Case Reports in Pulmonology
Volume 2012 (2012), Article ID 257827, 2 pages
EGFR-Mutant Lung Adenocarcinoma Mimicking a Pneumonia
1Medical Oncology Department, Hospital del Mar-Parc de Salut Mar, Passeig Maritim 25-29, 08003 Barcelona, Spain
2Radiology Department, IDIMAS-CRC, Hospital del Mar, Passeig Maritim 25-29, 08003 Barcelona, Spain
3PET Unit Molecular Imaging Center, CRC CIM-CRC Mar, Passeig Maritim 25-29, 08003 Barcelona, Spain
Received 3 April 2012; Accepted 13 July 2012
Academic Editors: F. L. Fimognari and M. Ip
Copyright © 2012 Álvaro Taus et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
PET-CT scan has demonstrated to be very effective in lung cancer diagnosis and staging, but lung cancer has multiple ways of presentation, which can lead to an error in diagnosis imaging and a delay on the beginning of specific treatment. We present a case of a 77-year-old man with an initial PET-CT scan showing high 18F-FDG intake, suggesting a bilateral pneumonia, who was finally diagnosed of an EGFR-mutant lung adenocarcinoma. EGFR-activating mutation allowed us to start treatment with the oral tyrosin kinase inhibitor Gefitinib, obtaining a rapid and sustained response. Histological confirmation of imaging findings is always necessary to avoid diagnostic errors.
Staging of nonsmall-cell lung cancer was one of the first approved indications for the use of positron emission tomography (PET) . Since 2001, combined PET and computed tomography (PET-CT scan) has rapidly replaced stand-alone PET and has become a key tool in the staging of lung cancer . Although Fluoro-2-deoxy-D-glucose (18F-FDG) has high sensitivity for cancerous conditions, there are benign processes that result in abnormal accumulation of and false positive images. These false positive results are due to conditions where 18F-FDG accumulation occurs in metabolically active tissue that is not cancerous, such as infection or inflammatory processes .
2. Case Report
We present a 77-year-old man, with no history of smoking, admitted to the emergency room with a 2 month history of malaise, shortness of breath, and weight loss. His medical history involved controlled heart failure, arterial hypertension, hypercholesterolemia, and obstructive sleep apnea syndrome. Blood count, liver, and renal functions were normal. Chest X-ray showed areas of consolidation in both lung bases, predominantly left.
A CT-scan of the chest demonstrated diffuse bilateral ground glass nodules, ill-defined areas of pulmonary opacities with “crazy-paving” pattern in right lower and middle lobes, and extensive air-space consolidation in left lung (Figures 1(a), 1(b), 1(c), and 1(d)). These findings suggested inflammatory or infectious process as first choice, being less likely neoplasic aetiology or organizing pneumonia.
The PET-CT scan (low-dose CT) reported an extensive and heterogeneous deposit of Fluoro-2-deoxy-D-glucose (18F-FDG) in both lungs with a maximum standardised uptake value (SUV) of 11.30, that correlated with morphological findings described on CT scan. In addition, hypermetabolic lymph nodes were detected in right supraclavicular, left mediastinal, and subcarinal regions (maximum SUV of 6,06). These PET-CT findings suggested as first choice a bilateral inflammatory or infectious process (Figure 2).
Bronchoscopy demonstrated serous secretions predominantly in the left bronchial tree. Bronchial aspirate, bronchoalveolar lavage, and bronchial biopsy resulted positive for adenocarcinoma. All bacteriological tests performed were negative.
In this case an activating mutation on exon 19 of epidermal growth factor receptor (EGFR) gene was found. Activating EGFR mutations derive in increase of response to EGFR tyrosin kinase inhibitors when comparing with standard chemotherapy [4, 5]. This finding allowed us to start treatment with the EGFR oral tyrosin kinase inhibitor Gefitinib. Rapid and sustained response was observed in the follow-up CT scan, and the patient remains on Gefitinib for 8 months without evidence of progression (Figures 1(e) and 1(f)) and excellent tolerance.
Lung cancer has multiple ways of presentation, which can lead to an error in diagnostic imaging, therefore histological confirmation is always necessary. Because EGFR-mutant tumours show lower 18F-FDG uptake in PET-CT scan , this case illustrates a rare presentation of EGFR-mutant lung adenocarcinoma with high 18F-FDG mutant lung adenocarcinoma.
In this case, with initial imaging/metabolic procedures suggesting bilateral inflammatory or infectious process, delay of histological confirmation would have had a negative impact in patient’s survival and quality of life.
Conflict of Interests
None of the authors have any conflict of interests to declare.
- J. McCann, “PET scans approved for detecting metastatic non-small-cell lung cancer,” Journal of the National Cancer Institute, vol. 90, no. 2, pp. 94–96, 1998.
- D. Lardinois, W. Weder, T. F. Hany et al., “Staging of non-small-cell lung cancer with integrated positron-emission tomography and computed tomography,” The New England Journal of Medicine, vol. 348, no. 25, pp. 2500–2507, 2003.
- K. D. M. Stumpe, H. Dazzi, A. Schaffner, and G. K. Von Schulthess, “Infection imaging using whole-body FDG-PET,” European Journal of Nuclear Medicine, vol. 27, no. 7, pp. 822–832, 2000.
- M. Maemondo, A. Inoue, K. Kobayashi et al., “Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR,” The New England Journal of Medicine, vol. 362, no. 25, pp. 2380–2388, 2010.
- T. Mitsudomi, S. Morita, Y. Yatabe et al., “Gefitinib versus cisplatin plus docetaxel in patients with non-small-cell lung cancer harbouring mutations of the epidermal growth factor receptor (WJTOG3405): an open label, randomised phase 3 trial,” The Lancet Oncology, vol. 11, no. 2, pp. 121–128, 2010.
- R. H. Mak, S. R. Digumarthy, A. Muzikansky et al., “Role of 18F-fluorodeoxyglucose positron emission tomography in predicting epidermal growth factor receptor mutations in non-small cell lung cancer,” The Oncologist, vol. 16, no. 3, pp. 319–326, 2011.