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Year : 2015  |  Volume : 11  |  Issue : 4  |  Page : 1043

Disseminated tuberculosis presenting as prolonged fever without source in a pediatric patient with acute lymphoblastic leukemia

1 Department of Medical Oncology, Cancer Institute, Adyar, Chennai, Tamil Nadu, India
2 Department of Pathology, Cancer Institute, Adyar, Chennai, Tamil Nadu, India

Date of Web Publication15-Feb-2016

Correspondence Address:
Venkatraman Radhakrishnan
Department of Medical Oncology, Cancer Institute (WIA), Adyar, Chennai - 600 020, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-1482.154030

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How to cite this article:
Panda S, Radhakrishnan V, Sundersingh S, Sagar T. Disseminated tuberculosis presenting as prolonged fever without source in a pediatric patient with acute lymphoblastic leukemia. J Can Res Ther 2015;11:1043

How to cite this URL:
Panda S, Radhakrishnan V, Sundersingh S, Sagar T. Disseminated tuberculosis presenting as prolonged fever without source in a pediatric patient with acute lymphoblastic leukemia. J Can Res Ther [serial online] 2015 [cited 2021 Jun 21];11:1043. Available from: https://www.cancerjournal.net/text.asp?2015/11/4/1043/154030


It is well-known that patients with acute leukemia are susceptible to various infections. [1] These infections are usually bacterial and fungal. Tuberculosis in such a setting is quite rare. Reports of tuberculosis in children undergoing treatment for cancer is scarce. [2],[3],[4] Pulmonary tuberculosis is more common and easier to diagnose than extrapulmonary tuberculosis. Extrapulmonary tuberculosis can present as pyrexia of unknown origin (PUO), especially in immunocompromised patients; and can be a challenge to diagnose due to difficulty in obtaining tissue diagnosis and demonstrating acid-fast bacilli. Positron emission tomography (PET) combined with computed tomography (CT) scan has been found to be helpful in diagnosis of extrapulmonary tuberculosis in patients with PUO. [5] We present an interesting case of precursor-Bacute lymphoblastic leukemia (ALL) in a child where prolonged fever without any identifiable source was encountered, which led to management dilemma.

A 5-year-old female presented to us with a history of fever for 1 month. She was diagnosed to have precursor-B ALL on bone marrow morphology and flowcytometry. Cytogenetics showed a normal female karyotype. Patient was started on induction chemotherapy with Berlin-Frankfurt-Munster (BFM)-95 ALL protocol. [6] The patient received induction chemotherapy with prednisolone for 28 days, three doses of vincristine and daunorubicin given every week, and five doses of L-asparginase. On day 24 of induction, she developed febrile neutropenia, which did not respond to antibiotics. The fever persisted after recovery of neutrophil counts, it was intermittent in nature and occurred daily with two to three spikes up to 103 F. Chest X-ray did not reveal any abnormality. A CT of chest and abdomen showed normal lung parenchyma and mediastinum, hypodense nodular lesions in liver, spleen, and both renal parenchyma. In view of persistent fever, a possibility of fungal infection was considered and patient was started on amphotericin-B. Her induction chemotherapy was compromised in view of persistent fever; however, her post-induction bone marrow aspirate was in remission. Bone marrow cultures, multiple peripheral blood cultures, and serological tests were negative for fungal infections, bacterial infections, and tuberculosis. CT-guided biopsy from the hypodense lesion of the liver was attempted thrice and showed only necrotic material and cultures for fungus, bacteria, and tuberculosis were sterile.

Patient was continued on ALL protocol despite of persisting fever. Patient underwent PET-CT and it showed metabolically active multiple hypodense lesions in liver, spleen, and kidneys [Figure 1]a-d]. Finally she underwent laparoscopy, which showed nodules in left lobe of liver and right subdiaphragmatic peritoneum. Biopsy from the left lobe lesion showed caseating granulomatous lesion comprising of Langhans giant cells, lymphocytes, and cellular debris with necrosis suggestive of tuberculosis [Figure 1]e and f]. Subsequent to the laparoscopic biopsy report, patient was started on antituberculosis drugs. Within a week of starting antituberculosis drugs, her fever lysed, her physical condition improved, and she started gaining weight. CT abdomen done 2 months after starting treatment for tuberculosis showed complete resolution of all previously seen lesions. Patient has completed 10 months of antituberculosis treatment and also her ALL treatment. On follow-up, she continued to be in remission.
Figure 1: (a and b) Coronal section of PET scan showing metabolically active lesions in liver (arrow). (c) Sagittal section in CT shows multiple, irregular, enhancing, hypodense lesions (arrow) in both lobes of liver. (d) The liver lesions seen in CT scan show increased metabolic activity (arrow) on PET-CT. (e) The biopsy shows caseating granulomatous lesion comprising of Langhans giant cells (arrow; ×100 magnification) suggestive of tuberculosis. (f) Lymphocytes and cellular debris with necrosis (arrow; ×40 magnification). PET = Positron emission tomography, CT = Computed tomography

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Pulmonary tuberculosis in ALL is much more common and easier to diagnose than disseminated extrapulmonary tuberculosis. [4] The patient had persistent fever for 2 months before a diagnosis of tuberculosis could be established and during this period she had received multiple prolonged courses of broad-spectrum antibiotics and antivirals. PET-CT has been found useful in identifying pathological sites in patients with PUO and has also been useful in identifying sites for guided biopsies. [7] PET-CT is not routinely recommended for diagnosing pulmonary tuberculosis as the diagnosis can be established with sputum studies or bronchoscopy. In a person with suspected malignancy, a tuberculous lesion on PET-CT can mimic a malignancy due to false positive uptake. Our case highlights the importance of selective use of PET-CT during a work-up for prolonged fever. This case is also reported for its rarity and to convey the importance of histopathological examination for confirmation of infective etiology, especially visceral tuberculosis.

 > References Top

Hakim H, Flynn PM, Knapp KM, Srivastava DK, Gaur AH. Etiology and clinical course of febrile neutropenia in children with cancer. J Pediatr Hematol Oncol 2009;31:623-9.  Back to cited text no. 1
Klossek A, Dannenberg C, Feuerhahn MR, Korholz D. Pulmonary tuberculosis in a child receiving intensive chemotherapy for acute myeloblastic leukemia. J Pediatr Hematol Oncol 2004;26:64-7.  Back to cited text no. 2
Chen CC, Huang LM, Chang YL, King CC, Lin KH. Acute respiratory distress syndrome due to tuberculosis in a child after allogeneic bone marrow transplantation for acute lymphoblastic leukemia. J Formos Med Assoc 1999;98:701-4.  Back to cited text no. 3
Lancioni C, LaBeaud AD, Esper F, Abughali N, Auletta J. Pulmonary tuberculosis presenting as fever without source in a pediatric patient with acute lymphoblastic leukemia. Pediatr Blood Cancer 2009;53:1318-20.  Back to cited text no. 4
Yu HY, Sheng JF. Liver tuberculosis presenting as an uncommon cause of pyrexia of unknown origin: Positron emission tomography/computed tomography identifies the correct site for biopsy. Med Princ Pract 2014;23:577-9.  Back to cited text no. 5
Moricke A, Reiter A, Zimmermann M, Gadner H, Stanulla M, Dordelmann M, et al. German-Austrian-Swiss ALL-BFM Study Group. Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: Treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95. Blood 2008;111:4477-89.  Back to cited text no. 6
Solav SV. FDGPET/CT in evaluation of pyrexia of unknown origin. Clin Nucl Med 2011;36:e81-6.  Back to cited text no. 7


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