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PubMed1990

Progressive multifocal leukoencephalopathy-remission with cytarabine.

A 51-year-old woman who was in complete remission from non-Hodgkin's lymphoma, developed a rapidly progressive dementia. Progressive multifocal leukoencephalopathy (PML) was diagnosed on the basis of a rising antibody titre to JC polyomavirus in cerebro-spinal fluid and serum and the presence of diffuse white matter changes on magnetic resonance imaging. She was treated initially with intravenous cytarabine and showed minimal improvement. Rapid improvement occurred when intrathecal cytarabine was added and the patient is in complete remission from both lymphoma and PML 20 months later.

Cytarabine↗
PubMedDate not supplied

Slow virus diseases of the central nervous system.

Slow virus diseases are characterized by a long asymptomatic period, often months or years in duration, between the introduction of the infectious agent and the appearance of clinical illness. Two distinct groups cause serious degenerative diseases of the brain and spinal cord. The first to be identified are those caused by "unconventional agents," kuru and Creutzfeldt-Jakob disease. The second category, "conventional virus diseases," include SSPE (subacute sclerosing panencephalitis), PML (progressive multifocal leukoencephalopathy), progressive rubella encephalitis, and HIV encephalopathy. The universal focus on acquired immune deficiency syndrome (AIDS) has stimulated new research on slow viruses. The extreme neurological deficits, the chronic nature of these diseases, and the possible concern with infection control make patients with these diseases a challenge to nursing.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Neuropathology of the acquired immune deficiency syndrome (AIDS): a report of 135 consecutive autopsy cases from Switzerland.

Neuropathological changes were studied in a consecutive autopsy series of 135 cases, comprising 73% of all patients who died of AIDS in Switzerland between April 1981 and December 1987. Central nervous system involvement was found in 119 patients (88%), 19 of which had multiple concomitant intracerebral lesions. Among the non-viral opportunistic infections, encephalitis due to Toxoplasma gondii was most frequent and occurred in 35 patients (26%), followed by central nervous system infection with Cryptococcus neoformans, which was found in five patients (4%). Cytomegalovirus (CMV) encephalitis was present in 14 patients (10%). Disseminated microglial nodules without morphological or immunocytochemical evidence of CMV was encountered in 18 patients (13%). However, in all but two of these patients there was evidence of extracerebral CMV infection, suggesting that CMV was responsible for these nodular encephalitides. Nine patients (7%) had progressive multifocal leukoencephalopathy (PML); in five of these, demyelination was associated with extensive tissue destruction and cyst formation. HIV-associated encephalopathy was observed in 21 patients (16%) and showed two characteristic morphological patterns: progressive diffuse leukoencephalopathy (PDL) and multifocal giant cell encephalitis (MGCE). PDL was observed in 13 cases and characterized by diffuse pallor and gliosis of the cerebral and cerebellar white matter with scattered multinucleated giant cells, but without significant inflammatory response. MGCE was found in eight patients and characterized by clusters of numerous multinucleated giant cells, rod cells, macrophages, lymphocytic infiltrates and occasional necroses. In our view, PDL and MGCE represent the two opposite variants of HIV-induced encephalopathies, with overlapping intermediate manifestations.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Altered CD4+/CD8+ T-cell ratios in cerebrospinal fluid of natalizumab-treated patients with multiple sclerosis.

BACKGROUND: Treatment with natalizumab, a monoclonal antibody against the adhesion molecule very late activation antigen 4, an alpha4beta(1) integrin, was recently associated with the development of progressive multifocal leukoencephalopathy, a demyelinating disorder of the central nervous system caused by JC virus infection. OBJECTIVE: To test the effect of natalizumab treatment on the CD4(+)/CD8(+) T-cell ratios in cerebrospinal fluid (CSF) and peripheral blood. DESIGN: Prospective longitudinal study. SETTING: Academic and private multiple sclerosis centers. PATIENTS: Patients with multiple sclerosis (MS) treated with natalizumab, untreated patients with MS, patients with other neurologic diseases, and human immunodeficiency virus-infected patients. MAIN OUTCOME MEASURES: CD4(+) and CD8(+) T cells were enumerated in CSF and peripheral blood. The mean fluorescence intensity of unbound alpha4 integrin on peripheral blood CD4(+) and CD8(+) T cells was analyzed before and after natalizumab therapy. RESULTS: Natalizumab therapy decreased the CSF CD4(+)/CD8(+) ratio of patients with MS to levels similar to those of human immunodeficiency virus-infected patients. CD4(+)/CD8(+) ratios in peripheral blood in patients with MS progressively decreased with the number of natalizumab doses, but they remained within normal limits. Six months after the cessation of natalizumab therapy, CSF CD4(+)/CD8(+) ratios normalized. The expression of unbound alpha4 integrin on peripheral blood T cells decreases with natalizumab therapy and was significantly lower on CD4(+) vs CD8(+) T cells. CONCLUSIONS: Natalizumab treatment alters the CSF CD4(+)/CD8(+) ratio. Lower expression of unbound alpha4 integrin on CD4(+) T cells is one possible mechanism. These results may have implications for the observation that some natalizumab-treated patients with MS developed progressive multifocal leukoencephalopathy.

Adolescent↗
PubMed2001

Successful treatment of aids related PML with HAART and cidofovir.

Progressive multifocal leukoencephalopathy (PML) is a progressive demyelinating infection of the central nervous system caused by the JC virus (JCV) in an advanced state of the acquired immunodeficiency syndrome (AIDS). Currently there are still no drugs with proven clinical efficacy against JCV, though highly active antiretroviral therapy (HAART) and the associated partial immune reconstitution have a beneficial effect on the survival time of AIDS-related PML. Various case reports have described an acceptable response under treatment with cidofovir which may be of particular benefit if HAART does not result in sufficient immune reconstitution. We report a patient with AIDS-related PML who improved under combined therapy with HAART and cidofovir. This suggests that the immediate combination of both drugs further improves the outcome of AIDS-related PML.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Types of immunological failure in the "slow-virus" encephalopathies and multiple sclerosis.

The pathogenesis of the slow virus encephalopathies and multiple sclerosis is reviewed within the framework of the immune response. The diseases are analyzed for the component of the immune response that appears to be crucial to the host's failure to control the disease. Thus, the absence of an immune response in the spongiform encephalopathies appears to reflect a failure of antigen recognition. Progressive multifocal leukoencephalopathy (PML), subacute sclerosing panencephalitis (SSPE), and progressive rubella panencephalitis (PRP) may result principally from a failure of effector mechanisms. In PML the failure usually occurs within the setting of an immunosuppressive illness. Conversely, in SSPE and PRP the effector failure seems to result from the nature of the host-virus interaction itself. Finally, evidence is accumulating that a defect of immunoregulation plays a significant role in multiple sclerosis.

Antigens, Viral↗
PubMedDate not supplied

A "progressive" visual loss.

An unusual cause of acute-onset and progressively worsening visual loss is presented. A 60-year-old woman was referred for left homonymous hemianopsia to our Emergency Medicine Department because of a suspected vascular accident. Ten years earlier she had been diagnosed as having chronic lymphocytic leukemia. Brain computed tomography and magnetic resonance imaging revealed "bilateral foci of white matter abnormalities in the occipital regions, compatible with a diagnosis of progressive multifocal leukoencephalopathy". Her cerebrospinal fluid was positive for papovavirus JC. Progressive multifocal leukoencephalopathy due to papovavirus JC, a typical complication in AIDS patients, is a rare complication in patients with other immunosuppressive conditions, such as chronic lymphocytic leukemia.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Management of infections by the human polyomavirus JC: past, present and future.

Progressive multifocal leukoencephalopathy is a fatal demyelinating disease caused by infection of oligodendrocytes by the human polyomavirus known as JC virus. Over the past 10 years, the disease has been documented almost exclusively in AIDS patients, who constitute a rapidly growing population of immunosuppressed individuals. More recently, progressive multifocal leukoencephalopathy has also been described in patients undergoing solid organ or cell transplant, as a result of immunosuppressive therapy to avoid graft rejection. Although there are several reports of successful treatment of progressive multifocal leukoencephalopathy, large-scale prospective trials have been few, and with mixed results. As more is discovered about the biology of JC virus infection and advances are made in targeted parenchymal delivery of therapeutic agents, there is hope for the development of an effective therapy for progressive multifocal leukoencephalopathy.

Antiviral Agents↗