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False-Positive Axillary Lymph Nodes Due to Silicone Adenitis on 18F-FDG PET/CT in an Oncological Setting

Journal of Thoracic Oncology, Volume 11, Issue 6, June 2016, Pages e73–e75

Abstract

The case of a 49-year-old transgender individual with a history of bilateral silicone breast implants and a right lung mass proven by biopsy to be a non–small cell lung cancer is presented. In addition to the primary malignancy, a positron emission tomography/computed tomography scan showed contralateral hypermetabolic adenopathy in the left axilla that was suggestive of nodal metastatic disease. Additional imaging and histological examination of the lymph nodes indicated silicone breast implant leakage and silicone adenitis as the underlying cause of the hypermetabolic axillary lymph node.

Case Report

A 49-year-old transgender (man to woman) smoker (40 pack-years) presented with coughing, dyspnea, and purulent sputum production. Clinical examination showed markedly lengthened expiration and wheezing. Chest radiography and computed tomography (CT) showed consolidation in the right lower lobe, and this consolidation did not resolve after antibiotic treatment. Bronchoscopy was performed, and the results of aspiration analysis and biopsy were negative for malignancy. Antibiotic treatment was continued for 2 weeks. A repeat CT scan showed that the consolidation in the right lower lobe had not changed significantly. F-18 Fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/CT scan was performed and showed the consolidation to be hypermetabolic (a maximal standardized uptake value [SUVmax] of 4.1) (Fig. 1). Furthermore, there was diffuse, moderately increased uptake of 18F-FDG around the left breast implant (Fig. 2) and two hypermetabolic lymph nodes in the left axilla (SUVmax of 4.7) (see Fig. 2). A repeat biopsy of the consolidation in the right lower lobe revealed an intermediate differentiated papillary adenocarcinoma of the lung. Digital mammography and ultrasound of the breasts showed bilateral silicone leakage of the prostheses. To evaluate for contralateral axillary lymph node metastatic disease, a biopsy was performed and revealed silicone vacuoles with a histiocytic reaction and absence of metastatic disease (Fig. 3).

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Figure 1

Maximum-intensity projection image (left), computed tomography image (top right), and non–attenuation-corrected positron emission tomography image (bottom right) of the hypermetabolic consolidation zone in the apical segment of the right lower lobe (black arrow).

 

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Figure 2

Axial computed tomography images (top row). Positron emission tomography images (middle row) of the thorax with visualization of diffuse hypermetabolism around the left breast implant (left image [yellow circle]) and visualisation of a hypermetabolic adenopathy in the left axillary region (right image). Fusion positron emission tomography/computed tomography image (bottom row [yellow circle]).

 

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Figure 3

Pathological findings from a left axillary lymph node (hematoxylin and eosin staining; magnification ×200 (top left) and ×400 (top right and bottom middle). The top left image shows lymph node architecture disturbed by large and smaller empty vacuoles where there was silicone inside before the washing process. There are still some small hyperchromatic lymphocytes in the background. The top right image represents a larger, pale-staining giant cell (yellow circle) with multiple nuclei in the periphery and with an intracytoplasmic vacuole in the lower part of the cell. The bottom middle image represents some histiocytes (yellow circles) with many intracytoplasmic phagocytic vacuoles.

 

Discussion

In this case, given the context of an oncological diagnosis and increased 18F-FDG uptake in the contralateral axillary lymph nodes suggestive of nodal metastatic disease, a biopsy was performed and revealed silicone adenitis. This entity consists of inflammatory lymph nodes containing free silicone surrounded by inflammatory cells (most often macrophages), and in this case, it is due to silicone leakage from the breast implants as confirmed by morphological imaging.1, 2, and 3 This case confirms previous reports that contralateral axillary lymph node involvement in the presence of an underlying lung carcinoma is rare. It has been postulated that there are different pathways for malignancy to disseminate to the contralateral axillary lymph nodes, although the most likely mechanism appears to be through intercostal lymphatics from mediastinal nodal metastasis.4 In the staging of non–small cell lung cancer, a single extrathoracic hypermetabolic focus on a PET/CT scan is potentially a metastasis and typically indicates nonresectable (M1b) disease. Accordingly, this finding requires careful clinical correlation, as well as additional imaging or biopsy to determine the diagnosis, clinical stage, and appropriate treatment. In this regard, a patient should not be denied the opportunity for curative treatment without appropriate evaluation.5 Specifically, the disease of the patient whose case is presented was staged by PET/CT scan as stage IV (M1b) but was determined to be at clinical stage of Ib (T2aN0M0) after tissue confirmation of benign pathology in a left axillary lymph node.

References

  • 1 S.L. Brown, B.G. Silverman, et al. Rupture of silicone-gel breast implants: causes, sequelae and diagnosis. Lancet. 1997;350:1531-1537 Crossref
  • 2 C.J. Chen, B.F. Lee, et al. A false positive 18F-FDG PET/CT scan caused by breast silicone injections. Korean J Radiol. 2009;10:194-196 Crossref
  • 3 V. Helyar, C. Burke, et al. The ruptured PIP breast implant. Clin Radiol. 2013;68:845-850 Crossref
  • 4 H. Satoh, H. Ishikawa, et al. Axillary lymph node metastasis in lung cancer. Med Oncol. 2009;26:147-150 Crossref
  • 5 G.A. Silvestri, A.V. Gonzalez, et al. Methods for staging non-small cell lung cancer: diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013;143:e211s-e250s Crossref

Footnotes

a Department of Nuclear Medicine, Algemeen Ziekenhuis Groeninge, Reepkaai 4, 8500 Kortrijk, Belgium

b Department of Nuclear Medicine, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium

c University of Leuven, Kulak, Etienne Sabbelaan 53, 8500 Kortrijk, Belgium

d Department of Pathology, Algemeen Ziekenhuis Groeninge, President Kennedylaan 4, 8500 Kortrijk, Belgium

Corresponding author. Address for correspondence: Ludovic D’hulst, MD, AZ Groeninge, Reepkaai 4, 8500 Kortrijk, Belgium.

Disclosure: The authors declare no conflict of interest.

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