Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We sought to determine whether the detectability of phytohemagglutinin-inducible p24 (PHA-p24) in short term cultures of peripheral blood mononuclear cells correlates with an increased risk of vertical transmission among human immunodeficiency virus type 1 (HIV-1)-infected pregnant women and more severe symptomatology among HIV-1-infected infants. The assay for PHA-p24 was performed on specimens obtained from HIV-1-infected women during their pregnancy and from infants during the first 6 months of life. Infants were followed prospectively to determine HIV-1 infection outcome and symptomatology. Among PHA-p24 positive women 9 of 19 (47.4%) gave birth to HIV-1-infected infants compared with 4 of 25 (16.0%) of PHA-p24-negative women (P = 0.02). Among women who tested PHA-p24-positive and had a CD4+ lymphocyte count < 500 cells/mm3, 8 of 15 (53.3%) gave birth to HIV-1-infected infants compared with 4 of 26 (15.4%) not meeting these conditions (P = 0.01). Among HIV-1-infected infants 4 of 5 (80%) of those testing PHA-p24-positive by one month of age developed an opportunistic infection or encephalopathy by 12 months of age, compared with none of the 11 infants testing PHA-p24-negative (P = 0.003). We conclude that PHA-p24 may be a useful in vitro measure for increased risk of vertical transmission among HIV-1-infected pregnant women and increased risk for rapid development of severe disease among HIV-1-infected infants.
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PMID:Phytohemagglutinin-inducible p24 in peripheral blood mononuclear cells as a predictor of human immunodeficiency virus type 1 vertical transmission and infant clinical status. 789 74

There are few reports of the behavioral manifestations in the pediatric population infected with human immunodeficiency virus type 1 (HIV-1). We report a case of a 4-year-old child with acquired immunodeficiency syndrome, whose initial manifestation of central nervous system involvement consisted of sudden onset of impulsivity, hyperactivity, initial insomnia, and aggressive behavior. This clinical picture may suggest an initial presentation of HIV-1 encephalopathy. Clonidine was helpful in ameliorating these behaviors.
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PMID:Case study: behavioral symptoms of pediatric HIV-1 encephalopathy successfully treated with clonidine. 789 70

Human immunodeficiency virus infection leads to a deregulated production of a number of cytokines. Some of them (IL-1, IL-6, TNF-alpha, interferon-gamma) are produced in increased amounts in vivo, whereas the production of IL-2 is decreased. This latter abnormality plays a pivotal role in the establishment of the immunodeficiency. Some cytokines (IL-1, IL-6, TNF-alpha) stimulate the in vitro replication of HIV, whereas others (mainly the interferons) inhibit it. The effect of cytokines in vivo in the spreading of HIV remains, however, largely unknown. Cytokines may also be involved in the development of many clinical manifestations associated with HIV infection. IL-1, IL-6 and TNF-alpha may play a role in tissue damages associated with opportunistic infections, in HIV-related encephalopathy and in cachexia. Cytokines, mainly IL-6, IL-10 and IL-13, may stimulate the growth of malignant cells during Kaposi sarcoma or lymphomas. Better knowledge of the role of cytokines during HIV infection should allow new therapeutic approaches based on the use of either recombinant cytokines or specific antagonists, with the aim of limiting both HIV spreading and the clinical manifestations of this infection.
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PMID:Cytokines in HIV infection. 792 84

Although computed tomography (CT) and magnetic resonance imaging scans often appear normal after mild head trauma, many patients experience attentional or other cognitive disturbances that are difficult to quantify by neuropsychological testing in the absence of a premorbid profile. Within 2 days of mild head trauma, 14 patients with normal-appearing brain CTs were studied with single-photon emission computed tomography (SPECT). They were compared to 15 normal control subjects and to 12 patients with mild human immunodeficiency virus (HIV) encephalopathy. Ten of 14 head trauma patients were separated from the normal control subjects by both independent readers, blinded to the clinical diagnosis. None of the SPECT results from normal control subjects were "read" as trauma. Trauma could not be differentiated from HIV encephalopathy. The observed percentage agreement between raters was 0.83 (kappa = 0.72). SPECT is more sensitive than CT in detecting brain injury after mild head trauma.
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PMID:Early single-photon emission computed tomography in mild head trauma. A controlled study. 794 53

In order to further study AIDS (acquired immunodeficiency syndrome) related neuropathologic findings, specifically progressive diffuse leuko-encephalopathy (PDL) and optic neuropathy, ten macaque monkeys (Macaca mulatta) were infected with simian immunodeficiency virus (SIV), observed for varying periods, and then sacrificed and tissue prepared for analysis. A marked difference from human AIDS pathology was found: in all monkeys, there was significant peripheral axonal dropout, as opposed to relatively little dropout in the central areas of the nerves (t stat. = -5.9, p < .001). In those monkeys infected with SIV for over one year, the axonal loss in the periphery was also greater than in the central optic nerve (t stat. = -5.03, p < .001); monkeys infected with SIV for less than one year had slightly less peripheral than central loss (t stat. = -4.5, p = .001). When compared with humans, however, it was found that the overall loss of axons was less (15% in monkeys vs. up to 45% in humans). There was also a lack of discernible retinal pathology, such as cotton wool spots, in the monkey tissue.
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PMID:Optic nerve morphometry following axonal degeneration from SAIDS in rhesus monkeys. 795 15

Infectious agents have been postulated as causes of multiple sclerosis for over a century. The possible role of a virus or viruses is supported by data that (1) a childhood exposure is involved and "viral" infections may precipitate exacerbations of disease, (2) experimental infections in animals and natural infections in humans can cause diseases with long incubation periods, remitting and relapsing courses, and demyelination, and (3) patients with multiple sclerosis have abnormal immune responses to viruses. The pathogenesis of three human demyelinating diseases of known viral etiology is discussed. In progressive multifocal leukoencephalopathy, a papovavirus selectively infects oligodendrocytes and causes focal areas of demyelination. In postmeasles encephalomyelitis, the virus is lymphotrophic and disrupts immune regulation that can result in an autoimmune perivenular demyelinating illness without evidence of infection of the central nervous system. In human immunodeficiency virus-encephalopathy and myelopathy virus is present in macrophages and microglia and the myelin abnormalities apparently are caused by soluble factors such as viral proteins, cytokines, or neurotoxins. These findings may have implications on how, when, and where to seek viruses in multiple sclerosis.
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PMID:The virology of demyelinating diseases. 801 89

The safety and efficacy of combined therapy with polyethylene glycolated (PEG) interleukin (IL)-2 and zidovudine was assessed in 19 human immunodeficiency virus type 1 (HIV-1)-seropositive subjects in a phase I/II open-label dose-ranging study. During courses of three weekly infusions of PEG IL-2, dose-limiting side effects were seen at 5 x 10(6) IU/m2 and reversible encephalopathy in 1 subject at 3 x 10(6) IU/m2. Significant increases were seen in CD4 cell counts (P < .01), NK cell activity (P < .05), and HIV-specific cytotoxicity (P < .01). Virologic monitoring (quantitative DNA polymerase chain reaction and p24 antigen assay) showed no evidence of increased HIV activation. Patients with CD4 cells < 200/mm3 were entered into a chronic dosing phase. PEG IL-2 was given at 14-day intervals at doses of 10(6) IU/m2 for 8 weeks and 3 x 10(6) IU/m2 for up to 16 weeks, resulting in mean CD4 cell count elevations of 16% and 33%, respectively. PEG IL-2 appears to warrant further investigation, especially in subjects with CD4 cell counts < 200/mm3, to determine whether increased lymphocyte numbers will translate into improved clinical outcome.
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PMID:Safety and efficacy of polyethylene glycol-modified interleukin-2 and zidovudine in human immunodeficiency virus type 1 infection: a phase I/II study. 809 58

From 1988 to 1991 the long-term efficacy of a combined therapy with a polyvalent immunoglobulin/cytomegalovirus (CMV) hyperimmunoglobulin, oral low dose zidovudine, oral cotrimoxazole or inhaled pentamidine was investigated in three groups of human immunodeficiency virus (HIV)-infected children. Group 1A consisted of three perinatally infected children with a CD4 cell decrease of > 400 cells/microliters per year. Group 1B were 17 perinatally infected children with a CD4 cell decrease of < 400 cells/microliters per year. Group 2 comprised eight haemophilic children infected by clotting factors. Despite combined therapy none of group 1A survived longer than 12 months showing a rapid loss of CD4 cell counts, progressive encephalopathy, wasting syndrome and severe bacterial, fungal and CMV reactivation. Under pure intravenous immunoglobulin (IVIG) therapy severe bacterial infections were seen in 1 of 12 children in group 1B. The majority of these patients showed increases or stabilisation of length and weight percentiles. In this group low dose zidovudine therapy was of benefit in HIV-associated neurological symptoms. Nevertheless combined therapy could not prevent further deterioration of CD4 cell counts. In group 2 severe bacterial infections were not seen under IVIG therapy. In this group a temporary increase (6 months) of CD4 cell counts under IVIG/zidovudine combined therapy occurred. Pneumocystis carinii pneumonia (PCP) prophylaxis with oral cotrimoxazole or inhaled pentamidine successfully prevented PCP in all three groups. Under CMV hyperimmunoglobulin (n = 22), ten out of ten patients did not acquire primary CMV infection, whereas CMV reactivations mainly located in the CNS could not be prevented in 5 of 12 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined therapy in human immunodeficiency virus-infected children--a 4-year experience. 810 91

Although neuropsychiatric abnormalities are common in subjects with the acquired immunodeficiency syndrome (AIDS), they are less frequent in asymptomatic human immunodeficiency virus (HIV) seropositive subjects. In contrast, others have reported high rates of electroencephalographic (EEG) abnormality among asymptomatic subjects. Here we report clinical and quantitative EEG findings across all stages of the disease in order to define when during the course of illness abnormalities are detectable. We studied 28 men with AIDS, 32 men with asymptomatic HIV infection, and 56 uninfected controls using clinical and quantitative EEG, measures of immunosuppression, and tests of neuropsychological performance. All were gay or bisexual without other significant risk factors for encephalopathy. We found very low rates of clinical EEG abnormality (less than 7%) among the asymptomatic HIV-infected group, a rate comparable to those of the uninfected group (7.1%). There were no differences between asymptomatic HIV-seropositive subjects and uninfected controls on quantitative EEG measures. Among AIDS patients 28.6% had abnormal clinical electroencephalograms. On quantitative measures, the greatest differences were found in the 6-10 Hz band, where AIDS patients had consistently increased absolute power, relative power, and coherence compared to the uninfected and asymptomatic seropositive groups. A subgroup (n = 9) of asymptomatic HIV-seropositive subjects had worsening performance on Trailmaking test, part B, at or after the time of recording. This subgroup had quantitative electroencephalographic measures similar to those of the AIDS patients and different from the remainder of the asymptomatic HIV-seropositive group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative EEG in patients with AIDS and asymptomatic HIV infection. 817 87

Quinolinic acid (QUIN) is a neurotoxin implicated in the neurologic deficits associated with human immunodeficiency virus type 1 (HIV-1) infection. Forty children with symptomatic HIV-1 disease had elevated (P < .001) cerebrospinal fluid (CSF) QUIN levels (55.8 +/- 8.9 nM) compared with controls (14.9 +/- 3.0 nM). Age-adjusted CSF QUIN concentrations in HIV-1-infected children were predicted by the general index of mental abilities (GIMA, from an age-appropriate intelligence test; r = -0.45, P < .01). Zidovudine therapy reduced CSF QUIN from 64.1 +/- 16.3 to 19.7 +/- 5.2 nM (P < .01; N = 16) and increased GIMA from 76.8 +/- 5.2 to 87.2 +/- 6.3 (P < .001). Encephalopathic HIV-1-infected patients had higher CSF QUIN levels than patients without encephalopathy (79.6 +/- 16.1 vs. 32.7 +/- 6.7 nM, P < .01). CSF QUIN concentrations were also higher (P < .001) in patients who died < or = 3 years after their baseline assessment, compared with those who were still alive. These results warrant further investigation of CSF QUIN in HIV-infected children as a mediator of neurologic dysfunction and a supplemental marker of neurologic disease, particularly when combined with measures of neurocognitive functioning.
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PMID:Quinolinic acid in the cerebrospinal fluid of children with symptomatic human immunodeficiency virus type 1 disease: relationships to clinical status and therapeutic response. 824 22


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