Progressive multifocal leukoencephalopathy after autologous bone marrow transplantation and alpha-interferon immunotherapy

Ré, Daniel; Bamborschke, S; Feiden, W.; Schröder, R; Lehrke, Ralph; Diehl, Volker; Tesch, Hans

doi:10.1038/sj.bmt.1701568

Cited by 59 publications

(32 citation statements)

References 11 publications

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“…6,[14][15][16] A retrospective study showed that 37% of allogeneic BMT patients developed neurological symptoms and the most frequent cause was the use of immunosuppressive drugs. 8 However, cerebrovascular events and CNS infections resulted in the most severe complications.…”

Section: Discussionmentioning

confidence: 99%

West Nile virus encephalitis causing fatal CNS toxicity after hematopoietic stem cell transplantation

Reddy¹,

Davenport

Ratanatharathorn³

et al. 2003

Bone Marrow Transplant

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Summary:We describe here a patient who died of progressive CNS deterioration following allogeneic stem cell transplant with West Nile virus as the sole pathogen on the cerebrospinal fluid and brain tissue analysis. A 50-yearold male with Philadelphia chromosome-positive acute lymphocytic leukemia (ALL) underwent allogeneic PBSCT from his HLA identical sister. After engraftment, the patient developed fever with progressive and ultimately fatal neurological deterioration. Imaging studies of the brain including CT and MRI scans were remarkable for mild low attenuation lesions of the white matter. CSF analysis was negative for neoplastic cells, bacteria, AFB, CMV, HSV, fungal infections and leukemic relapse. However, serological analysis of both the serum and CSF was positive for West Nile virus-specific IgM antibodies. At autopsy, West Nile virus PCR and cultures were positive in the mid-brain tissue. Electron micrographs showed evidence of viral particles. Given the recent increase in the spread of West Nile virus infections and the increased susceptibility of BMT patients to infectious complications, West Nile virus encephalitis should be considered in patients undergoing transplantation.

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Section: Discussionmentioning

confidence: 99%

West Nile virus encephalitis causing fatal CNS toxicity after hematopoietic stem cell transplantation

Reddy¹,

Davenport

Ratanatharathorn³

et al. 2003

Bone Marrow Transplant

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“…In this study, patients with JC virusspecific CD8-positive CTL had also a higher CD4 + cell count. In our series, CD4 + cell count was available in four of the 5 survivors: 3 had a baseline CD4 cell count higher than 0.34 Â 10 9 /L [33,34,44], and the fourth one had a lower count (0.149Â10 9 /L) that increased after IL2 therapy [31]. In this context, the use of JC virus-specific CTL produced in vitro or the use of peptide pulsed dendritic cells for selection of viral-specific T cells might also be explored [69].…”

Section: Discussionmentioning

confidence: 98%

“…Another explanation could be that the association between Hodgkin disease and PML is already well known and therefore not worth reporting. In contrast, after 1990, its appears that LPDs-associated PML is largely restricted to two groups of severely T-cell immunosuppressed patients: B-CLL patients who had received purine analogues [30,33,[35][36][37][39][40][41][42][46][47][48] and heavily pretreated patients with aggressive non-Hodgkin lymphoma after HDT/HSCT [29,31,34,[43][44][45]49].…”

Section: Discussionmentioning

confidence: 99%

“…All the patients in group A were diagnosed by histology (85% at autopsy). In group B, exclusive histologic diagnosis was made only in 16 patients (66.6%): 4 patients (16.6% of the total) were diagnosed at autopsy and 12 (50% of the total) by using stereotactic brain biopsy) [30][31][32][33][34][35][36][37][38][39]43,46,47]. The remaining 8 group B patients (33.3%) were diagnosed by clinical and/or neuroradiological criteria and the presence of a positive PCR for JC viral DNA in the CSF (Table I) [40][41][42]44,45,48,49].…”

Section: Clinical Findings and Diagnosismentioning

confidence: 99%

“…In group A, 21 patients (95.4%) died as a result of PML (median survival 3 months, range 10 days to 23 months), whereas 16 PML-related deaths (80%) in group B patients occurred within a median of 3 months (range 1-28 months) after the diagnosis of PML (Table IV). Only 5 patients (1 in group A and 4 in group B) survived the disease (Table V) [28,31,33,34,44]. Their median survival was 12 months (range, 10-28 months).…”

Section: Pml Therapy and Outcomementioning

confidence: 99%

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Changes in the natural history of progressive multifocal leukoencephalopathy in HIV-negative lymphoproliferative disorders: Impact of novel therapies

et al. 2005

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The aims of this study were to evaluate the clinical characteristics of HIV-negative patients affected by lymphoproliferative disorders (LPD) who developed progressive multifocal leukoencephalopathy (PML), to delineate the risk factors, and to analyze whether the new antineoplastic therapies are changing the natural history of this infectious disease. We retrospectively analyzed 46 cases with confirmed LPD-associated PML published from 1958 to 2004. Patients were stratified according to two different time periods: group A included patients diagnosed before 1989, and group B included patients diagnosed since 1990, after introduction of purine analogues. Group A patients (n = 22) had received alkylating agents and/or radiotherapy, and the majority (63.6%) had advanced Hodgkin disease. At univariate analysis, uncontrolled Hodgkin disease was the only risk factor for PML. In group B patients (n = 24), the most frequent treatments received were purine analogues (58.3%) and high-dose therapy with hematopoietic stem cell transplantation (33.3%; HDT/HSCT). B-cell chronic lymphocytic leukemia (45.8%) and aggressive non-Hodgkin lymphoma (24.9%) were the most frequent underlying LPDs. Patients treated with purine analogues were more likely to have active LPD, lower CD4 cell counts, and to be older and male than were HSCT recipients. The median interval from purine analogues or HDT/HSCT to PML was 11 months. In HDT/HSCT recipients, this interval was delayed for 10 months when peri-transplantation rituximab was used. Univariate analysis identified age >55 years, male sex, and CD4 cell counts £0.2 · 10 9 /L as risk factors for PML in patients treated with purine analogues. Mortality rates were 95.4% (group A patients), 90% (purine analogues), and 62.5% (HDT/HSCT recipients). At univariate analysis, the only factor that significantly correlated with recovery from infection was female sex. Our findings indicate (1) the possible reduction in reported cases associated with Hodgkin disease and the increasing number of published cases associated with the new antineoplastic therapies (purine analogues and HDT/ HSCT); (2) among patients treated with purine analogues, PML is more common in male patients with CD4 cell counts £0.2 · 10 9 /L; (3) the use of rituximab after HDT/ HSCT seems to delay the onset of PML; and (4) the prognosis is slightly better in transplant recipients. Am.

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Potential Risk of Progressive Multifocal Leukoencephalopathy With Natalizumab Therapy

Stüve¹,

Marra²,

Cravens³

et al. 2007

Arch Neurol

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Progressive multifocal leukoencephalopathy after autologous bone marrow transplantation and alpha-interferon immunotherapy

Cited by 59 publications

References 11 publications

West Nile virus encephalitis causing fatal CNS toxicity after hematopoietic stem cell transplantation

West Nile virus encephalitis causing fatal CNS toxicity after hematopoietic stem cell transplantation

Changes in the natural history of progressive multifocal leukoencephalopathy in HIV-negative lymphoproliferative disorders: Impact of novel therapies

Potential Risk of Progressive Multifocal Leukoencephalopathy With Natalizumab Therapy

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