Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine trends in progressive multifocal leukoencephalopathy (PML) mortality in the United States, we analyzed PML death rates and deaths for 1979 through 1994, using US multiple cause-of-death data. During the 16-year study period 3,894 PML deaths were reported. The age-adjusted death rate increased more than 20-fold, from less than 0.2 per million persons before 1984 to 3.3 per million persons in 1994. The increase was attributable to infection with human immunodeficiency virus (HIV) which was recorded on 2,267 (89.0%) of 2.546 death records from 1991 through 1994. PML age-adjusted death rates increased abruptly for all males beginning in 1984 and for black females in 1990. Only a small increase was observed for white females. In 1994, PML was reported in 2.1% of white males who died with HIV-associated disease compared with 1.2% of white females and 1.0% of black males and females who died of similar causes. The epidemic of PML deaths is increasing in parallel with the AIDS epidemic. The increase in HIV-associated PML deaths, first noted among males, has also become apparent among females and probably reflects the increasing importance of drug use and heterosexual transmission of HIV. The reason for the higher prevalence of PML among white males with HIV infection is unknown.
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PMID:Progressive multifocal leukoencephalopathy in the United States, 1979-1994: increased mortality associated with HIV infection. 977 96

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.
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PMID:Prognostic value of JC virus load in cerebrospinal fluid of patients with progressive multifocal leukoencephalopathy. 981 42

Two patients with human immunodeficiency virus (HIV) type 1 infection presented new-onset epilepsia partialis continua (EPC) as an early manifestation of progressive multifocal leukoencephalopathy (PML). EPC occurred with no other seizures and was associated with negative radiographic and electrophysiological findings for several weeks. PML represents an increasingly recognized cause of new-onset seizures in both seropositive and seronegative patients, with no report of EPC as a presenting complaint.
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PMID:HIV-associated PML presenting as epilepsia partialis continua. 987 2

Introduction of highly active antiretroviral therapy (HAART) has been associated with many changes in the complications of human immunodeficiency virus (HIV) infection. A cohort of 25 HIV patients with progressive multifocal leukoencephalopathy (PML) treated with HAART experienced a median survival of >46 weeks. This is an improvement in prognosis compared with recent historic experience and correlated with HIV RNA viral load reductions. We conclude that current HIV therapy is important in improving the outlook of PML in the setting of HIV.
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PMID:HAART improves prognosis in HIV-associated progressive multifocal leukoencephalopathy. 1002 68

Progressive multifocal leucoencephalopathy is an opportunistic JC virus-related pathology occurring in immunocompromised patients. We report a case of severe cellular immunodeficiency in a patient who underwent autologous bone marrow transplantation for acute myeloblastic leukemia, and who subsequently developed progressive multifocal leucoencephalopathy, an unusual pathology in this context. Progressive multifocal leucoencephalopathy was preceded by a peripheral demyelinating neuropathy. We discuss the possible link between these two neuropathies, the possible aggravation or activation from CMV infection, as well as the possible contribution of bone marrow purging in the resultant cellular immunodeficiency.
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PMID:Progressive multifocal leucoencephalopathy with peripheral demyelinating neuropathy after autologous bone marrow transplantation for acute myeloblastic leukemia (FAB5). 1010 May 86

We describe the clinical and virological outcome of human immunodeficiency virus-infected patients with progressive multifocal leukoencephalopathy (PML) treated with cytarabine. Twenty-seven patients received intrathecal cytarabine, 5 received concomitant intravenous cytarabine, and 20 received concomitant antiretroviral therapy. The median baseline CD4+ cell count was 28/mm3. After 4 weeks, 4 (19%) of 21 evaluable patients had stable disease, whereas the others progressed. The median survival from diagnosis and from onset was 66 and 128 days, respectively. Patients with Karnofsky scores of >50 and those previously taking antiretroviral medications had a higher probability of survival 3 months after diagnosis (P = .003 and P = .05, respectively). Overall, after 4 weeks, median JC virus load in CSF increased by 0.7 log10 copies/mL from baseline (P = NS). The mean JC virus load at 4 weeks was lower in patients with stable disease than in progressors (3.47 vs. 4.47 log10 copies/mL; P = .027). JC virus became undetectable in the only patient who had a long-term stable condition. The concentration of JC virus in CSF showed a correlation with clinical outcome.
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PMID:Clinical and virological monitoring during treatment with intrathecal cytarabine in patients with AIDS-associated progressive multifocal leukoencephalopathy. 1019 89

Recent reports suggest that human immunodeficiency virus (HIV)-associated progressive multifocal leukoencephalopathy (PML) may improve with highly active antiretroviral therapy (HAART). We observed three patients who developed PML while receiving HAART. All patients received HAART for 4-11 months and had low plasma levels of HIV-1 RNA before the onset of symptoms of PML. Antiretroviral therapy was changed in two patients, and their plasma HIV-1 RNA levels declined significantly. Despite this virologic response, PML did not improve in these patients. The third patient's HIV-1 RNA level became undetectable while he was receiving HAART, and his symptoms of PML improved after the addition of interferon alpha. Our observations suggest that PML can develop in patients who have shown clinical response to HAART. Furthermore, PML may not improve despite an adequate virologic response to HAART. Definitive therapy is still needed for PML.
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PMID:Progressive multifocal leukoencephalopathy in patients with AIDS receiving highly active antiretroviral therapy. 1045 51

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease resulting from lytic infection of oligodendrocytes by the papovavirus JC (JCV). PML has also been recognized as an AIDS-defining illness. The incidence of PML has increased since 1987 and it occurs in up to 4% of patients with AIDS. To date, there is no treatment available for PML and it usually results in death within 3-6 months of diagnosis. However, there are some reports of remission of PML after antiretroviral therapy. We report a 12-year-old child with hemophilia B and developing AIDS with the onset of PML. With highly active antiretroviral therapy, PML subsided with an increase of CD4 count from 10 to 300/microl in spite of about 1.0 X 10(4) human immunodeficiency virus (HIV)-1-RNA copies. He has survived more than 1 year without specific therapy against JCV. Highly active antiretroviral therapy appears to have improved his prognosis in HIV-associated PML.
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PMID:Remission of progressive multifocal leukoencephalopathy following highly active antiretroviral therapy in a patient with HIV infection. 1048 77

In progressive multifocal leukoencephalopathy (PML) the JC virus (JCV) load in the cerebrospinal fluid (CSF) is discussed as a parameter for disease progression. To investigate the evolution of viral shedding into the CSF, the JCV DNA concentration was quantified by competitive polymerase chain reaction (PCR) in multiple CSF samples from prior to and during an unsuccessful intrathecal salvage therapy in 2 human immunodeficiency virus-infected patients with biopsy-proven PML. With continuous clinical progression the virus load varied considerably intra- and interindividually, ranging from nondetectable to 1.2x108 genome equivalents/10 microliter CSF. Whereas an overall increase during progressive disease was confirmed, the virus burden was either constant or fluctuated irregularly during the intermediate stage of disease. This shows a variability of viral shedding during active disease that must be taken into account when the JCV load is measured by quantitative PCR for both the diagnosis of PML and monitoring under investigational treatment.
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PMID:Quantification of JC virus DNA in the cerebrospinal fluid of patients with human immunodeficiency virus-associated progressive multifocal leukoencephalopathy--a longitudinal study. 1051 34

The natural history of polyomavirus infection, and sensitivity of diagnostic assays remain unclear. A stratified group of 94 human immunodeficiency virus (HIV)-infected patients was studied for both virological and serological markers of active infection with both JC virus and BK virus. JC DNA was detected in the urine of 18 of 81 (22%) patients and BK DNA in 30 (37%) patients. Whilst patients with a low CD(4) cell count (P =.009), CD(4)/CD(8) ratio (P =.031) and beta2M concentration (P =.042) were significantly more likely to be excreting BK, JC excretion did not correlate with any of the immunological markers measured. Furthermore, when all the immunological factors were taken into account, there was no association between either BK or JC excretion and age of the patient (P =.149 for BK, P = 0.891 for JC). BK IgM antibody was detected in only 3 of 30 (10%) BK excretors. JC IgM was detected in 5 of 18 (27. 7%) JC excretors but also in 11 of 63 (17.5%) patients without demonstrable JC excretion. Therefore IgM was a very poor indicator of viruria. One year follow-up on a subset of patients showed that both DNA detection in urine and IgM antibody remain stable over many months despite falling CD(4) cell counts, and would indicate that events leading to enhanced viral production probably occur early after HIV infection. Replication of JC virus in the brain leading to the onset of progressive multifocal leukoencephalopathy (PML) could not be predicted using any of the markers studied.
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PMID:Prevalence of long-term BK and JC excretion in HIV-infected adults and lack of correlation with serological markers. 1053 29


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