Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have measured levels of soluble interleukin-2 receptor (sIL-2R) and soluble CD8 (sCD8) in serum and cerebrospinal fluid (CSF) of 127 human immunodeficiency virus (HIV)-seropositive and 51 HIV-seronegative individuals. Serum levels of sIL-2R and sCD8 were higher in HIV+ than in HIV- individuals. HIV+ individuals were grouped by neurological status: asymptomatic, abnormal on neuropsychological screening, HIV-related meningitis, inflammatory demyelinating polyneuropathy, opportunistic central nervous system (CNS) infections and HIV-related dementia, myelopathy or sensory neuropathy. Serum levels of sIL-2R and sCD8 were higher in all HIV+ categories compared to HIV- individuals. Patients with HIV-related meningitis had higher levels of sIL-2R and sCD8 than asymptomatic HIV+ individuals, and inflammatory polyneuropathy patients had higher levels of sCD8. CSF levels of sCD8 were higher in all categories of HIV+ than in HIV- individuals. Patients with HIV-related meningitis, inflammatory neuropathy and opportunistic infections had higher levels than asymptomatic individuals. Examination of the time course showed that serum and CSF levels of sIL-2R and sCD8 increased to very high levels during acute HIV infections. Serum levels then declined over several months to relatively stable elevated levels. By 1-2 years after HIV infection sIL-2R was relatively low in CSF, while sCD8 remained elevated with a gradual decrease over the subsequent years of follow-up.
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PMID:Soluble interleukin-2 receptor and soluble CD8 in serum and cerebrospinal fluid during human immunodeficiency virus-associated neurologic disease. 211 34

The AIDS dementia complex and peripheral neuropathy in AIDS are considered to be direct or indirect manifestations of HIV infection, yet the pathogenesis in unclear. There are parallels between AIDS and Tangier disease clinically and histopathologically and in lipid metabolism. The neurological disorders in AIDS may be caused by dysfunction of cellular cholesterol transport. Substitution of high density lipoprotein is recommended in the treatment of severe polyneuropathy and dementia in AIDS.
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PMID:Abnormalities in cholesterol metabolism cause peripheral neuropathy and dementia in AIDS--a hypothesis. 217 10

The brains of 65 individuals with antibodies to human immunodeficiency virus type 1 (HIV-1), 20 HIV-1 seronegative homosexual men, and 75 heterosexual controls were examined by a quantitative magnetic resonance imaging technique. A white matter aberration was detected most frequently in patients with AIDS-related complex (ARC) or AIDS, but also in asymptomatic HIV-1 seropositive persons and in HIV-1 seronegative homosexual men, of whom two of three tested were reactive for HIV-1 DNA by polymerase chain reaction. The aberration was not found in the control group. Brain atrophy was mainly confined to patients with ARC or AIDS. The brain lesions correlated with the presence of HIV-1 in cerebrospinal fluid and with elevated levels of beta 2-microglobulin and neopterin. The most pronounced brain aberrations were in patients with AIDS-dementia complex. These findings indicate that brain aberrations may occur in persons in the early stages of HIV-1 infection, although to no greater extent than in HIV-1 seronegative homosexual men. The occurrence of pronounced brain lesions seems to be associated with the presence of an advanced immunodeficiency.
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PMID:Quantitative detection of brain aberrations in human immunodeficiency virus type 1-infected individuals by magnetic resonance imaging. 223 Feb 57

The AIDS dementia complex (ADC) is one of the most common and important causes of morbidity associated with infection by human immunodeficiency virus type 1 (HIV-1). The evaluation of ADC in clinical trials is significant not only because of the clinical impact of this syndrome, but also because of the value of measuring its cardinal features as an index of drug efficacy and because of its emerging role as a major clinical end point. The objectives of therapy include both prevention of ADC in the presymptomatic patient and alleviation of established disease. At present, the pathogenesis of ADC is incompletely understood in several critical aspects, particularly the processes underlying the clinical manifestations of central nervous system (CNS) HIV-1 infection and, further, how such processes are related to systemic disease. Consequently, it is not yet clear to what extent, or in which patients, it is necessary to achieve "therapeutic" drug levels within the CNS. Nevertheless, the assessment of ADC prevention and treatment relies principally on the complementary approach of neurological examination for diagnosis and neuropsychological testing for quantitative serial measurement of treatment effects. Additionally, surrogate markers in cerebrospinal fluid (CSF) may hold promise for objective, rapid assessment of treatment response and dose adjustment. Other measurements, including more routine CSF analysis, neuroimaging, and neurophysiological assessments, are used principally for differential diagnosis rather than for monitoring ADC status. Accumulating experience with available antiviral agents suggests that ADC can be effectively prevented and treated, at least for some period of time, and that assessment of this condition is indeed a valuable approach for measuring antiviral therapy.
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PMID:Evaluation of the AIDS dementia complex in clinical trials. 223 3

HIV-infected patients are at increased risk of neurological disease. The most common symptom is an altered mental status, depicted by the progressive chronic stages of AIDS Dementia Complex. The ability to recognize this syndrome so as to be able to refer for evaluation is a key factor in the optometrist's role as primary care provider.
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PMID:Neurological manifestations of AIDS. 224 70

The case history is presented of the first patient with a fatal HIV-2 infection in The Netherlands, a Portuguese woman aged 51 yr. The infection resulted in AIDS, the AIDS-dementia complex and death. Her partner, a retired Cape Verde sailor, also proved to be infected with HIV-2. Epidemiology, virology and clinical manifestations of HIV-2 infection are discussed.
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PMID:[HIV-2 infection in a Portuguese woman with an AIDS-dementia complex living in The Netherlands]. 229 13

A patient presented with a subacute cerebellar syndrome in absence of cognitive impairment or other symptoms. He became demented several months after the onset of the disease. Necropsy demonstrated the typical features of the AIDS dementia complex and severe loss of Purkinje cells of the cerebellum. Patients with subacute cerebellar dysfunction should be evaluated for the presence of human immunodeficiency virus infection.
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PMID:Subacute cerebellar syndrome as the first manifestation of AIDS dementia complex. 232 31

In order to study the correlation between central nervous system (CNS) involvement and EEG abnormalities in HIV infection we studied 100 consecutive HIV patients. Patients were divided into 4 groups; Group I: 42 neurologically asymptomatic subjects; Group II: 6 patients with peripheral neuropathies; Group III: 28 patients with AIDS Dementia Complex; Group IV: 24 patients with secondary CNS involvement. The results of this study emphasize that abnormal EEGs are correlated with CNS involvement. Neurologically asymptomatic patients showed no abnormal tracings, but the presence of borderline EEGs (33%) in asymptomatic patients should be evaluated prospectively.
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PMID:Electroencephalogram and HIV infection: a prospective study in 100 patients. 236 56

Eighty people, all infected by HIV-contaminated drug injection equipment between 1983 and 1984, completed the National Adult Reading Test (NART) and selected revised Wechsler Adult Intelligence Scale (WAIS-R) subtests. Demographic variables (age, sex, years of education, and social class) were recorded as additional indices of premorbid functioning. Cross-sectional comparison of NART and WAIS-R scores showed that cognitive function was not more impaired with increasing severity of HIV illness, as defined by clinical staging. Nor were HIV-positive patients more impaired than a control group of seronegative drug users. Mean NART scores did not differ significantly from that predicted by a regression model, indicating that the NART can be reliably used to estimate premorbid intelligence for this population. However, current performance on WAIS-R subtests was below that expected from population models of cognitive function that combine measures of premorbid IQ and demographic factors, providing evidence of impaired intellectual function. Currently observed cognitive deficits are probably more due to drug use than to the insidious onset of AIDS dementia complex.
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PMID:The Edinburgh cohort of HIV-positive drug users: current intellectual function is impaired, but not due to early AIDS dementia complex. 239 57

AIDS/HIV counselling will increasingly become part of the role of occupational health professionals. Issues that arise in the occupational setting include: occupational transmission, knowledge and attitudes, problems with family and friends, AIDS dementia, and uncertainty. Dilemmas can occur in relation to contamination incidents, HIV positive employees, or staff refusing to work because of fears of HIV/AIDS. It it easier to deal with the problems that arise if the issues have been thought through beforehand. Examples are given of problems that have occurred in a setting of occupational health in the British Health Service and their resolution is discussed.
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PMID:AIDS/HIV counselling in occupational health. 248 87


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