SEARCH · PubMed Health

Results for “Leukoencephalopathy, Progressive Multifocal”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources

PubMed1999

[Progressive multifocal leukoencephalopathy: morphologic possibilities of diagnostic classification methods and in situ hybridization].

Progressive multifocal leucoencephalopathy is caused by infection with JC virus. The disease affects patients with immunodeficiencies, hematologic diseases, and patients treated with radiotherapy. The disease is characterised by foci of demyelinisation with atypical astrocytes and oligodendrocytes. Oligodendrocytes contain typical intranuclear inclusions. Progressive multifocal leucoencephalopathy and its verification is presented in three cases. Two patients died of progression of a malignant neoplasm and the leucoencephalopathy was a complication of the malignancy. The third case was a biopsy specimen taken from the brain of a patient who received a renal transplant. The material of all patients was analysed by light and electron microscopy, and in situ hybridisation with a probe specific for JC virus. In situ hybridisation proved to be the most specific and a simple method to demonstrate the infection in all cases. It is useful in instances in which the histologically detectable lesion is not characteristic, and in cells in which the conventional histologic methods fail to reveal the intranuclear inclusions of JC virus.

Aged↗

PubMed1994

Progressive multifocal leukoencephalopathy in a patient with Alzheimer's disease.

An 80-year-old woman with slowly progressive dementia of at least 1 year's duration died with an abrupt change in the rate and character of mental deterioration. Pathologic examination of the brain showed Alzheimer's disease as well as progressive multifocal leukoencephalopathy (PML) in the parietal and cerebellar areas. JC virus (JCV) was detected by polymerase chain reaction (PCR) amplification of paraffin sections from both PML and non-PML areas of the cerebrum. Analysis by in situ hybridization and reverse transcriptase PCR in situ localized JC viral DNA and RNA to the nuclei of oligodendrocytes only in the areas of demyelination. This case is noteworthy in that PML occurred in the setting of Alzheimer's disease by presumed activation of latent JCV in the absence of usual causes of immunocompromise.

Aged↗

PubMed1999

Progressive multifocal leukoencephalopathy: improved survival of human immunodeficiency virus-infected patients in the protease inhibitor era.

To examine factors affecting survival after diagnosis of progressive multifocal leukoencephalopathy (PML), we analyzed data from an observational cohort study, the Adult and Adolescent Spectrum of HIV Disease project. We identified 415 patients diagnosed with PML during 1990-1997. The median survival time after diagnosis was 1 month. By use of an extended proportional hazards, multivariate regression model, risk factors associated with decreased survival time included CD4 count <0.20 x 10(9) cells/L (risk ratio [RR], 2.1; 95% confidence interval [CI], 1.3-3.5) compared with >/=0.20 x 10(9) cells/L, whereas factors associated with increased survival time were prescription of antiretroviral medication that contained a protease inhibitor (RR, 0.2; 95% CI, 0.1-0.4) and prescription of other antiretroviral medication (RR, 0.6; 95% CI, 0.5-0.8) compared with no antiretroviral prescription. We conclude that protease inhibitor use (in combination antiretroviral therapy) is likely to favorably affect survival time after diagnosis of PML.

AIDS Dementia Complex↗

PubMed1994

Isolated motor control dysfunction related to progressive multifocal leukoencephalopathy during AIDS with normal MRI.

We describe the case of a human immunodeficiency virus-infected 34-year-old man with progressive multifocal leukoencephalopathy (PML). His case displayed unusual features, including a bizarre movement disorder, predominant involvement of the subcortical U fibers on neuropathologic examination, and the absence of MRI abnormalities suggestive of PML. Anatomic-clinical correlations are discussed.

AIDS Dementia Complex↗

PubMed1998

Prognostic value of JC virus load in cerebrospinal fluid of patients with progressive multifocal leukoencephalopathy.

JC virus (JCV) load was determined by using quantitative polymerase chain reaction in cerebrospinal fluid (CSF) of 12 patients with AIDS-associated progressive multifocal leukoencephalopathy (PML) and compared with clinical outcome. JCV loads varied widely (3-7 log10 JCV equivalents/mL of CSF) and were apparently not related to absolute CD4 cell counts or CSF and plasma human immunodeficiency virus type 1 loads. A significant correlation was observed between JCV load and survival time (Spearman's rank correlation, -0.83; P<. 01). Moreover, CSF JCV load decreased and then became undetectable in 1 PML patient receiving cidofovir treatment, and this was associated with clinical improvement. These results show that CSF JCV load may be useful as a prognostic parameter and in monitoring the effectiveness of anti-JCV therapies in PML patients.

AIDS Dementia Complex↗

PubMed2006

[Progressive multifocal leukoencephalopathy secondary to JC virus infection after liver transplantation and treatment of recurrent hepatitis C].

Progressive multifocal leucoencephalopathy due to JC virus is a rare complication of liver transplantation. Only four cases have already been described in the literature. This disease is difficult to differentiate from leucoencephalopathy associated with immunosuppressive drugs such as cyclosporin or tacrolimus. Positive diagnosis of progressive multifocal leucoencephalopathy no longer requires cerebral biopsy. It must be confirmed by positive JC virus RNA amplification in the cerebrospinal fluid. We report a case of progressive multifocal leucoencephalopathy occurring 18 months after liver transplantation for hepatitis C-related cirrhosis.

Female↗

PubMedDate not supplied

Rapidly progressive multifocal leukoencephalopathy with substantial cell-mediated inflammatory response and with cognitive decline of non-Alzheimer type in a 75-year-old female patient.

Autopsy findings of rapidly progressive and widespread multifocal leukoencephalopathy (PML) in a 75-year-old woman with no known predisposing disease are demonstrated. Originally she was given a clinical working diagnosis of syndrome of progressive supranuclear palsy (PSP). The neuropathological investigation revealed widespread white and gray matter changes consistent with PML, and the JC virus was verified by EM, in situ hybridization and immunohistochemistry. In contrast to the few chronic inflammatory cells generally seen in PML in this case there was a substantial cell-mediated inflammatory response reflected in numerous T-helper and T-killer cells. The uncommon, widespread distribution of lesions and substantial cell-mediated response reported might indicate that the rearrangement of viral genome, previously suggested of importance for viral growth in the central nervous system (CNS), is also important for viral spread within the CNS, infectivity of glial cells and for the activation of cell-mediated immunity.

Aged↗

PubMed1999

Immunohistochemical detection of JC virus in nontumorous renal tissue of a patient with renal cancer but without progressive multifocal leukoencephalopathy.

We performed immunohistochemical staining on the nontumorous renal tissue of 45 patients with renal cancer but without progressive multifocal encephalopathy using JCV-specific antibody. For one patient we found positive staining of the nuclei of the renal collecting ducts. Immunoelectron microscopic examination of the positive cell nuclei revealed electron-dense polyomavirus-like particles.

Antibodies, Viral↗

PubMed2006

[New trends in progressive multifocal leukoencephalopathy].

Infection by Polyomavirus JC is a model of chronic active viral infection, closely controlled by the immune system. Progressive multifocal leucoencephalopathy (PML) is a deadly demyelinating disease of the central nervous system, consecutive to the lytic infection of oligodendrocytes by JC virus. Reactivation of JC virus occurs only in the setting of severe cellular immune deficiency. During the last 25 years, the incidence of PML has significantly increased related to the AIDS pandemic and, more recently, to the growing use of immunosuppressive drugs. There is no specific antiviral treatment for PML. Nevertheless, the availability of highly active antiretroviral therapy has changed the clinical course of PML in HIV-infected individuals. One-year mortality has decreased from 90 percent to approximately 50 percent as a result of reconstitution of the immune system. Recent advances in JC virus biology give new perspectives to the pathogenesis of PML. New trends in the understanding of the cellular immune response against the JC virus have direct implications for patient management and may lead to develop future strategy of immunotherapies for PML.

Anti-HIV Agents↗

PubMed2001

Potent anti-retroviral therapy with or without cidofovir for AIDS-associated progressive multifocal leukoencephalopathy: extended follow-up of an observational study.

To analyze the clinical efficacy of cidofovir combined with highly active anti-retroviral therapy (HAART) in AIDS-related progressive multifocal leukoencepalopathy (PML), a multicenter observational study was performed. Consecutive HIV-positive patients with histologically or virologically proven PML and at least 4 weeks of treatment after diagnosis were examined: 27 patients were treated with HAART, whereas 16 patients were treated with HAART plus cidofovir 5 mg/kg intravenously per week for the first 2 weeks and every other week thereafter. JC virus DNA was quantified in cerebrospinal fluid (CSF) by PCR. Baseline virologic, immunologic, and clinical characteristics as well as HIV RNA and CD4 responses to HAART were homogeneous between the groups. The median follow-up was 132 weeks. In one case (6%), cidofovir was permanently discontinued because of severe proteinuria. One-year cumulative probability of survival was 0.61 with cidofovir and 0.29 without (log rank test P = 0.02). After adjusting for baseline CD4 counts, JC viral load in CSF, Karnofsky, and use of HAART prior to the onset of PML, the use of cidofovir was independently associated with a reduced risk of death (hazard ratio, 0.21, 95% confidence interval, 0.07-0.65; P = 0.005). A randomized study will definitively establish whether cidofovir confers significant advantage over HAART alone in AIDS-related PML.

AIDS-Related Opportunistic Infections↗

PubMed1970