Bone Marrow Aplasia: A Rare Complication of Disseminated Tuberculosis

Archives of Clinical Infectious Diseases. 2012 April; 7(2): 75-77.
Published Online 2012 April 13. Brief Report
Bone Marrow Aplasia: a Rare Complication of Disseminated Tuberculosis

1, * 1
Ravi Ambey , Veerbhadra CD
1 Department of Pediatrics, G.R. Medical College, Gwalior, India
*Corresponding author: Ravi Ambey, Department of Pediatrics, G.R. Medical College, Gwalior, India. Tel.: +91-7512403268, E-mail: ravi_ambey97@yahoo.co.in.
Received: February 10, 2012; Revised: February 20, 2012; Accepted: March 01, 2012
We report 11 year old male child, a case of acquired aplastic anemia as a complication of disseminated tuberculosis with acute onset, rapid
downhill course and refractory to both antitubercular drugs as well as immunosuppressive drugs.
Keywords: Anemia, Aplastic; Antitubercular Agents; Child
1. Introduction altered sensorium. Neurological examination revealed

meningoencephelitis with right sided hemiparesis with
We would like to share our experience with an eleven-
left sided facial palsy. The examination of other systems
year-old male, a case of acquired aplastic anemia as a
was within normal limits. Cerebrospinal fluid analysis
complication of disseminated tuberculosis with acute
revealed 432 mg/dL protein, 43 mg/dL glucose, 110 meq/L
onset, rapid downhill course, and refractory to both anti-
chloride with 160 cells out of which 75% was lymphocytes
tubercular as well as immunosuppressive drugs.
and 25% was polymorphs. Gram staining of the CSF was
2. Short Communication
unremarkable and culture was negative. However, CSF
PCR was positive for mycobacteria tuberculosis. There
Tuberculosis is known to cause wide variety of systemic were few signs of raised intracranial pressure without
complications when it disseminates in the body. Tubercu- active seizure. He was given supportive treatment with
losis, suppressing all three cell lines which causes pancy- intravenous fluids, mannitol, and dexamethasone. When
topenia, leading to aplastic anemia has been reported by he was stabilized on the second day, antitubercular ther-
very few case reports, either as the result of disseminated apy and nasogastric tube feeding were initiated. Brain CT
tuberculosis or as an adverse effect of anti-tubercular showed gyral swelling with patchy hemorrhage involv-
medicines (1-3). An eleven-year-old male, weighing 27 kg ing fronto-parieto-temporo-occipital lobe (meningo-en-
with poor nutritional status presented to our pediatric cephelitis) with grade 3 perifocal edema leading to mild
intensive care unit with history of fever for one month, leftward midline shift (Figure. 1).
headache and vomiting for 15 days and weakness of right Hematological deterioration continued as pancytope-
half of his body with right-sided deviation of the angle of nia was persistent on peripheral blood smear examina-
his mouth for 3 days. He also noticed bluish spots on the tion. Peripheral smear did not show any abnormal cells,
chest and trunk for one day. He lived in an overcrowded hemoparasites, or evidence of hemolysis. Bone marrow
house with illiterate parents and belonged to a family aspiration confirmed hypoplastic marrow with epithe-
with low socioeconomic status, but was immunized and loid cell granuloma and focal necrosis consistent with
had BCG scar with a history of contact with an active tu- tuberculosis. There were no features suggestive of he-
berculosis patient in his family. He did not have similar mophagocytic syndrome in bone marrow smear exami-
complaints in the past or any hospitalization or medi- nation. The bleeding time was 14 minutes. The clotting,
cation. On examination, the child was afebrile and nor- prothrornbin and partial thromboplastin time were
motensive, his heart rate was 110 beats per minute, and normal. The urine and stool examination did not show
respiratory rate was 27/min. He was severely pale, and any abnormality. Urine and blood cultures did not grow
petechiae were observed over the trunk accompanied any organisms. The direct and indirect Coomb’s tests
by subconjunctival hemorrhage. He was drowsy with were negative. Blood Widal, HIV ELISA and VDRL were
Implication for health policy/practice/research/medical education:

Tuberculosis is known to cause wide variety of systemic manifestations when it disseminate to the body. We are reporting a case of bone marrow aplasia
in a child due to disseminated tuberculosis. The case emphasizes that Tuberculosis continues to be a Pandora’s Box with many new surprises for clini-
cians.
Copyright © 2012, Shahid Beheshti University of Medical Sciencces;. This is an Open Access article distributed under the terms of the Creative Commons Attribution
License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work
is properly cited.
Ambey R et al.
non-reactive. We added anabolic steroids and later cyclo- bleeding due to severe thrombocytopenia, developed
sporine for which there was no response. There was no hypovolumic shock and died as the result of massive
possibility to transfer the patient to another center with uncontrollable upper gastrointestinal and pulmonary
facilities for bone marrow transplantation. In spite of hemorrhages after 19 days of hospital stay. Autopsy
two platelet-rich plasma transfusions, the child started could not be performed.
Volume Zoom A Volume Zoom A

Ex: 1 Ex: 1
ST PLAIN 8.0 H41s ST Contr 8.0 H41s
Se: 3/5 Se: 6/5
Im: 2/8 Im: 3/8
Ax: I100.0 Ax: I97.1 (COI)
NCCT HEAD CECT HEAD 8 MM
512x512 512x512
H41s H41s
R L R L
1200 kv
2600 mAs 1200 kv
GT:0.0 2600 mAs
TL: 1.0 s GT: -2.0
8.0 mm TL: 1.0 s
W: 80 L: 35 P DFOV: 20.0x20.0 cm 8.0 mm
W: 80 L: 35 P DFOV: 20.0x20.0 cm
Figure 1. Axial Contrast-Enhanced CT Scan Images of The Brain Demonstrating Patchy Gyral Hemorrhage With Leptomeningeal Enhancement Involving
the Right Temporo-Parieto-Occipital Region With Extensive Edema and Midline Shift
Literature shows the occurrence of pancytopenia in aplastic anemia in tuberculosis (5). Aplasia of the bone
disseminated tuberculosis is attributed to hypersplen- marrow was caused by an overwhelming toxemia. Sur-
ism, histiocytic hyperplasia and indiscriminate phago- prisingly no system was able to analyze the effect of the
cytosis of blood cells by histiocytes in the bone marrow, condition on bone marrow, disregarding the neurologi-
maturational arrest, or infiltration of the bone marrow cal aspects. In spite of limiting to two foci, severity of the
by caseating or noncaseating tubercular granulomas. bone marrow disease was rapidly progressive and did not
Tubercular granulomas may cause pancytopenia by re- respond to supportive treatment.
placement of marrow cells or suppression through re-
lease of interferon and lymphotoxin. However, despite Acknowledgements
presence of tuberculous granulomas in a high propor-
I acknowledge Dr Ajay Gaur, Head of the Department
tion of patients with disseminated tuberculosis, pancy-
and Dr GS Patel, Dean for motivating and supporting us
topenia is uncommon (1). Pathophysiology of acquired
to publish the case report.
aplastic anemia in tuberculosis is found to be immune-
Authors’ Contribution
mediated based on observation of recovery after im-
munosuppressant, but the present case was resistant to
this treatment (4). Veerbhadra CD collected the clinical data and prepared
the manuscript. Ravi Ambey reviewed the literature, re-
3. Conclusions vised the manuscript and is guarantor.
Financial Disclosure
There are several unusual features of interest in this
case. Amidst many reports which have not shown asso-
ciation between tuberculosis and aplastic anemia, our We declare that we have no financial interest related to
case brings back the old view to support the causation of material in manuscript.
76 Arch Clin Infect Dis. 2012;7(2)

Ambey R et al.
Funding/Support berculosis: interesting hematological observations. J Assoc Physi-

cians India. 2010;58:243-4.
The study did not receive any fund. 3. Kernohan EJ. Aplastic anaemia complicating miliary tuberculo-
sis. Br Med J. 1950;2(4675):399-400.
References 4. Young NS. Pathophysiologyic mechanism in acquired aplastic
anemia. Heamatol. 2006:72-7.
1. Yadav TP, Mishra S, Sachdeva KJ, Gupta VK, Siddhu KK, Bakshi G, 5. Hsu HC, Lee YM, Su WJ, Huang CY, Yang CF, Ho CK, et al. Bone mar-
et al. Pancytopenia in disseminated tuberculosis. Indian Pediatr. row samples from patients with aplastic anemia are not infected
1996;33(7):597-9. with parvovirus B19 and Mycobacterium tuberculosis. Am J Clin
2. Avasthi R, Mohanty D, Chaudhary SC, Mishra K. Disseminated tu- Pathol. 2002;117(1):36-40.
Arch Clin Infect Dis. 2012;7(2) 77

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Archives of Clinical Infectious Diseases. 2012 April; 7(2): 75-77.

Published Online 2012 April 13. Brief Report

Bone Marrow Aplasia: a Rare Complication of Disseminated Tuberculosis

Keywords: Anemia, Aplastic; Antitubercular Agents; Child

1. Introduction altered sensorium. Neurological examination revealed

Implication for health policy/practice/research/medical education:

Volume Zoom A Volume Zoom A

76 Arch Clin Infect Dis. 2012;7(2)

Funding/Support berculosis: interesting hematological observations. J Assoc Physi-

Arch Clin Infect Dis. 2012;7(2) 77

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