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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 3  |  Issue : 2  |  Page : 285-290

Pancreatic mass in a 95-year-old male: A rare presentation of tuberculosis


1 Department of Internal Medicine, St. Luke's University Hospital Network, Bethlehem, USA
2 Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA
3 Department of Anesthesiology and Critical Care, University of Pennsylvania Medical Center, Philadelphia, PA, USA
4 Department of Pathology, St. Luke's University Hospital Network, Bethlehem, USA

Date of Web Publication9-Jan-2018

Correspondence Address:
Dr. Sudip Nanda
Department of Internal Medicine, St. Luke's University Hospital Network, 801 Ostrum Street, Bethlehem, PA 18015
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2455-5568.222477

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  Abstract 


Due to the great increase of international travel and emigration, physicians the world over may face serious diagnostic challenges, resulting from the inability to recognize diseases totally alien to their culture, and diseases common to their culture but presenting with previously unseen complications. Over the past 50 years, the frequency of Mycobacterium tuberculosis (MT) infections, arising in the native populations of the United States and other industrialized countries, has been declining. However, the rate of infections in under-developed nations remains at a very high rate. Tuberculosis (TB) can occur in any organ or tissue and can mimic many other diseases. We present the case of a 95-year-old male immigrant from India, with abdominal pain and chronic anemia. Investigation of his abdominal pain revealed a large pancreatic mass with possible hepatic metastases consistent with pancreatic cancer. Fine-needle aspiration biopsy of the mass obtained by endoscopic ultrasound, demonstrated granulomatous inflammation and yielded cultures positive for MT. Antitubercular therapy resulted in progressive resolution of the pancreatic mass and the anemia. The initial clinical impression and radiological findings, in a 95-year-old patient, may well have prompted a harmful decision to opt for comfort care only. This was avoided in our patient by adherence to the strict standard of pursuing a definitive tissue diagnosis for all “masses of unknown origin.” The merits of this case report are in the thorough discussion and illustration of the unusual pathogenesis of TB of the elderly, the imperative of assessing socioeconomic status of patients, and the diagnostic considerations required to evaluate extrapulmonary TB.
The following core competencies are addressed in this article: Patient care and Medical knowledge.

Keywords: Extrapulmonary tuberculosis, pancreatic mass, pancreatic tuberculosis, pancreatic tumor


How to cite this article:
Duarte-Chavez R, Stone LE, Fegley MW, Amin A, Matin A, Longo S, Nanda S. Pancreatic mass in a 95-year-old male: A rare presentation of tuberculosis. Int J Acad Med 2017;3:285-90

How to cite this URL:
Duarte-Chavez R, Stone LE, Fegley MW, Amin A, Matin A, Longo S, Nanda S. Pancreatic mass in a 95-year-old male: A rare presentation of tuberculosis. Int J Acad Med [serial online] 2017 [cited 2019 Dec 14];3:285-90. Available from: http://www.ijam-web.org/text.asp?2017/3/2/285/222477




  Introduction Top


Mycobacterium tuberculosis (MT) organisms can primarily and secondarily infect practically any organ or tissue in the body. Once considered to be a nearly conquered infectious disease, tuberculosis (TB) has shown a great resurgence in both economically advanced nations and developing countries.

The great number of travelers and emigrants from areas with a significant endemic tubercular population has added additional challenges to physicians unfamiliar with the disease. In the United States, the annual incidence has been steadily declining from 10.4 cases per 100,000 population in 1992 to 3 cases per 100 000 population in 2014. Mortality also has decreased 67% overall from 1992 to 2014 although from 2013 to 2014 there was an 8% increase in mortality. HIV coinfection has decreased as well from 48% in 1993 to 6% in 2014.[1] Demographic data over the same two decades have confirmed two very useful facts. First, more than half of all the newly diagnosed cases of active TB in the United States occurred in foreign-born Asians or Hispanics. Second, the new cases of TB occurring in native-born Americans are usually associated with low socioeconomic status.[2],[3]

Active or inactive disease found primarily in the lungs and/or the adjacent regional lymph nodes (LNs) is called pulmonary TB (PTB). Active or inactive tubercular disease presenting outside of the lungs is called extra-PTB (EPTB) [Table 1].[4] However, detectable active or inactive lung involvement may be present in 10%–50% EPTB cases. By custom, these cases are classified as PTB. The classification of these cases as PTB reflects the consensus that EPTB is a de facto complication of PTB. This empirical paradigm requires physicians to carry out a complete diagnostic workup for PTB in all patients presenting with what appears to be only EPTB.
Table 1: Comparison between pulmonary tuberculosis and extrapulmonary tuberculosis in a case series from Korea

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Radiological imaging and bacteriological workup are required to determine if a case is infectious [Algorithm 1].[3],[4]



Either in localized or disseminated (miliary TB) forms, EPTB rarely occurs in immune competent patients. Conditions in which the incidence of EPTB may be increased include all cause immune incompetence, tardive reactivation disease (months to years after primary infection), and decline in cellular immune function [Table 2].[4],[5],[6] In 5%–10% of the cases of EPTB, identifiable factors predisposing the patient to reactivation TB are absent. The interplay between the virulence of the bacteria and the host's susceptibility is the main determinant of infection.[7],[8]
Table 2: Factors associated to decline in cellular immunity

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  Case Report Top


A 95-year-old male presented to the emergency department with a constant nonradiating midabdominal pain, which had been present for several days. The pain did not interfere with his daily routine, including long walks, and was unassociated with nausea, vomiting, diarrhea, weight loss, anorexia, fever, or chills. His medical history included valsartan treatment for hypertension and oral iron supplement for chronic anemia of 1-year duration. Personal history: retired salesman, immigrant from India, living in the USA since 1980. Over the years, he has made numerous trips to India. He is a former cigarette smoker. There were no risks factors for HIV infection. Family history: noncontributory with no history of cancer. Physical examination: no rash, adenopathy, or skin lesions were identified, lungs were clear to auscultation, the abdomen was mildly tender to palpation, and there were no palpable masses. Laboratory tests confirmed a microcytic, hypochromic anemia, with elevated ferritin and low iron. Differential white blood cell count was normal. A serum CA 19-9 level was also slightly elevated (37 U/mL reference values 0–35 U/mL).

A computed tomography (CT) of the abdomen revealed an intrapancreatic heterogeneous mass and dilation of the major pancreatic ducts. One isolated hepatic lesion was suspicious for metastasis [Figure 1]. A magnetic resonance imaging (MRI) corroborated the previous CT findings but raised concerns of possible tumor invasion of the superior mesenteric artery and splenic vein [Figure 2]. An endoscopic ultrasound (EUS) revealed an intrapancreatic hyperechogenic mass in the body/neck region with upstream dilatation of the pancreatic ducts [Figure 3], a 7 mm hypoechogenic lesion in the liver, a peripancreatic hypoechogenic mass posterior to the pancreas compressing the splenic vein, and a 12 mm celiac LN [Figure 4]. All these imaging features are described in literature as highly suspicious for malignancy. Fine-needle aspiration biopsy (FNAB) was obtained from all the lesions identified in EUS, except the liver lesion (being out of reach owing to its localization) and the peripancreatic lesion (due to proximity of the splenic vein). All the biopsies yielded numerous single and clustered chronic inflammatory cells, epithelioid histiocytes, and varyingly developed giant cell granulomata. There was no evidence of malignancy [Figure 5]. Bacteriologic stains were negative for acid-fast bacilli. Samples of aspirated tissue were sent for routine aerobic, anaerobic, and acid-fast organisms. The celiac LN was the only with a positive culture, growing only acid-fast organisms, consistent with Mycobacterium species. Confirmatory DNA probe analysis identified the cultured organisms as MT. The organisms were sensitive to anti-TB antibiotics. A chest X-ray was subsequently performed, which was negative for an evidence of active or chronic pulmonary disease. In the absence of pulmonary symptoms or findings, a sputum culture was not deemed necessary. At this point, a firm diagnosis of EPTB was made.
Figure 1: Computed tomography scan: (a) A pancreatic heterogeneous 50 mm × 25 mm mass (wide arrow) compressing the splenic vein (thin arrow). (b) Pancreatic duct dilation is appreciated. (c) A lesion suspicious for liver metastasis is observed

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Figure 2: Computed tomography scan and magnetic resonance imaging: (a and b) Pancreatic mass compressing splenic vein at the moment of diagnosis. (c) Twelve months later, after antibiotic therapy was finished, previously identified pancreatic body mass appears decreased in size with less mass effect on the splenic vein

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Figure 3: Endoscopic ultrasound: (a) A 2.5 by 2.3 cm mass is observed on the pancreatic head, the parenchyma was lobulated with hyperechoic strands. (b) Pancreatic duct was dilated in the upstream body and tail and measured 3.4 mm, multiple dilated side branches of the pancreatic duct were seen. There was a narrowing in the area of the body/neck, being normal downstream

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Figure 4: Endoscopic ultrasound: (a) A 7 mm hypoechoic lesion was identified on the liver. (b) A hypoechoic lesion of 11 mm was seen posterior/inferior to the pancreas in the retroperitoneum, with involvement and narrowing of the splenic vein and possibly the portal confluence, being unable to be sampled due to blood vessels being in the needle path. Multiple lymph nodes were seen in the peripancreatic region of the head of the pancreas, this lesion was not sampled. (c) A large celiac lymph node measuring 1.2 cm was seen and biopsied

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Figure 5: Fine-needle aspiration biopsy of celiac lymph node: (a) These two loosely clustered groups of cells are the most commonly seen cell aggregates in this fine-needle aspiration biopsy. At low power, the individual cells within the groupings did not suggest a specific type of inflammation. (b) Epithelioid histiocytes with lymphocytes, plasmacytes, and a prominent multinucleated cell of Touton forming a central ball defining a granuloma, negative for malignancy

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The treatment protocol for this patient included rifampin, isoniazid, pyrazinamide, and ethambutol for 2 months, followed by 7 months of isoniazid and rifampin. A follow-up evaluation occurred 1-year postdiagnosis. By MRI, there was approximately 50% shrinkage of the pancreatic mass but persistent dilatation of the pancreatic duct, considerably less compression of the splenic vein and superior mesenteric artery, and disappearance of the liver lesion [Figure 2]. There was complete resolution of the anemia.


  Discussion Top


The portal of entry of PTB infections is the upper airway [Figure 6]. MT organisms are carried as air-borne particle into the terminal respiratory bronchioles and alveoli, where they are engulfed by macrophages. Mycobacteria can survive and proliferate within phagocytes. During this initial infestation, the surviving mycobacteria may appear in the circulating blood stream or within lymphatic vessels within the lung, around the bronchi and mediastinum. One or more sites of infection within the lung parenchyma can occur as granulomatous inflammation characteristic of TB. The granulomatous infection can simultaneously occur within the hilar and peribronchial LNs. Contiguous lymphatic spread may extend into the carinal and midmediastinal LNs and the LNs of the anterior lower neck. In addition, spread of lymphatic extension of infection can occur through the intrathoracic pleural lymphatics which extend through the diaphragmatic hiatus into the retroperitoneum.
Figure 6: Pancreatic Mycobacterium tuberculosis infection through lymphohematogenous spread

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Organs and tissues with the richest blood supply and lymphatic connections are most vulnerable to infection [Table 3].[4],[5],[8],[9] Immune-competent persons generally mount a strong host response to the tubercle bacillus, and in the majority of the patient, the infection appears to be completely cleared. A very small percentage of infected patients will continue to harbor viable but dormant tubercle bacilli in any anatomic location. The tubercle bacilli remain as a latent infection but well-known to become reactivated TB by numerous documented factors.[6]
Table 3: Most common localization of extrapulmonary tuberculosis

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There are two basic mechanisms of spread of TB to the gastrointestinal tract (EPTB). The first occurs through hematogenous and lymphatic circulations (vascular spread). The second is by oral ingestion of tubercle bacilli [Figure 7]. After being swallowed, MT infects the (Peyer's patches) intramural lymphatics, particularly the terminal ileum and cecum. Both are areas of slow transit and rich concentration of lymphatic vessels. These are the common sites of intestinal mycobacterial infections. Lymphatic extension from adjacent lymphadenitis to the neighboring organs can occur later. Tuberculous lesions within the abdomen are extremely difficult for the physician to distinguish from tumors, inflammatory bowel diseases, and other infections.[10] Tuberculous infection of parenchymatous abdominal organs is generally seen with miliary TB.[5]
Figure 7: Pancreatic Mycobacterium tuberculosis infection through ingestion

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Pancreatic TB is most often associated with generalized dissemination of PTB and immune suppression [Table 4].[11],[12],[13],[14] This may reflect the inability of the pancreas to clear the infection due to its poor content of reticuloendothelial cells. Tubercular infection of the pancreas presents on imaging as a solitary mass lesion of the head and body that resembles a cancer but lacks features associated to neoplasia (e.g., vascular invasion or pancreatic duct dilation).[15] On ultrasound (USG), its appearance has been described as either cystic or as a hypoechoic mass with occasional central liquefaction. On CT, pancreatic masses are hypodense and hypovascular with adjacent lymphadenopathy. After imaging has been done, accurate diagnosis of pancreatic tuberculoma must rely on histological confirmation and bacteriologic criteria. FNAB has proven to be a useful and safe first-line method of tissue sampling. Inconclusive FNAB results warrant a laparotomy for definitive diagnosis. For accessible lesion, percutaneous USG or CT-guided FNAB can be used. EUS may provide the safest access to the lesions and greater resolution imaging of the pancreas, especially when malignancy is highly suspected and tumor seeding is a concern.[16],[17]
Table 4: Organs most commonly involved in miliary tuberculosis

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  Conclusions Top


The absence of vascular invasion, absence of pancreatic ductal dilation, and hypodensity/hypoechogenicity are characteristics of pancreatic TB infection.[18] We present a case of pancreatic TB which could not be differentiated from a neoplasm on imaging due to the presence of the tumor-associated findings: changes simulating vascular invasion, pancreatic duct dilation, and hyperechogenicity on USG. Our patient had an elevated serum CA 19-9. An elevated serum CA 19-9 level is not specific for neoplasm, but it is most strongly associated with gastrointestinal malignancies. Even with positron emission tomography CT, TB can resemble malignancy and uptake values of FDG can be as high as those found in neoplasia.[16] Hence, a thorough investigation with cytopathology is necessary in all the patient on risk for TB infection such as immigrants from countries with high incidence of TB (Asia and Latin America) and/or impaired cell-mediated immunity [Table 2], given the different prognosis and treatment of TB compared to malignancy.[19]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical conduct of research

The authors attest that this scholarly work was conducted in accordance with the recommendations of The International Committee of Medical Journal Editors. Patient consent was obtained prior to the submission of this manuscript for publication in the International Journal of Academic Medicine.



 
  References Top

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Lee JY, Diagnosis and treatment of extrapulmonary tuberculosis. Tuberc Respir Dis (Seoul) 2015;78:47-55.  Back to cited text no. 4
    
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Slavin RE, Walsh TJ, Pollack AD, Late generalized tuberculosis: A clinical pathologic analysis and comparison of 100 cases in the preantibiotic and antibiotic eras. Medicine (Baltimore), 1980;59:352-66.  Back to cited text no. 11
    
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Imani Fooladi AA, Hosseini MJ, Azizi T, Splenic tuberculosis: A case report. Int J Infect Dis 2009;13:e273-5.  Back to cited text no. 13
    
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Choudhary NS, et al. Tubercular lymph nodal mass mimicking pancreatic malignancy with extrahepatic biliary obstruction in a young woman. Endoscopy 2015;47(S 01):E53-4.   Back to cited text no. 15
    
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Yamada R, et al. Peripancreatic tuberculous lymphadenitis with biliary obstruction diagnosed by endoscopic ultrasound-guided fine-needle aspiration biopsy. Intern Med 2016;55:919-23.  Back to cited text no. 16
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Sharma V, et al. Pancreatic tuberculosis. J Gastroenterol Hepatol 2016;31:310-8.  Back to cited text no. 17
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Rana SS, et al. Vascular invasion does not discriminate between pancreatic tuberculosis and pancreatic malignancy: A case series. Ann Gastroenterol 2014;27:395-8.  Back to cited text no. 18
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Yang YJ, et al. Pancreatic tuberculosis mimicking pancreatic carcinoma during anti-tuberculosis therapy: A case report. World J Clin Cases 2014;2:167-9.  Back to cited text no. 19
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]


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