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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to assess the levels of prolactin (PRL) in cerebrospinal fluid (CSF) of HIV-infected patients with regard to nonHIV-infected patients, and to assess the levels of prolactin in the CSF of HIV-infected patients with and without neurological HIV-involvement. Seventeen HIV-infected patients with different degrees of immunological and neurological involvement were studied. A second group of six HIV-seronegative patients with varying clinical conditions requiring lumbar punctures were included as controls. CSF was collected from patients and controls. Patients were studied neurologically and neuropsychologically, and computed tomography of the brain were performed. They were staged according to CDC clinical classification for HIV infection, and on the basis of tomographic findings into one of five stages. An additional classification for neurological involvement in AIDS was used. CD4+ cell counts, CSF studies, serum-prolactin levels and CSF-prolactin levels were performed as principal laboratory tests. CSF PRL concentrations were significantly higher in the HIV-infected group (n = 17) than the nonHIV infected control group (n = 6) (mean +/- s.d.; 5.77 +/- 2.22 vs. 3.53 +/- 0.69 x 10(-6) g l-1, respectively; p = 0.009, Mann-Whitney U-test). Moreover, even CSF-PRL concentration was higher in HIV-infected patients without cognitive impairment (stage 0 of the clinical classification), (n = 12) in comparison with nonHIV infected controls (n = 6) (mean +/- s.d.; 5.51 +/- 2.31 vs. 3.53 +/- 0.69 x 10(-1) g l-1, respectively; p = 0.028, Mann-Whitney U-test). There was a good correlation between serum and CSF-PRL levels in HIV-infected patients when measured by the Spearman Rank Test (rs = 0.773; p = 0.005). PRL raised serum levels were found in 4 out of 13 patients (30.73%). We conclude that higher levels of CSF-PRL are more frequently found in HIV-infected patients in comparison to uninfected controls. High levels of circulating PRL were also found in HIV-infected patients corroborating results from other work. A good correlation coefficient was found between circulating and CSF-PRL levels in HIV-infected patients, suggesting that disruption of the blood-brain barrier might account for a possible pathogenic mechanism.
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PMID:Prolactin levels in the cerebrospinal fluid of patients with HIV infection and AIDS. 947 Oct 94

The aim of the Italian Multicentre Neuropsychological HIV Study is to assess the prevalence and natural history of cognitive deficit in intravenous drug users (i.v.DUs) during the asymptomatic phase of HIV infection. The study is currently being conducted in four centres (Napoli, Benevento, Verona and Pavia) whose catchment areas are characterized by different levels of prevalence of HIV infection. Cognitive evaluation is being performed by means of a standardized neuropsychological test battery. A total of 251 subjects (167 males and 84 females) have been recruited in the cross-sectional phase of the study, including 75 asymptomatic HIV-seropositive i.v.DUs (HIV+/i.v.DUs), 97 HIV-seronegative i.v.DUs (HIV-/i.v.DUs) and 79 non-i.v.DU seronegative controls matched to i.v.DUs with regard to sex, age and educational level. The prevalence of global cognitive impairment (performance at least 1.5 standard deviations worse than the average of the control group, on at least two out of five tests) was significantly higher in HIV+/i.v.DUs than in either HIV-/i.v.DUs (22.7% vs. 8.2%; P < 0.01) or healthy controls (22.7% vs. 2.5%; P < 0.001). The difference between HIV-/i.v.DUs and healthy controls was not statistically significant (8.2% vs. 2.5%; P = 0.19). The results of this study lend further support to the 'cerebral reserve' model. The cerebral reserve could indeed be reduced in i.v.DUs as a consequence of chronic exposure to the substance of abuse, so that these subjects become more vulnerable to direct and indirect neurotoxic effects of HIV.
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PMID:Early neuropsychological impairment in HIV-seropositive intravenous drug users: evidence from the Italian Multicentre Neuropsychological HIV Study. 951 7

Cognitive impairment is a frequent manifestation of advanced human immunodeficiency virus (HIV) infection. The response to antiretroviral medication is often partial and poorly sustained. Recent studies suggest that free radical production within the CNS and neuronal apoptosis may play important roles in the pathogenesis of HIV dementia. We conducted a randomized double-blind, placebo-controlled trial using a parallel group, 2 x 2 factorial design evaluating deprenyl, a monoamine oxidase B inhibitor and putative anti-apoptotic agent, and thioctic acid, an antioxidant, in 36 patients with HIV-associated cognitive impairment. Both deprenyl and thioctic acid were well tolerated with few adverse events. Deprenyl recipients showed significant improvement on tests of verbal memory compared with patients not taking deprenyl. Thioctic acid treatment did not improve cognitive function. These results suggest that deprenyl treatment is associated with cognitive improvement in subjects with mild HIV-associated cognitive impairment, whereas thioctic acid has no benefit. A larger efficacy trial is needed to assess the long-term effect of deprenyl on cognitive performance in patients with HIV infection.
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PMID:A randomized, double-blind, placebo-controlled trial of deprenyl and thioctic acid in human immunodeficiency virus-associated cognitive impairment. Dana Consortium on the Therapy of HIV Dementia and Related Cognitive Disorders. 1037 54

As part of a Kenyan Medical Research Institute study of sexually transmitted diseases, psychiatric and neuropsychological functioning was assessed and related to HIV status. All 373 workers in the food industry who attended an occupational health clinic in Kenya's Nyanza Province for statutory annual health checks during a 10-week period in 1994, were eligible for study enrollment. Of the 337 study volunteers (mean age, 29.1 years), HIV status was available for only 230 subjects due to the loss of specimens between collection and laboratory delivery or the illegibility of numerical codes on specimen tubes; psychiatric and neuropsychological data were collected from 229. 78 workers (34%) were HIV-positive and another 14 (6%) had indeterminate results. No substantial differences in psychiatric morbidity, including depression or performance on neuropsychological tests, were found between HIV-positive workers and HIV-negative controls. Previous studies have documented substantial psychiatric morbidity and cognitive impairment in HIV-infected patients. The methodology of the present study differed from previous research, however, in that volunteers were asymptomatic and unaware they were being tested for HIV and interviewers were uninformed as to the subject's HIV status.
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PMID:Psychological morbidity and HIV in Kenya. 957 Apr 86

Neuropsychiatric disorders make up a large proportion of medical conditions causing disability and death worldwide. This paper reviews the most significant neurological disorders, emphasizing the preventability of most of them. The worldwide impact of cerebrovascular disease, protein-energy malnutrition causing cognitive impairment, tetanus, dementia, meningitis, and epilepsy is summarized. The burden of neurological dysfunction as a complication of tuberculosis, measles, road accidents, congenital anomalies, malaria, falls, war, violence, alcohol, HIV, diabetes, syphilis, and rheumatic heart disease might also be lessened by preventive measures. As in other health problems, major risk factors are poverty, poor access to health care, and social instability.
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PMID:Preventable neurological diseases worldwide. 959 82

Mounting evidence suggests that cognitive dysfunction developing as a result of HIV-1 infection is mediated at least in part by generation of excitotoxins and free radicals in the brain. This syndrome is currently designated HIV-1-associated cognitive/motor complex, was originally termed the AIDS Dementia Complex, and for simplicity, is called AIDS dementia in this review. Recently, brains of patients with AIDS have been shown to manifest neuronal injury and apoptotic-like cell death. How can HIV-1 result in neuronal damage if neurons themselves are only rarely, if ever, infected by the virus? Experiments from several different laboratories have lent support to the existence of HIV- and immune-related toxins in a variety of in vitro and in vivo paradigms. In one recently defined pathway to neuronal injury, HIV-infected macrophages and microglia, or immune-activated macrophages and astrocytes (activated by the shed HIV-1 envelope protein, gp120, or other viral proteins and cytokines), appear to secrete excitants and neurotoxins. These substances may include arachidonic acid, platelet-activating factor, free radicals (NO. and O2.-), glutamate, quinolinate, cysteine, amines, and as yet unidentified factors emanating from stimulated macrophages and reactive astrocytes. A final common pathway for neuronal susceptibility is operative, similar to that observed in stroke and several neurodegenerative diseases. This mechanism involves excessive activation of N-methyl-D-aspartate (NMDA) receptor-operated channels, with resultant excessive influx of Ca2+ and the generation of free radicals, leading to neuronal damage. With the very recent development of clinically tolerated NMDA antagonists, there is hope for future pharmacological intervention.
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PMID:Neuronal injury associated with HIV-1: approaches to treatment. 959 52

HIV-1-associated cognitive impairment has only been preliminarily investigated for associations with mortality. The authors examined 119 HIV-1-positive homosexual men (asymptomatic: n = 96; early symptomatic: n = 23). At follow-up (to 3.5 years), there were 105 survivors and 14 nonsurvivors. Those at the 25th percentile in response speeds and in long-term memory retrieval accuracy were at 6.4 (P < 0.02) and 3.5 (P < 0.05) times increased mortality risk, respectively, of those at the 75th percentile--independent of baseline CDC clinical stage, CD4 cell count, hemoglobin level, antiretroviral and prophylactic medication use, and sociodemographics. Cognitive impairment should be identified early--for maximization of both functional status and survival time.
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PMID:Mild cognitive impairment and risk of mortality in HIV-1 infection. 960 1

Human immunodeficiency virus (HIV) infection results in a chronic course of disease progression and eventual death. With this disease progression comes decreases in health-related quality of life and cognitive function in many patients. We evaluated the construct and discriminant validity of the Medical Outcomes Study four-item and six-item cognitive function scale in a sample of 162 patients with HIV disease. The patients were assessed at baseline and after 4 months with the cognitive function scale, a cognitive functioning transition item, the Reitan trail making test (TMT) and the Centers for Epidemiologic Studies Depression (CES-D) scale. The results found that the four- and six-item cognitive function scales varied by HIV disease stage, CD4 count, self-reported change in cognitive function, TMT-based cognitive impairment and depression. The differences in the cognitive function scores were attenuated, but still remained statistically significant even after controlling for depression. The cognitive function scales predict cognitive impairment based on the TMT. The results support the construct validity of these self-report cognitive function scales.
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PMID:Discriminant validity of the Medical Outcomes Study cognitive function scale in HIV disease patients. 973 45

In this consecutive autopsy study, the pathological evidence of HIV encephalitis, which included the presence of giant cells and/or HIV p24 immunopositivity, was found more frequently in drug users (25 of 45; 56%) than in homosexual men (6 of 35; 17%) with AIDS (P < 0.01). Productive infection, as shown by HIV p24 positivity, was found in frontal lobe white matter in 29 of the 31 HIV encephalitis cases, but was also present in grey matter in 50% of the HIV encephalitis cases. Immunopositivity was confined to microglia, monocytes and most but not all giant cells. HIV-1 proviral load was determined by quantitative PCR in 65 of the 80 cases (separately in grey and white matter in 49 of these), and correlated well with the presence of HIV encephalitis (P < 0.001). Twenty-five patients with AIDS (13 male homosexuals, 12 drug users) showed no HIV encephalitis, opportunistic infection or cerebral lymphoma, while 18 (2 male homosexuals, 16 drug users) showed pure HIV encephalitis. Cognitive function had been assessed prospectively in this cohort and graded as normal or mildly, moderately or severely impaired. Because opportunistic infections and lymphomas of the brain may also lead to dementia, patients found to have these conditions at autopsy were excluded from the final analysis of the cases with dementia, so that the precise correlation between cognitive impairment and pure HIV encephalitis could be determined in this cohort without possible confounding variables. Fourteen of 18 patients with pure HIV encephalitis had shown cognitive impairment. Severe dementia correlated better with pure HIV encephalitis in cases in which grey matter involvement was present (7 out of 9) than in those in which only white matter was involved (2 out of 9) (P < 0.05), although milder degrees of cognitive impairment had been present in a further 5 HIV encephalitis cases. No correlation was found between zidovudine therapy and the degree of cognitive impairment. Systemic and cerebral opportunistic infections and lymphoma showed a negative association with HIV encephalitis, being more common in homosexuals than in drug users, despite comparable CD4 counts in the two groups. These findings suggest that neocortical productive HIV infection is a significant factor in AIDS-related dementia, although this may reflect merely a higher overall viral burden in the brain.
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PMID:HIV encephalitis, proviral load and dementia in drug users and homosexuals with AIDS. Effect of neocortical involvement. 982 65

This preliminary investigation examined neuropsychological performance in a sample of human immunodeficiency virus (HIV)-positive and HIV-negative African-American women with a history of drug use. The study population was comprised of 10 HIV-negative, 9 asymptomatic HIV-positive, 13 symptomatic HIV-positive, and 10 acquired immunodeficiency virus (AIDS) patients. A neuropsychological battery designed to assess attention, psychomotor processing, verbal memory, and visual memory was administered to participants. No evidence of HIV-related cognitive impairment was found in patients in the early stages of HIV infection. Multivariate analyses of variance revealed significant deficits in psychomotor processing and verbal recall in persons with AIDS. These individuals showed greater difficulty in tasks requiring maintained attention and performed poorly on measures of immediate and delayed verbal recall. In contrast, HIV status was not related to visual memory, verbal recognition, or the number of errors made during a verbal recall task. The pattern of cognitive deficits observed in persons with AIDS resembles that commonly associated with subcortical pathology. The cognitive deficits observed were not related to depression or recentness of drug use.
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PMID:Neuropsychological functioning in HIV-positive African-American women with a history of drug use. 982 81


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