Cerebral lesions in hematological malignancies: a case report
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Published on: November 28, 2015
Nicoletta D'Ettore1, Valentina Scheggi2, Brunetto Alterini2
1Division of General Cardiology, Cardiothoracovascular Department, Azienda Ospedaliero-Universitaria Careggi, University of Florence, Largo Brambilla 3, 50133, Florence, Italy. nicoletta.dettore@gmail.com.
Insights
A rare central nervous system disease, progressive multifocal leukoencephalopathy (PML), can occur in patients treated with monoclonal antibodies. This case highlights the importance of considering PML in patients with neurological symptoms and suspicious MRI findings, especially those on immunosuppressive therapy.
Area of Science:
- Neurology
- Infectious Diseases
- Oncology
Background:
- Progressive multifocal leukoencephalopathy (PML) is a rare, fatal demyelinating disease of the central nervous system.
- Reactivation of the John Cunningham virus (JCV) causes PML.
- Monoclonal antibody therapy is an emerging risk factor for PML.
Observation:
- A 62-year-old man presented with right homonymous hemianopia.
- Initial MRI and biopsy suggested relapsed lymphoma but revealed macrophages.
- Worsening neurological symptoms prompted a second MRI, showing demyelinating lesions.
Findings:
- Cerebrospinal fluid analysis detected high levels of John Cunningham virus DNA (over 9 million units/μL).
- The patient received supportive care, but the outcome was poor.
Implications:
- PML should be considered in the differential diagnosis of cerebral lesions in patients with hematologic malignancies.
- Early suspicion and diagnosis of PML are crucial, particularly in patients on immunosuppressive or immunomodulatory drugs.
- Multidisciplinary assessment aids in diagnosing cerebral lesions in immunocompromised patients.
Background:
Progressive multifocal leukoencephalopathy is a rare central nervous system disease, resulting from reactivation of latent John Cunningham virus. Monoclonal antibodies have recently become a relevant risk factor for developing progressive multifocal leukoencephalopathy. We report the case of a 62-year-old Caucasian man who was admitted to our department in June 2020 because of right homonymous hemianopia. Magnetic resonance imaging findings were first interpreted as an intracranial relapsed lymphoma, so brain biopsy was performed, but no neoplastic cell was found. Histological sample only showed a large number of macrophages. The patient came back to our attention because of the worsening of neurological symptoms. A second magnetic resonance imaging showed widespread lesions suggestive of a demyelinating process. John Cunningham virus DNA was detected by polymerase chain reaction assay of the cerebrospinal fluid (over 9 million units/μL). The patient was treated supportively, but the outcome was poor.
Discussion:
A multidisciplinary assessment should be performed for differential diagnosis of cerebral lesions in hematologic malignancies. Progressive multifocal leukoencephalopathy should be suspected in cases of subacute neurological symptoms and imaging findings consistent with it, especially if the patient received immunosuppressive or immunomodulatory drugs.
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