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

Between 1989 and 1993, 22 HIV negative patients with primary central nervous system lymphoma (PCNLS) were treated with three different regimens. In group A, 13 patients received preradiotherapy systemic and intrathecal methotrexate (MTX), radiotherapy (RT) and three courses of post-RT chemotherapy (CT) with thiotepa and procarbazine. In group B, 4 patients received a similar CT only after RT and without intrathecal MTX in 3/4 cases. In group C, 5 elderly patients received CT alone. In group A, 9/13 patients achieved response after pre-RT CT and 12/13 were in complete response (CR) after RT. After a median follow-up of 27 months, 8/13 (62%) patients are alive but 4 have leucoencephalopathy and cognitive dysfunction. In group B, all 4 patients were in CR after RT but the 3 patients who did not receive intrathecal MTX died within 10 months with meningeal recurrence. In group C, 4/5 patients had a response to CT. 2 patients died of recurrent tumour at 5 and 10 months, and 2 are living in CR 11+ and 21+ months after diagnosis, 1 after salvage CT. Combined treatment with RT and CT is useful in PCNSL but adequate treatment of the meninges is required. CT alone is sometimes of value in elderly patients in whom RT is not indicated.
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PMID:Primary central nervous system lymphoma: treatment with chemotherapy and radiotherapy. 856 56

The CNS is frequently involved in human immunodeficiency virus (HIV) infection. In recent studies using proton magnetic resonance spectroscopy, investigators found a significant reduction in N-acetyl aspartate, a metabolic marker of neurons, in late stages of dementia. To further understand the relationship between proton magnetic resonance spectroscopy changes and clinical disease and dementia, we compared 20 HIV-infected patients presenting at varying stages of acquired immunodeficiency syndrome (AIDS) dementia complex and infection to 10 age-matched controls. We found a significant reduction in N-acetyl aspartate/creatine only in patients who had advanced dementia and CD4 counts less that 200/microliter. By contrast, a significant elevation in compounds containing choline was present in patients in the early stages of HIV infection of who had CD4 counts greater than 200/microliter, in patients with normal MRI scans, and in all AIDS dementia complex groups, including subjects with no or minimal cognitive impairment. An elevated choline level also occurred in later stages of HIV infection (CD4 < 200/microliter). Our results suggest that an increase in choline occurs before N-acetyl aspartate decrements, MRI abnormalities, and the onset of dementia, and may therefore provide a useful marker for early detection of brain injury associated with HIV infection.
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PMID:Brain choline-containing compounds are elevated in HIV-positive patients before the onset of AIDS dementia complex: A proton magnetic resonance spectroscopic study. 861 83

HIV infection has been associated with decline in a number of cognitive functions that are components of 'working memory'. Thus, tests of working memory that require the interaction of these components may be particularly sensitive to cognitive dysfunction that arises from HIV infection. To assess this possibility, working memory was examined in 147 HIV-seropositive (HIV+) and 38 HIV-seronegative (HIV-) males using the Reading Span Test and the Digit Span subtest from the Wechsler Memory Scale-Revised (WMS-R). Speed of information processing, a component of some working memory tasks, was assessed with a version of the Sternberg Memory Scanning task. Results indicated that symptomatic HIV+ subjects were impaired relative to HIV- control subjects on the Reading Span and Digit Span tests. Asymptomatic and mildly symptomatic HIV+ groups exhibited a trend toward impairment on these tests, and on the whole, a greater proportion of HIV+ subjects than HIV- subjects were impaired. The groups did not differ significantly in information processing speed. These results indicate that deficits in working memory are apparent in at least a subset of HIV-infected individuals. These deficits are most apparent in symptomatic HIV+ individuals, but the decline may begin during the asymptomatic phase of infection.
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PMID:Decline in working memory associated with HIV infection. HNRC Group. 863 52

Seventy-eight asymptomatic HIV-seropositive (aHIV) subjects were examined by means of an extensive neuropsychological test battery in comparison with 32 HIV-seronegative controls. They were also tested with regard to CD4+ and serum p24 antigen. Fifty-six of them completed a clinical follow-up of 12 up to 36 months and 35 also underwent a second session of neuropsychological, CD4+ and p24 antigen assessments at a 12- to 18-month interval from the first session. Results obtained lead to the following conclusions: (a) even among aHIV subjects there is a significant prevalence (28.2%) of cognitive abnormalities for which no cause other than HIV can be found, and therefore this suggests the possible development of HIV-related brain damage since the earliest stages of infection; (b) most sensitive to early HIV-related cognitive impairment are timed psychomotor tasks and memory tasks which require attention, learning and 'active' monitoring or retrieval of information; (c) during the early asymptomatic stages of HIV infection, there is no clear-cut evidence of a cross-sectional relationship between cognition and immunological/ virological markers (at least in the high ranges of CD4+ cell counts considered here); only in relatively more advanced stages does this relationship become evident in the subgroup of aHIV subjects with cognitive abnormalities; (d) the presence of cognitive abnormalities in early HIV infection is predictive of a further decrease in cognitive functioning and faster progression to AIDS-this latter reflected by a faster rate of decline in the number of CD4+ cells and by an increase in positivity of serum p24 antigen.
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PMID:Cognitive impairment in asymptomatic stages of HIV infection. A longitudinal study. 873 40

Utilizing an expanded concept of level of burden, the impact of multiple problems experienced by women in a residential drug abuse treatment program on treatment retention and outcomes is investigated. Level of burden is defined in this study as the number and severity of problems, including psychological problems, cognitive impairment, chronic health problems, HIV/AIDS status, as well as substance abuse. In the first study of 260 women, the ability to retain women in treatment as a function of their level of burden is examined using the technique of survival analysis. Results indicate that early in the course of treatment, high-burden clients tend to be the highest risks for early termination. In addition, there is a significant interaction between time in the program and level of burden. In the second study of 68 women, partial correlations between level of burden and ratings of outcomes by program staff at time of discharge are examined. Results show that many of the treatment outcomes are significantly negatively correlated with the initial levels of burden. Implications for treatment providers and directives for future studies are discussed.
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PMID:Level of burden: women with more than one co-occurring disorder. 878 90

Central nervous system involvement is common in the later stages of HIV infection. The pathophysiology for the development of cognitive impairment in HIV infection is still unclear. Magnetic resonance imaging shows brain atrophy and non-specific white matter abnormalities in some of the patients with HIV dementia. In vivo magnetic resonance spectroscopy (MRS) provides a biochemical profile of the brain and shows promise for furthering the understanding of the pathophysiology associated with HIV-related dementia. Moreover, MRS is a practical and non-invasive method which can help to differentiate the focal lesions of the most frequent opportunistic infections in AIDS.
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PMID:In vivo magnetic resonance spectroscopy in HIV and HIV-related brain diseases. 884 75

The relationship between subjective awareness and objective neuropsychological status in HIV-1 infection remains unclear. Forty-six HIV-1 seropositive males were administered a battery of neuropsychological measures assessing episodic memory, metacognition, and depression. Results of ANOVA revealed a dissociation between subjects' self-complaint of neuropsychological impairment and objective performance, with subjects who denied cognitive impairment performing worse on memory testing. Three subgroups were identified: A group whose self-reported cognitive impairment exceeded deficits demonstrated on memory testing (37% of subjects); a group who denied impairment but evidenced deficits on memory testing (26% of subjects); and a group whose self-appraisal was consistent with performance (37% of subjects). These data suggest that self-report of cognitive dysfunction among HIV-1 infected subjects is frequently at variance with objective neuropsychological testing and that diminished awareness of decline among medically symptomatic HIV-1 infected subjects can be identified.
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PMID:Actual versus self-reported cognitive dysfunction in HIV-1 infection: memory-metamemory dissociations. 887 26

Previous studies in patients receiving interferon-alpha (IFN-alpha) therapy and patients with systemic lupus erythematosus have demonstrated that elevated cerebrospinal fluid (CSF) levels of IFN-alpha are associated with cognitive dysfunction. We measured IFN-alpha levels in CSF and blood by ELISA in human immunodeficiency virus (HIV)-positive patients with (n = 21) and without (n = 23) dementia and HIV-negative controls (n = 48). IFN-alpha was significantly elevated in the CSF of HIV-positive patients with dementia compared to those without dementia and controls. An increasing amount of IFN-alpha in the CSF was correlated with the clinical parameter of increasing Memorial Sloan Kettering scores; although these correlations were not statistically significant, they further suggest an association of increased CSF IFN-alpha with neurocognitive dysfunction in AIDS. Immunocytochemical staining of brains demonstrated IFN-alpha-positive macrophages and astrocytes in frontal cortex and white matter and IFN-alpha mRNA was detected by reverse transcriptase-polymerase chain reaction, further indicating that IFN-alpha is made by cells within the brain and suggesting that the significant increases of IFN-alpha protein found in the CSF of patients with HIV-associated dementia complex are derived from intrinsic brain cells such as macrophages and astrocytes. Increased local production of IFN-alpha during HIV infection may contribute directly or indirectly to the pathogenesis of HIV-associated dementia.
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PMID:A potential role for interferon-alpha in the pathogenesis of HIV-associated dementia. 890 53

Indirect mechanisms are implicated in the pathogenesis of the dementia associated with human immunodeficiency virus-type 1 (HIV-1) infection. Proinflammatory molecules such as tumor necrosis factor alpha and eicosanoids are elevated in the central nervous system of patients with HIV-1-related dementia. Nitric oxide (NO) is a potential mediator of neuronal injury, because cytokines may activate the immunologic (type II) isoform of NO synthase (iNOS). The levels of iNOS in severe HIV-1-associated dementia coincided with increased expression of the HIV-1 coat protein gp41. Furthermore, gp41 induced iNOS in primary cultures of mixed rat neuronal and glial cells and killed neurons through a NO-dependent mechanism. Thus, gp41-induced NO formation may contribute to the severe cognitive dysfunction associated with HIV-1 infection.
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PMID:Immunologic NO synthase: elevation in severe AIDS dementia and induction by HIV-1 gp41. 894 6

The spreading of human immunodeficiency virus (HIV) infection and its increasing scientific knowledge keep the medical staff involved with these patients in permanent need of updating themselves. The different neurologic manifestations caused by HIV are related to a variety of pathogenic mechanisms, as follows: immunodeficiency, autoimmunity, direct effects of the virus on the nervous system, and toxic and metabolic effects. The opportunistic infections are caused by the immunodeficiency due to the action of the virus on CD4+ T cells and on cells of the monocytic-macrophage lineage. Demyelinating polyradiculoneuropathy and polymyositis-like syndromes are related to autoimmune mechanisms involving, probably, the non-specific stimulation of T cells by viral proteins. The primary action of the virus on the nervous system brings out aseptic meningitis, cognitive dysfunction, dementia, vacuolar myelopathy and sensory polyneuropathy probably through liberation of neurotoxic products by the infected macrophages. Antiretroviral drugs and others used to treat patients with AIDS may also have neurotoxic effects. The better understanding of the neuropathogenesis of HIV infection will permit the use of new, and more specific, therapeutical options in the future as well as a more precocious control of its neurologic complications.
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PMID:[Neuropathogenesis of HIV infection]. 898 98


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