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SHORT COMMUNICATION
Year : 2016  |  Volume : 5  |  Issue : 1  |  Page : 80-82

A case of tuberculosis and adenocarcinoma coexisting in the same lung lobe


Houston Medical Center, Warner-Robins, GA, USA

Date of Web Publication8-Feb-2017

Correspondence Address:
Ayman Rihawi
Infectious Disease Clinic, 104 Borders Way, Suite 400, Warner-Robins, GA 31088
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.ijmyco.2015.07.001

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  Abstract 


Tuberculosis and lung cancer rarely coincide together but have been proven to have a definitive link. In this case we describe tuberculosis and adenocarcinoma diagnosed together in the same lobe of the lung. The patient was found to have an epidermal growth factor receptor exon 19 deletion, which has been shown to have an association with tuberculosis.

Keywords: Communicable diseases, Adenocarcinoma, Tuberculosis


How to cite this article:
Rihawi A, Huang G, Al-Hajj A, Bootwala Z. A case of tuberculosis and adenocarcinoma coexisting in the same lung lobe. Int J Mycobacteriol 2016;5:80-2

How to cite this URL:
Rihawi A, Huang G, Al-Hajj A, Bootwala Z. A case of tuberculosis and adenocarcinoma coexisting in the same lung lobe. Int J Mycobacteriol [serial online] 2016 [cited 2019 Mar 24];5:80-2. Available from: http://www.ijmyco.org/text.asp?2016/5/1/80/199747




  Introduction Top


Tuberculosis (TB) and lung cancer are common diseases that cause substantial morbidity and mortality worldwide [1]. Although the two rarely occur together, a relationship has been established between them. A study conducted by the National Cancer Institute found that patients with pulmonary TB had increased risk of lung cancer [2] and another estimated a twofold elevation in risk of lung cancer in men with TB [1]. The coexistence of TB and lung cancer is estimated at ~2% [3],[4] and typically found in the upper lobes [5]. Here, we describe a case of TB and adenocarcinoma coexisting in the same lung lobe.


  Case report Top


A 44-year-old African-American male presented to the emergency room with a one-day history of nausea and fever. He had no history of significant medical ailments and did not smoke. An initial exam indicated that he was afebrile, had blood pressure of 196/111 mmHg, a pulse of 103 beats/min, respiratory rate of 18 breaths/min, and an oxygen saturation of 98%. His physical examination was normal, with no abnormalities on auscultation of the lungs. Laboratory studies indicated an elevated white blood cell count of 10.9×103 cells/μL (local control=3.8–10.7×103 cells/μL) with 81.5% neutrophils (local control=40–79%). C-reactive protein was also elevated at 4.089 mg/dL (local control<0.748 mg/dL).

A chest X-ray showed a suspicious right upper lobe mass with fullness in the right hilum ([Figure 1]). Computer topography scanning without contrast enhancement showed a soft tissue mass ([Figure 2]) along with a soft tissue lesion in the right hilum and multiple lytic lesions in the vertebrae, left-humeral head, and sternum. A bone scan to isolate the lytic lesions was performed using 25 millicurie Technetium-99 medronic acid, with results showing multiple foci of increased uptake. Given the location, bronchoscopy was performed to obtain a tissue biopsy of the right upper lobe mass. This showed invasive adenocarcinoma classified as Stage IV due to distal metastasis to the bone [6]. Epidermal growth factor receptor (EGFR) tyrosine kinase domain mutations were then evaluated in exons 18–21, with a mutation subsequently detected in exon 19. Based on genomic results, he began taking 150 mg erlotinib daily to treat the cancer.
Figure 1: Chest X-ray showing a 3.9 cm × 4.5 cm mass in the right upper lobe with mild fullness of the right hilum (circled).

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Figure 2: Computer topography scan of the chest showing a 5.0 cm × 3.2 cm mass in the right upper lobe with spiculated margins (circled).

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Pooled lung secretions from the surrounding area were collected and cultured to isolate acid-fast bacilli. QuantiFERON-TB Gold In-Tube test (QFT-G; Cellestis Limited, Carnegie, Victoria, Australia) was negative, however, direct amplification of rRNA using the Amplified Mycobacterium Tuberculosis Direct test (MTD; Gen-Probe, San Diego, CA, USA), returned positive results. The presence of Mycobacterium tuberculosis was confirmed using the BACTEC MGIT 960 Mycobacterial Detection System (Becton Dickson Diagnostic Systems, Sparks, Maryland, United States) based on susceptibility to isoniazid, rifampin, and ethambutol. The patient was then placed on 750 mg levofloxacin, 300 mg isoniazid, 50 mg pyridoxine, 2000 mg pyrazinamide, and 1600 mg ethambutol daily for tuberculosis (TB). This particular drug regimen was chosen given that rifampin, a first-line TB treatment [7], reduces erlotinib efficacy [8]. The patient began taking levofloxacin instead, which has similar efficacy in patients lacking tolerance for rifampin [7].


  Discussion Top


Pathogenesis of coexisting TB and lung cancer remains unclear. One hypothesis suggests that the tumor arises from a previous TB lesion called a scar cancer [4]. Additionally, TB may cause sustained inflammation leading to fibrosis, scarring, and host-tissue damage [1]. The fibrosis from the old TB lesion may cause lymphostasis, enhancing carcinogen deposition in the area [4]. Given the distal metastasis found in this patient, we felt that surgery was not appropriate. The diagnosis of scar cancer is typically made following tumor resection [5], so we were unable to determine if this was indeed the case.

There are many other theories concerning the relationship between TB and lung cancer. One is that TB mycobacterial cell wall components may induce nitric oxide production and reactive oxygen species, both implicated in carcinogenesis [9]. Another suggests that carcinoma may reactivate TB [5]. We were unable to determine disease chronology in this patient, given that TB and lung cancer were discovered simultaneously.

There may be a link between pulmonary TB and adenocarcinomas displaying the same mutation present in our patient. Data show that patients with old TB lesions have a statistically significant association with the EGFR mutation, specifically in exon 19, as compared with patients with lung adenocarcinoma without TB [10]. This same study also demonstrated that a higher proportion of patients with EGFR mutations and exon 19 deletion displayed lung cancer and old TB lesions within the same lobe or the same side of the lung as compared with patients having cancer and TB lesions located on opposite sides [10].

One of the most interesting results associated with this patient was the negative QFT-G. We believe this was a false-negative result. The high specificity for the test is 96–99%, however, the sensitivity is 81–89% [11]. Furthermore, our patient displayed pooled secretions identified as M. tuberculosis by direct amplification of rRNA using an MTD test kit with a specificity of 98.9% [12]. Carcinomas of the head, neck, and lung display decreased response to the tuberculin skin test in patients with TB. These conditions may also decrease production of IFNγ in the QFT-G assay. Thus, a negative QFT-G result alone would not be sufficient to exclude a diagnosis of TB in our patient [11].

Diagnosis of concurrent TB and lung cancer is important, but may be difficult. TB lesions can mask lung cancers, delaying the diagnosis [4]. Patients who initially present with active TB and lung cancer have lower survival rates than those having lung cancer without TB [13]. Surgical resection for early-stage lung cancer with anti-TB therapy is a potential treatment, however, there are currently no established guidelines [3],[4]. One suggestion is that newly diagnosed TB cases be followed up periodically with chest X-ray, bronchoscopy, and sputum cytology to enable early diagnose of lung cancer [4].

Although rarely occurring together, TB and adenocarcinoma have an established connection. Diagnosis of simultaneous occurrence is difficult, given that one can mask the other, however, recognition of the diseases is important and can impact outcomes and patient treatment options.

Conflicts of interest

All authors have no conflicts of interest to declare.



 
  References Top

1.
M.S. Shiels, D. Albanes, J. Virtamo, et al, Increased risk of lung cancer in men with tuberculosis in the alphatocopherol, beta-carotene cancer prevention study, Cancer Epidemiol. Biomarkers Prev. 20 (2011) 672–678.  Back to cited text no. 1
    
2.
A.V. Brenner, Z. Wang, R.A. Kleinerman, et al, Previous pulmonary diseases and risk of lung cancer in Gansu Province, China, Int. J. Epidemiol. 30 (2001) 118–124.  Back to cited text no. 2
    
3.
M. Sakuraba, M. Hirama, A. Hebisawa, et al, Coexistent lung carcinoma and active pulmonary tuberculosis in the same lobe, Ann. Thorac. Cardiovasc. Surg. 12 (2006) 53–55.  Back to cited text no. 3
    
4.
S. Cicenas, V. Vencevicius, Lung cancer in patients with tuberculosis, World J. Surg. Oncol. 5 (2007) 22.  Back to cited text no. 4
    
5.
Y.I. Kim, J.M. Goo, H.Y. Kim, et al, Coexisting bronchogenic carcinoma and pulmonary tuberculosis in the same lobe: radiologic findings and clinical significance, Korean J. Radiol. 2 (2001) 138–144.  Back to cited text no. 5
    
6.
P. Goldstraw, J. Crowley, K. Chansky, et al, International association for the study of lung cancer international staging committee; participating institutions. The IASLC lung cancer staging project: proposals for the revision of the TNM stage groupings in the forthcoming (seventh) edition of the TNM classification of malignant tumours, J. Thorac. Oncol. 2 (2007) 706–714.  Back to cited text no. 6
    
7.
L.E. Ziganshina, A.A. Vizel, S.B. Squire, Fluoroquinolones for treating tuberculosis, Cochrane Database Syst. Rev. 20 (2005). CD004795.  Back to cited text no. 7
    
8.
S. Marchetti, N.A. de Vries, T. Buckle, et al, Effect of the ATPbinding cassette drug transporters ABCB1, ABCG2, and ABCC2 on erlotinib hydrochloride (Tarceva) disposition in in vitro and in vivo pharmacokinetic studies employing Bcrp1-/-/Mdr1a/1b-/-(triple-knockout) and wild-type mice, Mol. Cancer Ther. 7 (2008) 2280–2287.  Back to cited text no. 8
    
9.
M.E. Falagas, V.D. Kouranos, Z. Athanassa, et al, Tuberculosis and malignancy, Q. J. Med. 103 (2010) 461–487.  Back to cited text no. 9
    
10.
Y.H. Luo, C.H.Wu,W.S.Wu, et al, Association between tumor epidermal growth factor receptor mutation and pulmonary tuberculosis in patients with adenocarcinoma of the lungs, J. Thorac. Oncol. 7 (2012) 299–305.  Back to cited text no. 10
    
11.
G.H. Mazurek, J. Jereb, P. Lobue, et al, Division of tuberculosis elimination, national center for HIV, STD, and TB prevention, centers for disease control and prevention (CDC): guidelines for using the QuantiFERON-TB gold test for detecting Mycobacterium tuberculosis infection, United States, MMWR Recomm. Rep. 54 (2005) 49–55.  Back to cited text no. 11
    
12.
J.S. Bergmann, G. Yuoh, G. Fish, et al, Clinical evaluation of the enhanced GEN-PROBE AMPLIFIED Mycobacterium tuberculosis Direct Test for rapid diagnosis of tuberculosis in prison inmates, J. Clin. Microbiol. 37 (1999) 1419–1425.  Back to cited text no. 12
    
13.
Y.M. Hen, J.Y. Chao, C.M. Tsai, et al, Shortened survival of lung cancer patients initially presenting with pulmonary tuberculosis, Jpn. J. Clin. Oncol. 26 (1996) 322–327.  Back to cited text no. 13
    


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