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CASE REPORT
Year : 2018  |  Volume : 6  |  Issue : 1  |  Page : 39-44

Pancreatic tuberculosis causing biliary obstruction and mimicking pancreatic malignancy


1 Faculty of Medicine, Umm Al-Qura University, Makkah, KSA
2 Radiology Department, Al Noor Specialist Hospital, Makkah, KSA

Date of Web Publication8-Jan-2018

Correspondence Address:
Noura Abdulaziz Al Najdi
Umm Al-Qura University, Makkah
KSA
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DOI: 10.4103/jhs.JHS_106_17

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  Abstract 

Tuberculosis (TB) is a bacterial infection which can affect any part of the body from head to toe and has various presentations depending on the site of the infection. Pancreatic TB is very rare and usually happens as a part of disseminated or miliary TB, whereas isolated pancreatic TB is even rarer. Here, we present a case of pancreatic TB at a TB endemic zone which presented with obstructive jaundice and pancreatic lesions mimicking pancreatic malignancy. A 46-year-old Saudi female patient presented with right upper quadrant abdominal pain associated with dark coloured urine and pale stool. The patient had been admitted to the surgical ward as a case of acute cholecystitis for further evaluation. On abdominal ultrasound (US), findings demonstrated dilated common bile duct (CBD), but the distal part was difficult to be visualised; hence, further evaluation by magnetic resonance cholangiopancreatography (MRCP) was recommended to look for CBD stones. The MRCP showed two focal pancreatic lesions causing the distal CBD obstruction with no stones at CBD. Based on these findings, malignancy was considered and computed tomography-guided fine-needle aspiration biopsy from the pancreatic neck lesion was performed. This demonstrated multiple granulomas and lymphocytes with no malignant cell which indicated pancreatic TB. The patient became well after a course of anti-TB medications. pancreatic TB should be included in the differential diagnosis of pancreatic masses, especially in those patients who live in an endemic area of TB. A biopsy is necessary to establish the diagnosis and start the appropriate treatment for this curable disease as soon as possible.

Keywords: Biliary obstruction, pancreatic malignancy, pancreatic tuberculosis


How to cite this article:
Al Najdi NA, Felemban BA, Abou Issa AH. Pancreatic tuberculosis causing biliary obstruction and mimicking pancreatic malignancy. J Health Spec 2018;6:39-44

How to cite this URL:
Al Najdi NA, Felemban BA, Abou Issa AH. Pancreatic tuberculosis causing biliary obstruction and mimicking pancreatic malignancy. J Health Spec [serial online] 2018 [cited 2020 Jul 7];6:39-44. Available from: http://www.thejhs.org/text.asp?2018/6/1/39/222462


  Introduction Top


Tuberculosis (TB) is a bacterial infection which can affect any part of the body from head to toe and has various presentations depending on the site of the infection. It is an endemic disease in developing countries with around 9.7 million cases reported annually.[1] It most commonly appears as necrotic granulomas in the lungs.[2] Extrapulmonary TB is found in 10%–30% of all cases [3] while the prevalence of abdominal TB in developing countries is as high as 12%,[4] and there, it often involves the peritoneum, gastrointestinal tract particularly ileum and caecum, liver, spleen and lymph nodes.[3]

Pancreatic TB is very rare and usually happens as a part of disseminated or miliary TB. Isolated pancreatic TB is rarer.[4] The nature of pancreatic involvement is still unclear, and its diagnosis remains a challenge since the clinical picture is indefinite and mimics another disease, especially pancreatic carcinoma even on radiological imaging. However, of all TB cases, pancreatic TB has a good response towards the anti-TB treatment as the diagnosis uses image-guided tissue biopsy.[3]

In this report, we present a case of pancreatic TB which presented with obstructive jaundice and pancreatic lesions mimicking pancreatic carcinoma.


  Case Report Top


A 46-year-old Saudi female presented to the emergency department complaining of right upper quadrant (RUQ) abdominal pain for the past 2 weeks.

Since its initiation, the pain was increasing and gradually getting worse over the past 2 days before admission. It was aggravated by food intake with no relieving factors. It was radiating to her right shoulder and back. The intensity of this pain was moderate according to the patient. The patient also has reported dark coloured urine and pale stool over the past 3 days. There was no fever, night sweating or loss of weight.

Her medical history was significant for intestinal TB and cholelithiasis. She did not have any previous surgeries. No known allergies were reported.

On physical examination, she was vitally stable. The chest was clear. Abdominal examination revealed RUQ tenderness. No other findings were detected.

The patient was admitted to the surgical ward as a case of acute cholecystitis for further evaluation.

Laboratory investigation results showed high blood level of total bilirubin 4.1 mg/dl (normal 0–1 mg/dl), direct bilirubin 2.57 mg/dl (normal 0–0.2 mg/dl), ALT 231 IU/L (normal 0–65 IU/L), AST 188 IU/L (normal 0–38 IU/L), alkaline phosphatase 168 IU/L (normal 40–136 IU/L), amylase 161 IU/L (normal 25–115 IU/L) and lipase 903 IU/L (normal 31–186 IU/L). The complete blood count was within the normal limits.

Abdominal ultrasound (US) findings demonstrated dilated common bile duct (CBD) measuring 15 mm (normal is <4 mm) [Figure 1]. The distal CBD was difficult to be visualised due to overlying bowel gases. No CBD stones were detected within these limitations. Mild intrahepatic biliary dilatation was also noted [Figure 2]. The gallbladder was normal in calibre with a large mobile stone in the neck [Figure 3]. Further evaluation by magnetic resonance cholangiopancreatography (MRCP) was recommended to look for CBD stones.
Figure 1: Abdominal ultrasound through the porta hepatis in colour Doppler mode demonstrating dilated common bile duct reaching up to 15 mm (red arrow). The portal vein is also shown demonstrating partial Doppler signa

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Figure 2: Abdominal ultrasound, dual scan through the right liver lobe. The one on the left is in greyscale mode and the one on the right in colour Doppler mode. Multiple mildly dilated intra-hepatic bile ducts are demonstrated (red arrows). The portal vein is also demonstrates with patent flow

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Figure 3: Abdominal ultrasound, scan of the gallbladder shows a normally sized and shaped gallbladder. A large stone was noted in the neck (red arrow). This stone was mobile

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MRCP demonstrated a dilated CBD along with mild-to-moderate intrahepatic biliary dilatation [Figure 4]. The pancreatic duct was dilated measuring 3 mm (normal is <2 mm). There was a large gallstone measuring 10 mm [Figure 5] and [Figure 6]. No stones were detected in the CBD. The liver demonstrated homogeneous parenchyma with no focal lesions.
Figure 4: Magnetic resonance cholangio-pancreatography, maximum intensity projection reformat series. There was marked common bile duct dilatation and mild intra-hepatic biliary duct dilatation. The gallbladder was also demonstrated with a large oval-shaped filling defect indicting a gallstone (blue arrow)

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Figure 5: Magnetic resonance cholangio-pancreatography, axial T2 turbo spin echo sequence. A well-defined round T2 hyperintense lesion was noted in the proximal part of the body of pancreas (red arrow). Focal dilatation of the pancreatic duct was noted between this lesion and the more proximal lesion located in the neck of pancreas (blue arrow). A gallstone was noted in the neck of gallbladder (green arrow)

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Figure 6: Magnetic resonance cholangio-pancreatography, axial T2 STIR sequence. A well-defined round T2 hyperintense lesion was noted in the proximal part of the body of pancreas (red arrow). A gallstone was noted in the neck of gallbladder (green arrow)

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Two focal pancreatic lesions were detected. The first one was located in the neck of the pancreas, extending posteriorly to the uncinate process, measuring 34 mm × 25 mm [Figure 7] and [Figure 8]. The second one was located in the proximal body of pancreas, measuring 25 mm × 25 mm [Figure 5] and [Figure 6]. Both were faintly hyperintense on T2-weighted images (WIs). Due to the study protocol, neither T1-WIs nor contrast-enhanced sequences were obtained. The neck lesion was the lesion causing the distal CBD obstruction. There was a focally dilated segment between the neck lesion and the proximal body lesion [Figure 5].
Figure 7: Magnetic resonance cholangio-pancreatography, axial T2 turbo spin echo sequence. A well-defined lobulated T2 hyperintense lesion was noted in the neck of pancreas extending to the uncinate process (red arrow)

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Figure 8: Magnetic resonance cholangio-pancreatography), axial T2 STIR sequence. A well-defined lobulated T2 hyperintense lesion was noted in the neck of pancreas extending to the uncinate process (red arrow)

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Multiple enlarged, T2 hyperintense, peripancreatic, and paraaortic lymph nodes were detected. The largest measured 27 mm × 19 mm [Figure 9].
Figure 9: Magnetic resonance cholangio-pancreatography, axial T2 STIR sequence. A large, T2 hyperintense, left para aortic lymph nodes was demonstrated (red arrow)

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The other visible viscera, namely, the spleen and adrenal glands were normal. The kidneys were not completely visualised.

Based on these findings, malignancy such as lymphoma, pancreatic adenocarcinoma or metastasis (breast cancer, lung cancer, etc.) was considered. Due to the prior history of intestinal TB, it was considered in the differential diagnosis but to a lesser degree.

The patient underwent a focused history and physical examination for malignancy by the treating team. Focused laboratory work was ordered.

Computed tomography (CT) chest, abdomen and pelvis were recommended to detect other abnormalities and for staging purposes. The pancreatic lesions were redemonstrated which were hypodense in pre-contrast series and minimally enhanced in relation to normal pancreas [Figure 10] and [Figure 11]. The nearby blood vessels, mainly the superior mesenteric artery and the portal vein, were patent, normal in calibre and were not encased by the pancreatic lesions [Figure 10] and [Figure 11]. Intra- and extra-hepatic biliary dilatation was again identified [Figure 12]. Multiple, peripancreatic and para-aortic lymph nodes were detected [Figure 13]. No enhancing hepatic lesions were detected. A small enhancing mass was noted in the lower pole of the right kidney, measuring 28 mm × 21 mm [Figure 14]. The left kidney was atrophied showing no focal lesions [Figure 14]. The rest of major viscera were normal.
Figure 10: Computed tomography chest, abdomen and pelvis, late arterial phase. A well-defined, hypodense, hypovascular lesion was noted in the proximal part of body of pancreas (red arrow). The nearby vessels were intact and were not encased

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Figure 11: Computed tomography chest, abdomen and pelvis, late arterial phase. A well-defined, irregularly-outlined, hypodense, hypovascular lesion was noted in the neck of pancreas (red arrow). The nearby vessels were intact and were not encased. A calcified gallstone is noted (green arrow)

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Figure 12: Computed tomography chest, abdomen and pelvis, portal venous phase coronal reformat. Markedly dilated common bile duct with mild intra-hepatic biliary dilatation was noted. Small amount of peri-hepatic fluid was identified (red arrow)

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Figure 13: Computed tomography chest, abdomen and pelvis, portal venous phase coronal reformat. Multiple enlarged para-aortic lymph nodes were identified (red arrows)

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Figure 14: Computed tomography chest, abdomen and pelvis, portal venous phase coronal reformat. Small solid lesion was noted in the lower pole of right kidney (red arrow). The left kidney was atrophied

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After detecting the right kidney lesion, malignancy was highly considered. The possibilities were renal cell carcinoma (RCC) with pancreatic metastasis versus pancreatic cancer with renal metastasis or two synchronous malignancies at the same time.

CT-guided fine-needle aspiration biopsy from the pancreatic neck lesion was performed [Figure 15]. This demonstrated multiple granulomas and lymphocytes with no malignant cell which indicated pancreatic TB. Exclusion of RCC was needed and another sample from the right renal lesion was performed by CT-guided core biopsy [Figure 16]. This also demonstrated numerous granulomas with surrounding lymphocytes indicating renal TB.
Figure 15: Computed tomography guided fine needle aspiration biopsy. A 20 G Chiba needle was inserted through anterior abdominal wall. Samples were obtained from the pancreatic neck lesion

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Figure 16: Computed tomography guided core biopsy. An 18 G side cutting needle was inserted through right posterior abdominal wall through a 17 G co-axial needle. Three samples were from the lower pole right renal lesion

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Based on these findings, the patient had been given a course of anti-TB medications for 6 months.

Follow-up abdominal US demonstrated interval resolution of the pancreatic and renal lesions with interval resolution of biliary obstruction [Figure 17] and [Figure 18].
Figure 17: Abdominal ultrasound through the porta hepatis in colour Doppler mode demonstrating interval reduction of common bile duct (red arrow) diameter from 15 mm as noted in Figure 1 to 7 mm. The portal vein was also shown demonstrating patent colour Doppler signal

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Figure 18: Abdominal ultrasound through lower pole of right kidney greyscale mode demonstrating no focal lesions in the lower pole

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  Discussion Top


Isolated TB of the pancreas is not common, even in those endemic areas with a high prevalence of TB. Less than 100 cases have been reported worldwide and it is not so far known clearly how the infection can solitary affect the pancreas.[5] The pancreas is biologically protected from being infected by Mycobacterium tuberculosis[6] since pancreatic enzymes have been reported to have an antitubercular impact in vitro.[5] The slow course of the disease and unclear presentation together with non-specific laboratory and radiological findings demand greater attentiveness.

In 1944, Auerbach's reported the fi rst case of pancreatic TB.[7] A study was done in 1966, found pancreatic involvement on autopsy in 2% of 526 patients with miliary TB. Therefore, even in cases of miliary TB, where visceral involvement is more common, the pancreatic TB is very rare.[8]

The prevalence of pancreatic TB is almost equal among men and women, with higher prevalence among young persons or persons with past history of TB infection. Immunocompetent as in this case and immunocompromised populations both can be affected by pancreatic TB, while it affects the immunocompromised more frequently.[9],[10]

Pancreatic TB can present with deferent and non-specific symptoms. Commonly reported symptoms are abdominal pain, nausea, vomiting, fever, weight loss and if the inflammatory mass is located at the head of the pancreas, it may present as obstructive jaundice.[7],[9],[11] Other less common presentations include acute or chronic pancreatitis, gastrointestinal bleeding and portal hypertension.[12]

Physical examination is usually indistinguishable, making the clinical diagnosis difficult along with the vague symptoms.[13]

The radiological findings also fail to differentiate between pancreatic TB and malignancy.[13] On ultrasound (US) of the abdomen, the lesions can appear as a hypoechoic or cystic lesion. On CT, pancreatic TB generally presents as an enhancing hypodense mass commonly at the head or the body of the pancreas with irregular borders or diffuse enlargement of the pancreas and enlarged peripancreatic lymph nodes.[10],[14] On magnetic resonance imaging, features of pancreatic TB include sharply delineated lesions, showing heterogeneous enhancement. They are hypointense on fat-suppressed T1-WIs and show a mixture of hypointensity and hyperintensity on T2-WIs.[15]

All these findings are non-specific and mimicking the other differential diagnosis, like cystadenocarcinomas, pancreatic adenocarcinomas and pancreatic pseudocysts. These make the need for more invasive techniques such as US or CT-guided biopsy a must to confirm the diagnosis.[10],[14]

Histological findings of caseating granulomatous inflammation and positive acid-fast bacilli stain are confirmatory evidence of pancreatic TB.[13],[14]

Once the diagnosis is established, anti-TB treatment should be started for 6–12 months.[3] Most of the cases respond well to the treatment and have a good prognosis.[16]

When the diagnosis cannot be established, you can start anti-TB treatment based on clinical presentation and image findings, especially in young patients living in an endemic area of TB. There should be improvement or deterioration of symptoms after 6 weeks of anti-TB treatment. Otherwise, the diagnosis should be re-established.[3]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgement

The authors would like to thank Dr. Alaa Almarzouki, radiologist senior registrar, as she has reported the first MRCP; Dr. Wael Ahmad, consultant radiologist, as he has reported the CT; Dr. Riyadh Elerian, consultant urologist, who insisted on taking a sample from the kidney; and the histopathologist, Dr. Amal Hasan.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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1.
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Ray S, Das K, Mridha AR. Pancreatic and peripancreatic nodal tuberculosis in immunocompetent patients: Report of three cases. JOP 2012;13:667-70.  Back to cited text no. 3
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González A, Baudagna G, Gutiérrez SC, Villaverde M, Monteverde A. Pancreatic tuberculosis. Acta Gastroenterol Latinoam [Internet]. 2008;38:199-201. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18979900. [Last cited on 2017 Apr 26].  Back to cited text no. 12
    
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Pramesh CS, Heroor AA, Gupta SG, Krishnamurthy S, Shukla PJ, Jagannath P, et al. Pancreatic tuberculosis: An elusive diagnosis. HPB (Oxford) 2003;5:43-5.  Back to cited text no. 13
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18]


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