Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 4, 2011, pp. 628-630

Neurology India, Vol. 59, No. 4, July-August, 2011, pp. 628-630

Letter to Editor

Meningeal tuberculoma mimicking chloroma in a patient with chronic myeloid leukemia on imatinib

Pravin Salunke¹, Kirti Gupta², Navneet Singla¹, Harnarayan Singh¹, Paramjeet Singh³, Kanchan K Mukherjee¹

¹ Department of Neurosurgery, PGIMER, Chandigarh, India
² Department of Histopathology, PGIMER, Chandigarh, India
³ Department of Radiodiagnosis Histopathology, PGIMER, Chandigarh, India
Correspondence Address: Kanchan K Mukherjee, Department of Neurosurgery, PGIMER, Chandigarh, India, kkmneuro@yahoo.in

Date of Submission: 27-Apr-2011
Date of Decision: 30-Apr-2011
Date of Acceptance: 19-May-2011

Code Number: ni11187

PMID: 21891950

DOI: 10.4103/0028-3886.84354

Sir,

Central nervous system (CNS) lesions complicating chronic myeloid leukemia (CML) are rare and a meningeal enhancing lesion in a patient with CML is usually suspected to be a chloroma. ^[1] We report meningeal tuberculoma mimicking chloroma in a patient with CML on imatinib.

A 43-years-female, a known case of CML on imatinib 400 mg per day since 6 years, presented with headache and vomiting without fever and other constitutional symptoms of one week duration. Examination revealed bilateral papilledema and no signs of meningitis. Abdominal ultrasound revealed no hepato-splenomegaly and the chest X-ray was normal. Investigations: Hemoglobin 8.8 g/dl, total leucocyte count (TLC) 11,700/cu mm, and platelet count 5,68,000/cu mm. Patient was started on dexamethasone and the dose of imatinib was stepped up from 400 mg to 600 mg per day. Contrast magnetic resonance imaging (MRI) brain revealed a left temporal meningeal lesion with intense meningeal enhancement. There was an evidence of uncal herniation. The adjacent bone diploe appeared normal [Figure - 1]a-d. In view of features of raised intracranial pressure and temporal mass with uncal herniation, decompression with biopsy was planned. The lesion was adherent to the adjacent dura matter, firm to hard in consistency and had both solid and soft areas. Cisternal cerebrospinal fluid (CSF) and tumor fluid analysis were noncontributory. Post-op recovery was complicated by high grade fever of unknown origin and did not respond to broad spectrum antibiotics. Post-op TLC was 19,300/cu mm. Biopsy confirmed meningeal-based tubercoma. [Figure - 2]a-d. She was started with anti-tubercular therapy (ATT). Response to ATT was promising initially and she became afebrile by day-6. In addition, she was on imatinib and steroids. However, a month later, she presented with altered sensorium. Contrast MRI showed basal exudates and infarcts secondary to vasculitis [Figure - 1]d and e. Lumbar puncture done at this stage revealed mild pleocytosis and was negative for Acid Fast Bacilli and culture. She continued to be on altered sensorium, intermittently opening her eyes and moving her limbs, despite being on 8 weeks of steroids and ATT.

CNS involvement in leukemias is rare and is usually seen in acute myeloid leukemia (AML). Meningeal or parenchymal lesion in these patients is likely to be chloroma/granulocytic sarcoma. ^[2] The leukemic cells possibly migrate from bone marrow via haversian canals to the periosteum and then infiltrate the dura matter and brain parenchyma by subarachnoid perivenous adventitial tissue or by direct hematogenous spread or hematopoetic cell differentiation in embryonic cells in CNS. ^[2] In the absence of acute leukemia, chloroma suggests imminent conversion to AML or blast crisis and is an ominous sign. ^[2] Typically on MRI, the lesion appears isointense or slightly hypointense in T ₁ - and T ₂ -weighted images with homogeneous contrast enhancement. ^[3] Associated bone marrow (diploe) involvement helps differentiating these tumors from other intracranial lesions. ^[3] Meningeal chloroma can mimic meningioma, lymphoma, metastasis, and even herpes simplex encephalitis. ^[2],[4]

Imatinib is the first-line treatment for CML. Isolated CNS relapse in cases of CML on imatinib has been reported. ^[1] Low levels of imatinib in the CSF due to its active out transport by the membrane-bound transport protein (P-glycoprotein) makes the CNS a sanctuary site for leukemic cells. ^[1] Tyrosine kinase plays an important role in T-cell receptor signal transduction and imatinib has been shown to affect T-cell receptor signal transduction, thereby, affecting the cellular immunity; leaving the host susceptible to reactivation of tuberculosis. ^[5] This is true for extra CNS tuberculosis and its role in CNS tuberculosis is unclear. Meningeal based tuberculoma is a rare manifestation of CNS tuberculosis. In this patient, repeat CSF showed pleocytosis. Whether it is related to tuberculous pathology or CNS leukemia is uncertain. ^[6] Generally, the response to ATT in CNS tuberculosis is favorable unless the disease is severe at the start of the treatment. ^[6] Our patient illustrates the fact that one should have a high index of suspicion of CNS tuberculosis in patients with CML on imatinib with meningeal based lesion, more in countries endemic to tuberculosis. Biopsy of the lesion helps differentiate tuberculosis from chloroma.

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