Mediastinal Adenopathy with Brain lesions


A 26 year old male patient presented with fever of five days duration. The complete haemogram showed a haemoglobin of 13.2g/dL, WBC count of 13500/mm3 with a differential count of 75% polymorphs, 21% lymphocytes, 2% eosinophils and 2% monocytes and a platelet count of 232,000/mm3. The smear did not show plasmodium and the serology for dengue and HIV was negative. The liver and kidney functions and the X-ray Chest was normal.

A CT scan of the chest was performed which showed mediastinal adenopathy which showed patchy enhancement on injection of contrast. The site was deemed as inaccessible for a biopsy

The patient was initiated on four drug anti-tuberculous therapy. The fever subsided in a week.

About two weeks after discharge the patient has a left sided seizure with unconsciousness. He was admitted to the hospital anti-convulsants given and an MRI of the brain preformed.

The MRI showed multiple ring enhancing lesions in the bilateral fronto-parietal temporal lobes with significant peri-lesional oedema and a significant midline structures to the left due to the right frontoparafalcine lesion.

Lymphoma is a highly curable tumour that mimics tuberculous lymphadenitis. Delay in treatment of high grade lymphomas compromises the chance of cure. Lymph node biopsy is an invasive procedure sometimes needing laparotomies and thoracotomies. The issues that arise when a lymph node is relatively inaccessible are:

Is biopsy needed for all patients with lymphadenopathies?

Patients with lymphadenopathy and an infective/inflammatory pathology in the drained areas need not be biopsied. Patients with inflamed nodes need not be biopsied. Patients with deep seated nodes in whom a certain diagnosis can be made by non-invasive tests need not be biopsied. All other patients should be biopsied. FNAC, unless it yields a specific diagnosis, is an inadequate investigation for lymphadenopathy. An excision biopsy is ideal. A large wedge biopsy is acceptable for large nodes and a trucut biopsy is appropriate for deep seated nodes. Many patients have succumbed to an advanced lymphoma because of delayed diagnosis from an inappropriate or inadequate biopsy. From the pathologists point of view the diagnosis of lymphoma may be one of the most challenging. Not everyone is experienced enough to make the diagnosis. Even the experienced pathologists can only report on the material provided. Providing appropriate material is the responsibility of the clinician. When one is treating on a clinical diagnosis the patients needs a close monitoring for signs of treatment failure and an alternative diagnosis.

Is there a blood test for the diagnosis of lymphomas?

Lymphomas are of two types Hodgkin’s and non-Hodgkin. Non-Hodgkin’s lymphoma is a collection of about 30 distinct malignancies of the lymphoid cells. Non-Hodgkin’s lymphomas have a leukaemic phase i.e. the phase when the malignant cells spill into the blood. Leukaemic phase occurs early in the course of the disease in patients with low grade lymphomas e.g. small lymphocytic lymphoma, follicular lymphomas and splenic marginal zone lymphomas and very high grade lymphomas e.g. Burkitt’s lymphoma and lymphoblastic lymphoma. The leukaemic phase of small lymphocytic lymphoma is chronic lymphocytic leukaemia and that of very high grade lymphomas is acute lymphoblastic leukaemia. Blood tests can only diagnose lymphomas which are in the leukaemic phase. There are no other blood tests for the diagnosis of lymphomas

Does an MRI scan differentiate a lymphoma from tuberculosis?

A tuberculous granuloma caseates resulting in ring enhancement and oedema around the lesion. The other ring enhancing lesions include primary brain tumour (glioblastoma), metastasis (especially post chemotherapy), abscess, Toxoplasma and Cryptococcus in HIV, resolving hematoma (10-21 days), radiation necrosis, and aneurysm. The MRI features of a primary CNS lymphoma in an immune competent host are quite distinct. The tumour is isointense on T1 and show pronounced uniform enhancement and very little peri-lesional oedema. Ring enhancement is seen rarely. In immunocompromised patients ring enhancement, multiple lesions, spontaneous haemorrhage and non-enhancing lesions are common making it difficult to distinguish CNS lymphoma from infections in these patients. A patient with high index of suspicion of lymphoma must undergo a biopsy.

Could these CNS lesions be from a lymphoma?

The MRI picture is inconsistent with a lymphoma in an immune competent patient. Synchronous CNS and systemic lymphomas are very rare and have been reported only in immunocompromised patients. One report of AIDS related lymphomas described synchronous CNS involvement in 5/19 patients (Annals of Oncology 18 (Supplement 9): ix178–ix182, 2007, abstract 71). Synchronous CNS involvement has also been described in a child with immunodeficiency J Pediatr Hematol Oncol. 2008 Apr;30(4):317-9. Isolated CNS relapse from a lymphoma is seen in less than 1% of the patients. This patient was treated as tuberculosis.

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