Diffuse Lung Disease: Student/Resident Case Report Poster - Diffuse Lung Disease |

Oxaliplatin-Induced Exacerbation of Idiopathic Pulmonary Fibrosis FREE TO VIEW

Evan Orlikow, MD; Marcus Blouw, MD
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Internal Medicine, University of Manitoba, Winnipeg, MB, Canada

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):515A. doi:10.1016/j.chest.2016.08.529
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SESSION TITLE: Student/Resident Case Report Poster - Diffuse Lung Disease

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM

INTRODUCTION: FOLFOX (5-fluorouracil, leucovorin, and oxaliplatin) is a common chemotherapy regimen for colorectal adenocarcinoma. Preliminary research demonstrated gastrointestinal, neurologic and hematologic side effects1. Subsequent literature revealed that interstitial lung disease (ILD) occurs or is exacerbated by FOLFOX in 0 to 4.2% of cases with oxaliplatin having been established as the causative agent by process of exclusion1,2. We now present a unique case of reversible exacerbation of Idiopathic Pulmonary Fibrosis (IPF) after administration of oxaliplatin.

CASE PRESENTATION: A 64-year-old female with IPF was diagnosed with stage IIIa cecal adenocarcinoma. Prior to the diagnosis of cancer, her IPF was characterized by stable dyspnea (MRC class 1-2), bibasilar and sub-pleural reticular opacities with traction bronchiectasis on CT scan, and mild lung volume restriction and moderate diffusion impairment on pulmonary function testing (PFT). The patient underwent right hemi-colectomy and received FOLFOX adjuvant chemotherapy. After six cycles of FOLFOX her dyspnea worsened dramatically (MRC Class 4). Further chemotherapy was suspended. PFT’s revealed a significant deterioration of her diffusing capacity and lung volumes. CT scan demonstrated air-bronchograms and traction bronchiectasis bilaterally. Bronchoscopy did not reveal evidence of infection, malignancy, or endobronchial pathology. Antimicrobials failed to provide relief. By process of exclusion, the deterioration was attributed to oxaliplatin. Subsequently her symptoms and PFT abnormalities returned to baseline. Open lung biopsy then demonstrated usual interstitial pneumonitis, consistent with the prior clinico-radiologic diagnosis of IPF.

DISCUSSION: Respiratory deterioration in known cases of IPF can be due to infection, heart failure, progression of IPF, or acute interstitial pneumonitis (AIP). In our case, infection and heart failure were excluded by clinical investigations. The reversible course excludes progression of IPF. Although AIP was considered, treatment with high-dose corticosteroids was not initiated due to concerns about side effects. While a prior case of oxaliplatin-exacerbated ILD responded to corticosteroids, it is uncertain whether corticosteroids would have been beneficial in this case2.

CONCLUSIONS: This case demonstrates the potential for oxaliplatin to induce rapid exacerbation of pre-existing IPF. However, clinical recovery can be achieved with prompt discontinuation of the offending agent. This case highlights the importance of close surveillance of patients with IPF while on oxaliplatin-containing chemotherapy.

Reference #1: Wilcox, B.E., et al. 2008. Exacerbation of pre-existing interstitial lung disease after oxaliplatin therapy: a report of three cases. Respiratory Medicine. 102(2). 273-279.

Reference #2: Park, C.K., et al. 2013. Multiple Cancers in a Patient with Systemic Sclerosis and Aggravated Interstitial Lung Disease by Chemotherapy. Tuberculosis and Respiratory Diseases. 75(3). 111-115.

DISCLOSURE: The following authors have nothing to disclose: Evan Orlikow, Marcus Blouw

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