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AJR 2005; 184:50-54
© American Roentgen Ray Society


Original Report

Tuberculosis of the Pancreas: MRI Features

A. I. De Backer1, K. J. Mortelé2, P. Bomans3, B. L. De Keulenaer4, I. J. Vanschoubroeck3 and M. M. Kockx5

1 Department of Radiology, Stuivenberg, Ziekenhuisnetwerk Antwerpen, Lange Beeldekensstraat 267, Antwerp B-2060, Belgium.
2 Department of Radiology, Division of Abdominal Imaging and Intervention, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St., Boston, MA 02115.
3 Department of Internal Medicine, Stuivenberg, Ziekenhuisnetwerk Antwerpen, Antwerp B-2060, Belgium.
4 Intensive Care Unit, Royal Darwin Hospital, Rocklands 0810, TIWI, Northern Territory, Australia.
5 Department of Pathology, Stuivenberg, Ziekenhuisnetwerk Antwerpen, Antwerp B-2060, Belgium.

Received January 9, 2004; accepted after revision April 28, 2004.

 
Address correspondence to A. I. DeBacker (adelard.debacker{at}skynet.be).


Abstract
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
OBJECTIVE. The purpose of this study was to describe the MRI features of tuberculosis of the pancreas.

CONCLUSION. Pancreatic tuberculosis can be focal or diffuse. If focal, it presents as a sharply delineated mass located in the pancreatic head, showing heterogeneous enhancement. Lesions are hypointense on fat-suppressed T1-weighted images and a mixture of hypo- and hyperintense on T2-weighted images. The appearances of common bile duct and main pancreatic duct are normal. Diffuse involvement is characterized by pancreatic enlargement with narrowing of the main pancreatic duct and heterogeneous enhancement. Signal intensity abnormalities indicating diffuse involvement include hypointensity on fat-suppressed T1-weighted images and hyperintensity on T2-weighted images.


Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
The incidence of tuberculosis in the developed countries is increasing, mainly among immigrants and immunocompromised patients. The predominant manifestation of tuberculosis is pulmonary disease. The abdomen, however, is a common site of extrapulmonary involvement. The most common sites of involvement in the abdomen are the mesentery, small bowel, peritoneum, liver, and spleen [1]. Tuberculosis of the pancreas is considered to be uncommon, but its true incidence is unknown. Tuberculosis of the pancreas usually occurs as a complication of miliary tuberculosis and immunodeficiency, with isolated involvement of the pancreas being exceedingly rare [2, 3]. The diagnosis usually is not suspected before laparotomy unless there is evidence of tuberculosis elsewhere or a relevant clinical history [3].

We describe three patients with tuberculosis of the pancreas and discuss the disease features seen on MRI.


Materials and Methods
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Patients
We reviewed the medical records of three patients (mean age, 33 years; range, 23–47 years) with pancreatic tuberculosis who were seen at our institution over a 3-year period. All patients, one man and two women, were immigrants. The findings at physical and histopathologic examinations, results of laboratory tests, and MRI studies were available for all three patients.

MRI Technique
MRI was performed with a 1.5-T magnet (Signa EchoSpeed Plus, GE Healthcare) using a phased-array torso coil. Thin-section and thick-slab T2-weighted single-shot fast spin-echo and T1-weighted fat-suppressed gradient-recalled-echo images were obtained. Parameters used in T2-weighted single-shot fast spin-echo imaging were TR/TE, infinite/60 and 4-mm section thickness for the thin-slice technique and infinite/> 600 and 40-mm thickness for single thick slab techniques. Parameters used in gradient-recalled-echo imaging were 105/1.6; 256 x 512 matrix; rectangular field of view to reduce the number of phase-encoding views; 5-mm section thickness with a section gap of 2 mm or less; and flip angle of 60°. Contrast-enhanced gradient-recalled-echo images were obtained 25 sec, 60 sec, and 3 min after IV administration of 0.1 mmol of gadobenate dimeglumine (Multihance, Bracco-Altana) per kilogram of body weight.


Results
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Clinical Findings
Presenting symptoms in all three patients consisted of general weakness, malaise, loss of body weight, and chronic lower back pain. Cervical lymphadenopathy, fever, night sweats, hemoptysis, and productive cough were present in two patients. Intermittent pain of moderate intensity localized to the upper abdomen, dry cough, a fistula with purulent discharge in the ventral wall of the abdomen, enlarged lymph nodes in the groin, and epileptic insult associated with meningeal signs were present in one patient each.

Laboratory Analysis and Histopathology
In two patients, the biochemical analysis showed an elevated erythrocyte sedimentation rate (67 and 23 mm/h; normal values, 0–20 mm/h) and C-reactive protein level (10 and 1.69 mg/dL; normal values, < 1 mg/dL). In one patient, elevated WBC (11.8 x 109/L; normal values, 3.7–10.1 x 109/L), platelets (456 x 109/L; normal values, 155–366 x 109/L), and levels of alkaline phosphatase (174 U/L; normal value, 38–126 U/L), and y-glutamyl transpeptidase (143 U/L; normal values, 12–43 U/L) were noted. In all three patients, hemoglobin, total bilirubin, serum amylase, and lipase levels were normal, and results of tests for the HIV antibody using ELISA (enzyme-linked immunosorbent assay) methods were negative. The diagnosis of tuberculosis was based on results of a highly specific polymerase chain reaction–based assay for mycobacterial DNA on bronchioalveolar lavage fluid (n = 1), lumbar puncture of cerebrospinal fluid (n = 1), and a surgical lymph node biopsy (n = 1) and was proven by the growth of Mycobacterium tuberculosis on culture (n = 3). In all patients, tuberculous involvement of the pancreas was confirmed by improvement of abnormalities on abdominal CT and MRI after administration of antituberculous chemotherapy.

MRI Fin`dings
A sharply delineated heterogeneous mass, located in the head of the pancreas, was present in two patients (Figs. 1A, 1B, 2A, 2B, and 2C). The largest diameter of the lesion was 4.0 and 2.5 cm, respectively. In these patients, unenhanced T1-weighted fat-suppressed images showed the lesion as hypointense compared with normal pancreatic tissue. On T2-weighted images, heterogeneous signal intensities were noted, with areas of increased and decreased signal intensities. On gadolinium-enhanced T1-weighted fat-suppressed gradient-recalled-echo images, rim enhancement with focal areas of enhancement within the lesions resulted in a multiloculated appearance. The biliary and pancreatic ducts were unremarkable on MR cholangiopancreatography (MRCP) images in both patients.



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Fig. 1A. 30-year-old man with tuberculous involvement of head of pancreas and spleen and tuberculous spondylitis. T2-weighted single-shot fast spin-echo image shows heterogeneous mass with increased and decreased signal intensities. No dilatation of main pancreatic duct is seen.

 


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Fig. 1B. 30-year-old man with tuberculous involvement of head of pancreas and spleen and tuberculous spondylitis. Gadolinium-enhanced T1-weighted gradient-recalled-echo image obtained with fat suppression shows sharply delineated heterogeneous mass with multiloculated appearance.

 


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Fig. 2A. 23-year-old woman with tuberculous involvement of head of pancreas and "wet" peritoneal tuberculosis. T2-weighted single-shot fast spin-echo image shows heterogeneous mass in head of pancreas with central and peripheral hyperintensities. Obstruction and dilatation of main pancreatic duct is not present.

 


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Fig. 2B. 23-year-old woman with tuberculous involvement of head of pancreas and "wet" peritoneal tuberculosis. On unenhanced T1-weighted gradient-recalled-echo image obtained with fat suppression, lesion is hypointense compared with normal pancreatic tissue.

 


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Fig. 2C. 23-year-old woman with tuberculous involvement of head of pancreas and "wet" peritoneal tuberculosis. Gadolinium-enhanced T1-weighted gradient-recalled-echo image obtained with fat suppression shows sharply delineated mass with peripheral and central areas of enhancement.

 

In the third patient (Figs. 3A, 3B, 3C, and 3D), diffuse enlargement of the pancreatic gland was associated with increased signal intensity on T2-weighted images, with heterogeneous decreased signal intensity on T1-weighted fat-suppressed gradient-recalled-echo images and with heterogeneous enhancement after IV administration of gadolinium. MRCP showed diffuse narrowing of the main pancreatic duct.



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Fig. 3A. 47-year-old woman with diffuse enlargement of pancreas and abdominal lymphadenopathy caused by Mycobacterium tuberculosis. T2-weighted single-shot fast spin-echo image shows diffusely enlarged, hyperintense pancreas.

 


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Fig. 3B. 47-year-old woman with diffuse enlargement of pancreas and abdominal lymphadenopathy caused by Mycobacterium tuberculosis. On MR cholangiopancreatography image, diffuse narrowing of main pancreatic duct is noted.

 


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Fig. 3C. 47-year-old woman with diffuse enlargement of pancreas and abdominal lymphadenopathy caused by Mycobacterium tuberculosis. T1-weighted gradient-recalled-echo image obtained with fat suppression shows heterogeneously decreased signal intensity of pancreas.

 


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Fig. 3D. 47-year-old woman with diffuse enlargement of pancreas and abdominal lymphadenopathy caused by Mycobacterium tuberculosis. Slightly heterogeneous enhancement is seen on gadolinium-enhanced T1-weighted gradient-recalled-echo image obtained with fat suppression.

 

In all three patients, peripancreatic and paraaortic enlarged lymph nodes were detected with signal intensity changes comparable to those of the enlarged pancreas.


Discussion
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Although its true incidence is unknown, pancreatic involvement is considered extremely rare in patients with miliary tuberculosis. Auerbach [2] reported 1,656 autopsies performed during an 8-year period in patients who had tuberculosis. Generalized miliary tuberculosis was noted in 297 cases, but pancreatic involvement was noted in only in 14 of these cases. Paraf et al. [4] also reviewed autopsy studies of 526 cases of miliary tuberculosis. Pancreatic or peripancreatic involvement was found in only 11 cases. Isolated tuberculous involvement of the pancreas, in which the pancreas is the only site of reactivation of tuberculosis, is even more uncommon [3].

The rare occurrence of pancreatic tuberculosis has been proposed to be the result of antibacterial pancreatic factors. Intraparenchymal injection of M. tuberculosis causes destructive lesions only if an enormous amount of inoculum is used. Furthermore, an antimycobacterial effect from pancreatic extracts and purified lipases and deoxyribonucleases has been reported [5].

The exact mode of transmission of M. tuberculosis to the pancreas is not well understood, and several hypotheses have been proposed. Lymphatic and hematogenous dissemination after pulmonary exposure has been theorized to result in infection of the pancreas. Other possible mechanisms are abdominal contamination by M. tuberculosis as a result of ingestion of infected material from an active pulmonary focus with subsequent lymphatic spread; reactivation of a previously latent pancreatic tuberculosis induced by alcoholism, pancreatitis, treatment with steroids, or surgical manipulation; and direct extension through the pancreas from adjacent organs such as contiguous lymph nodes. Finally, a toxic-allergic reaction of the pancreas as a result of generalized tuberculosis, probably reflecting a nonspecific inflammatory host response to mycobacterial antigens rather than an infection per se, has also been suggested [5, 6]. In our patients, concomitant pancreatitis or toxic-allergic reaction to systemic tuberculosis seemed unlikely because laboratory evaluation showed normal levels of serum amylase and lipase, and the signal intensities of the peripancreatic and paraaortic lymph nodes were comparable to those of the affected portions of the gland.

Pancreatic tuberculosis may have different clinical presentations. These may include obstructive jaundice, gastrointestinal bleeding, acute or chronic pancreatitis, portal vein obstruction, and pancreatic mass mimicking abscess, carcinoma, and peripancreatic abscess [57]. In addition, constitutional symptoms such as low-grade fever, night sweats, weight loss, anorexia, nausea, acute or chronic abdominal pain, and malaise may be present.

Focal tuberculous involvement of the pancreas has been reported to occur most frequently in the pancreatic head, followed by the pancreatic body and tail [8]. Diffuse pancreatic involvement is exceedingly rare [8]. In our series, a sharply delineated heterogeneous mass, located in the head of the pancreas, was present in two patients. Sonography and CT may show a focal hypoechoic or hypodense lesion, often displaying internal echoes or densities [9]. On contrast-enhanced CT, this well-defined mass may show irregular margins with peripheral enhancement. Areas of central enhancement may result in a multiloculated appearance. These features, however, are nonspecific and may resemble those of inflammatory or neoplastic cystic lesions of the pancreas. Rarely, diffuse enlargement of the pancreas along with hypodense areas may be seen [10]. The latter morphologic abnormalities are also nonspecific and may be seen with pancreatitis and lymphoma. Diffuse enlargement of the gland with pancreatic duct narrowing may also be seen in patients with autoimmune pancreatitis.

To the best of our knowledge, no prior reports have focused on the MRI findings of tuberculous involvement of the pancreas. In two of our patients, T1-weighted fat-suppressed images showed the lesion as hypointense compared with normal pancreatic tissue. On T2-weighted images, heterogeneous signal intensities were noted, with areas of increased and decreased signal intensities. On gadolinium-enhanced T1-weighted fat-suppressed gradient-recalled-echo images, peripheral enhancement with areas of central enhancement was noted, resulting in a multiloculated appearance. In our third patient, diffuse enlargement of the pancreatic gland was associated with increased signal intensity on T2-weighted images, heterogeneous decreased signal intensity on T1-weighted fat-suppressed gradient-recalled-echo images, and heterogeneous enhancement after IV administration of gadolinium. Obstruction and dilatation of the common bile duct with dilatation of the intrahepatic ducts and distention of the gallbladder have been reported to be rare in patients with pancreatic tuberculosis [7]. Furthermore, a normal pancreatogram on ERCP, even if the tuberculous mass is centrally positioned in the pancreatic head, has been reported to be typical in tuberculous pancreatic involvement [11]. However, displacement and stenosis of an otherwise normal main pancreatic duct without prestenotic dilatation have been reported sporadically [12].

In conclusion, we described the MRI features of involvement of the pancreas by M. tuberculosis in three patients. The presence of a mass in the pancreatic head or a diffuse enlargement of the gland in patients with miliary tuberculosis or other types of abdominal tuberculosis should raise the possibility of tuberculous involvement of the pancreas.


References
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 

  1. Hulnick DH, Megibow AJ, Naidich DP, et al. Abdominal tuberculosis: CT evaluation. Radiology1985; 157:199 -204[Abstract/Free Full Text]
  2. Auerbach O. Acute generalized miliary tuberculosis. Am J Pathol 1944;20:121 -136
  3. Yokoyama T, Miyagawa S, Noike T, Shimada R, Kawasaki S. Isolated pancreatic tuberculosis. Hepatogastroenterology1999; 46:2011 -2014[Medline]
  4. Paraf A, Menager C, Texier J. La tuberculose du pancreas et la tuberbulose des ganglions de l'etage superieur de l'abdomen. Rev Med Chir Mal Foie 1966;41:101 -126[Medline]
  5. Knowles KF, Saltman D, Robson HG, Lalonde R. Tuberculous pancreatitis. Tubercle1990; 71:65 -68[Medline]
  6. Stock KP, Rieman JF, Stadler W, Rosch W. Tuberculosis of pancreas. Endoscopy 1981;13:178 -180[Medline]
  7. Crowson MC, Perry M, Burden E. Tuberculosis of the pancreas: a rare cause of obstructive jaundice. Br J Surg1983; 71:239
  8. Ladas SD, Vaidakis E, Lariou C, et al. Pancreatic tuberculosis in non-immunocompromised patients: reports of two cases and a literature review. Eur J Gastroenterol Hepatol1998; 10:973 -976[Medline]
  9. Akhan O, Pringot J. Imaging of abdominal tuberculosis. Eur Radiol2002; 12:312 -323[Medline]
  10. Desai SR, Bhanthunmavin K, Hollands M. Primary pancreatic tuberculosis: presentation and diagnosis. Aust N Z J Surg 2000:70;141 -143[Medline]
  11. Evans JD, Hamanaka Y, Olliff SP, Neoptolemos JP. Tuberculosis of the pancreas presenting as metastatic pancreatic carcinoma. Dig Surg 2000; 17:183 -187[Medline]
  12. Fischer G, Spengler U, Neubrand M, Sauerbruch T. Isolated tuberculosis of the pancreas masquerading as a pancreatic mass. Am J Gastroenterol 1995;90:2227 -2230[Medline]

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