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2017, Volume 33, Number 1, Page(s) 062-065
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DOI: 10.5146/tjpath.2014.01228 |
Primary Pulmonary Mucinous (Colloid) Adenocarcinoma that Arose in the Cavernomyoplasty Area in a Patient with Tuberculosis: A Rare Case Report |
Neşe A. YENER1, Nesrin SARIMAN2, Mehmet M. ATASOY3, Ahmet MİDİ1, Alpay ÖRKİ4 |
1Department of Pathology, Maltepe University, Faculty of Medicine, İSTANBUL, TURKEY 2Department of Chest Disease, Maltepe University, Faculty of Medicine, İSTANBUL, TURKEY 3Department of Radiology, Maltepe University, Faculty of Medicine, İSTANBUL, TURKEY 4Department of Chest Surgery, Maltepe University, Faculty of Medicine, İSTANBUL, TURKEY |
Keywords: Lung neoplasms, Mucinous adenocarcinoma, Tuberculosis |
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Primary pulmonary mucinous (colloid) adenocarcinoma is a rare type
of lung cancer. Its arising in the cavernomyoplasty area has not been
reported before. We here describe a sixty-year-old man with a previous
history of multidrug-resistant and surgically-treated tuberculosis
who was diagnosed as primary mucinous adenocarcinoma in the
cavernomyoplasty site. We discuss the relevant literature on this rare
entity. |
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Primary pulmonary mucinous (colloid) adenocarcinoma is
a rare type of lung cancer with distinct histopathological
features 1,2. Its arising in the lung areas adjacent to the
tuberculosis sequela 3,4 or its arising in patients with
history of thoracoplasty 5 was reported in the literature.
However, its occurrence in the cavernomyoplasty site has
not been reported before. We here describe a sixty-yearold
man with a previous history of multidrug-resistant
and surgically-treated tuberculosis who has got primary
pulmonary mucinous adenocarcinoma that arose in the
cavernomyoplasty site. We discuss the relevant literature on
this rare entity. |
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Abstract
Introduction
Case Presentation
Disscussion
References
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A sixty-year-old man applied to our emergency service
with one-month history of cough, fever and weight
loss. He has got eight-pack-year history of smoking and
stopped smoking ten years ago. His past medical history revealed that he had been treated for multidrug-resistant
tuberculosis 30 years prior. Ten years after this, he applied
to the emergency service with massive hemoptysis. Due
to his insufficient cardiopulmonary reserve resulted from
extensive tuberculosis sequela, he didn't undergo anatomic
resection for the cavities but cavernomyoplasty to control
his hemoptysis. He continued to come for follow-up
for many years since his last referral to our hospital for
left-sided empyema. Sputum smear and pleural fluid
was microbiologically negative for tuberculosis bacilli.
Radiologically, the X-ray image revealed increased
pulmonary opacities and patchy consolidation of the left
lung (Figure 1A). CT scan and PET-CT fusion images
showed cavitations in the left lung (Figure 1B,C). These were
thick-walled cavitary mass lesions with air-fluid level. There
were also traction bronchiectasis, pleural and parenchymal
fibrotic changes that resulted in lung volume depletion,
highly suggestive findings for tuberculosis sequela in both
lungs (Figure 1B).
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Figure 1: A) X-ray image revealed increased pulmonary opacities
and patchy consolidation of the left lung. b,c) CT scan and PETCT
fusion images at the same level showed cavitary lesions in
the left lung. In figure 1b, traction bronchiectasis (arrows) and
pleural and parenchymal fibrotic changes, highly suggestive for
tuberculosis sequela in both lungs. In figure 1c, there is a cavitary
mass lesion with air-fluid level in the left lung. |
Then, the patient was undertaken video-assisted thoracoscopy
with the presumptive diagnosis of empyema.
Extensive debridement of the diffuse cavitary lesions of
the left lung was made. Grossly, the material was totally
gelatinous (Figure 2). Microscopically, it was an invasive
tumor composed of large pools of mucin with sparse
neoplastic cells floating within the mucin pools (Figure 3).
These cells were in goblet cell morphology in some areas
whereas they were in signet ring cell morphology in others.
 Click Here to Zoom |
Figure 2: Grossly, the resected material was almost totally
gelatinous. |
 Click Here to Zoom |
Figure 3: Large mucin pools destroying alveolar septae and
neoplastic cell clusters within them. |
Immunohistochemically, they were strongly positive for
CK20, CEA and MUC2 (Figure 4A-C) and negative for
CDX2 (Figure 4D), CK7 and TTF-1. The large mucin pools
of the tumor stained positively for CEA and MUC5AC (Figure 4E). Then, the specimen was entirely submitted
to show any granulomatous inflammation. There wasn't
any sign of granulomatous inflammation or tuberculosis
bacilli with Ziehl-Neelsen stain. The diagnosis of mucinous
adenocarcinoma (colloid carcinoma) was made. The case
was accepted as primary lung cancer after a careful systemic
investigation including CT, PET scan and colonoscopy
revealed no other abnormalities. No adjuvant therapy was
given. His postoperative course and two-year follow up was
uneventful without any sign of recurrence or metastasis.
 Click Here to Zoom |
Figure 4: Neoplastic cells were positive for (a) CK20, (b) MUC2,
(c) CEA; (D) and the tumor was negative for CDX2 (E) large
mucin pools were positive for MUC5AC. |
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Top
Abstract
Introduction
Case Presentation
Disscussion
References
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The coexistence of tuberculosis and the lung cancer was first
described by Bayle in 1810 5. Since then, there has been
several studies on this subject 3,4. The incidence of this
coexistency is reported as 2.1-30.2% 3,4. In these series,
the incidence of lung tuberculosis –either active or inactiveassociated
with the pulmonary adenocarcinoma is between
21.7%-56.1% 3,4. The subtype of adenocarcinoma was not
given in these series. It is concluded that post-tuberculosis
chronic inflammation resulting in deformation of bronchi
and alveoli, and the subsequent epithelial dysplasia might
be the risk factors for the development of lung cancer.
Chronic inflammation in the lung also causes goblet cell
proliferation by up-regulation of several mediators such as
interleukin-13 and several transcription factors 6.
On the other hand, Tamura et al reported their experience
on a series of patients who develop lung cancer after having
been operated on to treat their pulmonary tuberculosis5. In this series, male gender dominance (85%), high
rate of smoking habbit among them and finally, high rate
of having long interval (≥21 years) between the time of
thoracotomy and the lung cancer development in these
patients was reported as significant5. Our patient is a
sixty-year-old, a formerly heavy smoker man. This is an
interesting case because radiologically, the patient had signs
of tuberculosis sequela in both lungs and also had a tumor
developed at the area of cavernomyoplasty which was done
for the treatment of tuberculosis twenty years back. In
this context, we focus on the carcinogenesis triggered by
the cavernomyoplasty operation. It is possible that long
term deposition of carcinogens due to lymphostasis at the
operation site and also post-tuberculosis changes causing
destruction of bronchi and alveoli might have initiated the
malignant process. We think that chronic inflammation
might probably induced excessive goblet cell proliferation
and subsequently initiated this malignancy of mucinous
type.
According to the International Association for The Study
of Lung Cancer/American Thoracic Society/European
Respiratory Society Classification suggested in 2011,
mucinous (colloid) adenocarcinoma is suggested as a rare
low grade variant of invasive adenocarcinoma of the lung
composed of either tall-columnar goblet cells, signetring
cells or both1,2. The presence of abundant mucin
pools destructing the alveolar septae and having neoplastic
cells within these mucin pools is typical2. Metastatic tumor from a primary mucinous adenocarcinoma of the
alimentary tract, ovary, or pancreas to the lungs should be
ruled out by performing a careful systemic investigation.
Immunohistochemically, mucinous adenocarcinoma of
goblet cell type is usually positive for CK202. Although
less intense and diffuse than in conventional lung
adenocarcinoma, CK7 and TTF-1 positivity may be useful
for confirming the pulmonary origin2. In our case, large
mucin pools with neoplastic cells within were destructing
the alveolar septae in all areas. The tumor cells were negative
for CK7, TTF-1, CDX2 and positive for CK20, CEA and
MUC2. The large mucinous matrix stained positively for
MUC5AC. Hence, the immunostains were not useful
to rule out any metastatic lung disease. Intense clinical,
imaging and laboratory tests were employed to decide the
origin of the tumor as being the lung.
In conclusions; primary mucinous (colloid) adenocarcinoma
is a rare type of low grade malignancy of the lung.
Though rare, its arising in cavernomyoplasty site in patients
with history of lung tuberculosis should be kept in mind.
Differential diagnosis with metastatic colorectal adenocarcinoma
is also challenging and requires appropriate clinical
investigation especially when immunohistochemical findings
are deceiving. |
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Abstract
Introduction
Case Presentation
Discussion
References
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1) Travis WD, Brambilla E, Noguchi M, Nicholson AG, Geisinger
K, Yatabe Y, Powell CA, Beer D, Riely G, Garg K, Austin JH,
Rusch VW, Hirsch FR, Jett J, Yang PC, Gould M; American
Thoracic Society. International Association for the Study of
Lung Cancer/American Thoracic Society/European Respiratory
Society. International multidisciplinary classification of lung
adenocarcinoma: Executive summary. Proc Am Thorac Soc.
2011;8:381-5.
2) Rossi G, Murer B, Cavazza A, Losi L, Natali P, Marchini A, Capitanio
G, Brambilla E. Primary mucinous (so-called colloid) carcinomas
of the lung. A clinicopathologic and immunohistochemical study
with special reference to CDX-2 homeobox gene and MUC
expression. Am J Surg Pathol. 2004;28:442-52.
3) Cicënas S, Vencevièius V. Lung cancer in patients with
tuberculosis. World J Surg Oncol. 2007;5:22.
4) Dacosta NA, Kinare SG. Association of lung carcinoma and
tuberculosis. J Postgrad Med. 1991;37:185.
5) Tamura A, Hebisawa A, Hayashi K, Sagara Y, Kawabe Y,
Nagayama N, Machida K, Fukushima K, Yotsumoto H, Mori
M. Lung cancer in patients who had received thoracoplasty for
pulmonary tuberculosis. Jpn J Clin Oncol. 1999;29:541-5.
6) Turner J, Jones CE. Regulation of mucin expression in respiratory
diseases. Biochem Soc Trans. 2009;37:877-81. |
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Abstract
Introduction
Case Presentation
Discussion
References
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