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Progressive multifocal leukoencephalopathy in a 16‐year‐old patient with pancytopenia after autologous bone marrow transplantation for relapsed Hodgkin lymphoma

To the Editor: Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease caused by an opportunistic infection by the John Cunningham (JC) virus [1]. PML occurs most commonly in immunocompromised adults, such as those with human immunodeficiency virus (HIV) infection and those with hematological malignancies treated with aggressive chemotherapy including bone marrow transplantation (BMT) [1–4]. We report on a 16-year-old adolescent in whom PML developed 7 months after autologous BMT was performed to treat relapsed Hodgkin lymphoma. The 14-year-old Japanese patient was sequentially treated with following chemotherapy regimens for Hodgkin lymphoma (mixed cellularity classical type, stage IIIB): 2 cycles each of OEPA (vincristine, etoposide, prednisone, and doxorubicin), ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine), and COPP (cyclophosphamide, vincristine, procarbazine, and prednisone). The patient then underwent radiotherapy. Complete remission was achieved. However, the patient relapsed at the age of 15 years, 1 year 2 months after the initial diagnosis. After undergoing chemotherapy for relapsed disease consisting of 1 cycle each of OEPA, ABVD, and COPP regimens, the patient underwent high-dose chemotherapy including busulfan and cyclophosphamide followed by autologus BMT. A second complete remission was achieved. At the age of 16 years, 7 months after undergoingautologus BMT, the patient was readmitted to our hospital because of neurological symptoms, including apathy, speech disability, and progressive weakness of the upper and lower extremities. Hematologic examination revealed pancytopenia: white blood cell count, 950/ml (neutrophils, 6.0%; lymphocytes, 64.0%; and monocytes, 30.0%); hemoglobin, 5.6 g/dl; platelet count, 3.9 10/ml. Bone marrow examination revealed severe hypocellularity without blastic cells. In addition, gallium scintigraphy and magnetic resonance imaging (MRI) of the chest revealed no sign of relapsed Hodgkin lymphoma. Theanalysisofcerebrospinalfluid(CSF)wasnormal.BloodandCSF cultures yielded no pathogens. A test for (1,3)-b-D-glucan an antigen test for cryptococcus, and antibody tests for toxoplasma and HIV in the serum were negative. A MRI scan of the brain revealed lowintensity lesionsonT1-weighted images (Fig.1A)andhigh-intensity lesions on T2-weighted images (Fig. 1B) and fluid attenuated inversion recovery (FLAIR) images (Fig. 1C) of the left frontal and temporal robes, right frontal white matter, and right midbrain. Polymerase chain reaction (PCR) assays of the CSF samples were negative for herpes simplex and Epstein–Barr virus DNA but were positive for JC virus DNA, leading to the diagnosis of PML. Treatment with risperidone did not improve the neurologic symptoms. The patient’s condition deteriorated rapidly, and he died of multiple organ failure 2 months after readmission. Although PML is a rare in childhood, PML should be considered as a possible diagnosis in children who treated with aggressive chemotherapy, showing central nervous system symptoms. Although PCR of the CSF has emerged as a promising tool for detecting JC virus, false negativity remains a difficult problem due to the sensitivity for JC virus of 50–75% [5]. Moreover, the optimal treatment for HIV-negative patients with PML has not been defined.Further investigation isneeded todeveloprapid andaccurate diagnostic tools and effective treatments.