain and multiple lymph node metastases (Fig. 1A). Fluorescence in situ hybridization analysis revealed the presence of ALK gene rearrangement. Crizotinib (250 mg twice daily) was administered as first-line chemotherapy. On day 27, the patient developed high-grade fever and exertional dyspnea. Chest computed tomography (CT) revealed a decrease in tumor size; however, there was new extensive bilateral ground-glass opacity (GGO) and airspace consolidation with traction bronchiectasis (Fig. 1B). With the patient on oxygen at a flow rate of 5 l̸min via a mask, the arterial blood gas analysis revealed a PaO 2 of 48.5 mmHg. Although the chest CT revealed bilateral pleural effusions, there was no evidence of left heart failure. There were also no signs of infection. Based on thes...

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“…• des traitements particuliers : [34,35], le crizotinib [36,37], la gemcitabine [3] et le nivolumab [18] ; -en milieu non oncohématologique : le méthotrexate, l'ibuprofène, l'aténolol, l'intoxication chronique à l'aspirine.…”

Section: Pneumopathies Alvéolaires Aiguësunclassified

“…En milieu oncologique, les pneumopathies interstitielles aiguës ou subaiguës sont observées avec les chimiothérapies (le méthotrexate, le melphalan, la bléomycine, le cyclophosphamide, la gemcitabine, la carmustine, le docétaxel, la mitomycine, le chlorambucil, le nilutamide, l'hydroxyurée, l'idélalisib), un grand nombre inhibiteur des tyrosines kinases (gefitinib, sorafénib, sunitinib, erlotinib, crizotinib…) [9,14,22,36], les inhibiteurs des points de contrôle de l'immunité (nivolumab…) [12,18], les anticorps monoclonaux (rituximab [près de 4 % des patients traités pour un lymphome non hodgkinien] [41], le trastuzumab), et les inhibiteurs de la voie de signalisation mTOR [15]. Les pneumopathies radiques, apparaissant généralement trois semaines à six mois après la fin de l'irradiation, répondent à ce cadre sémiologique, mais s'en individualisent par des lésions très focalisées aux champs d'irradiation.…”

Section: Pneumopathies Interstitielles Aiguës Et Subaiguësunclassified

“…L'évolu-tion de ces IRAM est en réalité difficilement prévisible ; dans notre expérience, le recours à la corticothérapie est fré-quent avec une efficacité d'autant plus importante que son initiation est précoce [16]. Dans la littérature, notamment japonaise, des fortes doses (500 mgr-1 gr j1-j3 avec un relais à 1 mgr/kg par jour) sont rapportées, en tout cas, recommandées en cas d'hémorragie intra-alvéolaire [36]. Nous utilisons plutôt de fortes doses les trois premiers jours puis nous diminuons à 1 mgr/kg avec ensuite une décrois-sance d'autant plus lente que le médicament a une longue demi-vie ; ainsi pour l'amiodarone la durée de traitement pourra être de six mois.…”

Section: Quel Traitement ?unclassified

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Toxicité pulmonaire des médicaments : ce que le réanimateur doit connaître ?

Parrot

Gibelin

Issoufaly

et al. 2018

Méd. Intensive Réa.

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Résumé Le diagnostic d'insuffisance respiratoire aiguë d'origine médicamenteuse est un véritable défi. Les traitements à l'origine d'une toxicité pulmonaire sont très nombreux. Les nouveaux traitements, notamment en oncohématologie (thé-rapie ciblée, immunothérapie), ne sont pas en reste. L'expression clinique très hétérogène est sous-tendue par des mécanis-mes lésionnels très différents. Après avoir écarté une infection ou un oedème pulmonaire, il faut savoir évoquer une pneumopathie médicamenteuse. La réalisation d'un scanner thoracique et d'une fibroscopie bronchique avec lavage bronchoalvéolaire peut être utile pour exclure une pathologie infectieuse et suggérer une pathologie médicamenteuse. Le traitement est l'arrêt du médicament et repose fréquemment dans ces formes graves sur une corticothérapie. Mots clés Détresse respiratoire · Pneumopathie médicamenteuse · Toxicité pulmonaireAbstract Acute respiratory failure related to drug toxicity is challenging. Several drugs, also including targeted therapy and immunotherapy, have been reported to induce lung toxicity. Clinical and pathological presentations are heterogeneous suggesting different toxicity pulmonary mechanisms. Infection or pulmonary edema should be ruled out, and then drug-induced pneumonitis diagnosis should be considered. CT scan and bronchoscopy with bronchoalveolar lavage are helpful for the disease diagnosis. Due to the severity, the identified drug should be stopped and more frequently steroids should be started.

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Crizotinib Associated with Ground-Glass Opacity Predominant Pattern Interstitial Lung Disease: A Retrospective Observational Cohort Study with a Systematic Literature Review

Cited by 49 publications

References 31 publications

Immune-checkpoint inhibitors associated with interstitial lung disease in cancer patients

Immune-checkpoint inhibitors associated with interstitial lung disease in cancer patients

Alectinib as a treatment option following recovery from crizotinib-induced interstitial lung disease in patients with anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer

Toxicité pulmonaire des médicaments : ce que le réanimateur doit connaître ?

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