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

Postmortem neuropathologic changes were evaluated in 141 consecutive patients dying with human immunodeficiency virus infection at publicly supported hospitals affiliated with the University of Texas Southwestern Medical Center in Dallas, between August 1984 and September 1990. Morphologic abnormalities were identified in 112 cases (79%). Cytomegalovirus was the most common opportunistic infection encountered, with characteristic viral inclusions identified in 23 patients, and presumptive evidence of infection in six additional patients. Progressive multifocal leukoencephalopathy was present in four patients. Gram-positive bacterial infections were identified in six patients, and mycobacterial infections in three patients. Opportunistic fungal infections included cryptococcosis (13 cases), histoplasmosis (two cases), and coccidioidomycosis (one case). Toxoplasmosis was uncommon, with active or quiescent lesions identified in five patients. Lymphoma was present in nine patients and was primary in the central nervous system in five patients. Multinucleate giant cell (human immunodeficiency virus) encephalitis was identified in 28 patients. In an additional 26 patients, microglial nodules and/or more generalized white-matter abnormalities were encountered in the absence of multinucleate giant cells, cytomegalovirus inclusions, or systemic cytomegalovirus infection. Vacuolar change was present in 21% of spinal cords, and was highly correlated with cytomegalovirus infection in the nervous system. Mixed infections and/or neoplasms were identified in 24 patients. This survey documents a high frequency of neuropathologic abnormalities in human immunodeficiency virus-infected individuals in a geographical region of the United States not represented in previous series. Variations noted in the frequencies of specific central nervous system disorders between this and other study populations reinforce the need for continuing documentation of geographical trends in human immunodeficiency virus-associated disorders.
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PMID:The neuropathology of human immunodeficiency virus infection. The Dallas, Texas, experience. 174 29

A case of intracerebral malignant B cell lymphoma associated with encephalitis typical of Human Immunodeficiency Virus (HIV) infection is described in a 4 year old child, with post-transfusion Acquired Immune Deficiency Syndrome (AIDS) and severe pre-existing cystic encephalomalacia. This report further documents B cell lymphoma as the commonest cause of an intracerebral mass, and an important cause of death in paediatric AIDS. That more than one pathological process may be responsible for neurological symptoms in paediatric AIDS is also emphasised.
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PMID:Cerebral lymphoma and HIV encephalitis in a case of paediatric AIDS, with pre-existing multicystic encephalomalacia. 175 41

Two cases of peripheral facial paralysis associated with infection by the human immunodeficiency virus in young intravenous drug abuser patients are reported. One patient manifested AIDS-related complex (ARC) and the other fulfilled the Center for Disease Control (CDC) criteria for AIDS. Clinical symptoms and signs occurred as facial paralysis and headache. One patient presented progressive motor slowing and the computerized tomography (CT) of the brain showed a wide hypodense lesion in the left temporal-anterior region and the involvement of the left basal ganglia. In this patient the impairment of the facial nerve was associated with a HIV-related encephalitis. In the second patient the CT did not show cerebral lesions and the etiology of the paralysis was unknown.
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PMID:[Peripheral facial paralysis and HIV infection]. 175 30

In order to further characterize the pathogenesis of Toxoplasma gondii infection in patients with AIDS and AIDS-related complex (ARC), a cohort of HIV- and Toxoplasma-infected individuals were identified and prospectively followed. Four hundred and 10 HIV-infected individuals followed in the San Francisco General Hospital AIDS Clinic were screened for antibodies to Toxoplasma between November 1986 and November 1988. Of the 67 (16%) individuals seropositive for Toxoplasma antibodies, 33 (49%) were followed monthly for a mean duration of 7.5 months. One hundred and 11 follow-up blood samples were obtained in order to determine Toxoplasma serology and the incidence of parasitemia. In general, Toxoplasma immunoglobulin (Ig) G antibodies remained stable over time. Detection of Toxoplasma antigenemia and parasitemia was uniformly negative, including those specimens obtained from two individuals within 45 days of their developing toxoplasmic encephalitis.
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PMID:Toxoplasma serology, parasitemia and antigenemia in patients at risk for toxoplasmic encephalitis. 176 86

Health workers took blood samples from 94 HIV positive patients (cases) and 86 HIV negative patients (controls) at the Kenyatta National Hospital in Nairobi, Kenya. Researchers compared the serological results of both groups to determine if any serological evidence of reactivation of latent infection existed and, if so, whether this reactivation could be related to acute toxoplasmosis. Laboratory personnel tested all serum with EIA and latex agglutination and dye tests to determine the presence of anti-Toxoplasma antibodies (Toxoplasma IgG). Both the EIA and latex test were more sensitive and specific in detecting Toxoplasma IgG than the dye test. The dye test revealed 54% of all patients had Toxoplasma IgG. Further 22% of the cases had IgG levels 180 units/ml whereas only 1% of controls had these levels. None of the patients exhibited any signs or symptoms of toxoplasmic encephalitis. Further no correlation between high Toxoplasma IgG titers and signs of central nervous system dysfunction or confusion occurred. Even though 35% of cases had considerable lymphadenopathy, it was not associated with Toxoplasma IgG levels. Moreover Toxoplasma IgG levels were not related to AIDS or death. The researchers concluded that high serum IgG levels were indicative of early Toxoplasma reactivation and necessarily associated with disease.
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PMID:Toxoplasma antibodies in HIV-positive patients from Nairobi. 180 45

The frequency of neurological manifestations was evaluated in 653 HIV infected patients admitted in a university hospital in Rio de Janeiro city, Brazil, in the 1985-1989 period. A total of 172 (26%) patients developed neurological symptoms. Central nervous system complications included: cerebral toxoplasmosis (80), cryptococcal meningitis (57), subacute encephalitis (17), tuberculosis (8) and aseptic meningitis (2), progressive multifocal leukoencephalopathy (2) and vacuolar myelopathy (6). Peripheral neuropathy occurred in three cases. The clinical and tomographic aspects were analysed. The majority of the patients died within six months after the onset of the neurological disease.
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PMID:[Neurological complications in acquired immunodeficiency syndrome: experience at the Hospital Universitario Clementino Fraga Filho-Universidade Federal do Rio de Janeiro]. 181 Feb 33

The human immunodeficiency virus infected persons frequently have manifestations of central nervous system disfunction. These can be primary involvement or secondary processes such as infections or tumors. The present paper presents a short review of radiologic CNS findings in patients with AIDS as seen on CT and or MRI. The radiologic findings of HIV-1 encephalitis, toxoplasmosis, primary CNS lymphoma, PMLE, cryptococcosis, histoplasmosis, CMV encephalitis, HVS and varicella are presented. We expect this will ultimately help in the management of the AIDS patient.
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PMID:CNS involvement in AIDS patients as seen with CT and MR: a review. 181 9

A 19-year-old male intravenous drug abuser, was admitted to hospital with a one-week history of lower limb weakness and urinary retention. He was known to have been HIV-seropositive for 3 years and had been treated for cerebral toxoplasmosis. Neurological examination confirmed flaccid paraparesis with weak ankle jerks and bilateral extensor plantar responses. There was no obvious sensory deficit. Neurological examination was otherwise normal. CSF contained 63 mg/dl protein and 10 leucocytes/mm3. Myelography was normal. He died 1 month later from septic peritonitis. Neuropathological examination showed chronic lesions of toxoplasmosis in brain. Small necrotic foci with myelin loss, proliferation of microglia, macrophages and multinucleated giant cells (MGC) were disseminated in the whole spinal cord, mostly in the white matter, but the brain was spared. Immunohistochemistry demonstrated p24 and p17 HIV antigens in macrophages, MGC and microglial cells. These lesions resemble those of so called 'multifocal giant cell encephalitis'. The present case demonstrates that HIV-related multifocal inflammatory changes may be restricted to the spinal cord and may be a cause of myelopathy in AIDS patients.
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PMID:Multifocal multinucleated giant cell myelitis in an AIDS patient. 185 90

HIV establishes a chronic infection in the central nervous system (CNS) of AIDS patients. The immunopathogenesis of this chronic encephalitis is unknown. Because of the importance of major histocompatibility (MHC) class I and class II antigens in modulating the immune response, we examined the tissue expression of MHC molecules in relation to CNS damage and expression of viral antigens. By immunocytochemical staining we found that beta 2-microglobulin (beta 2M) expression is elevated in all cases with signs of viral encephalitis. beta 2M was expressed at high levels on endothelial cells, macrophages and possible oligodendroglia within regions of histopathology. In histologically normal regions elevated expression of beta 2M was noted only on endothelial cells. MHC class II expression was elevated only in the HIV encephalitis cases, and was restricted to macrophages/microglia and occasional endothelial cells. When compared with other viral encephalitides these findings suggest that the intra-CNS immune response to HIV is appropriate for viral presentation; however, the absence of responsive systemic T cells may lead to chronic viral infection.
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PMID:Expression of major histocompatibility complex and HIV antigens within the brains of AIDS patients. 186 5

Clinical and pathological evidence of subcortical central nervous system (CNS) damage is observed commonly in patients with human immunodeficiency virus (HIV) encephalitis. Whether other CNS regions are also affected has not been well studied. We report neocortical damage in patients with HIV encephalitis. Using quantitative techniques, we demonstrate statistically significant thinning of the neocortex, with a loss of large cortical neurons. Qualitative and quantitative assessments of neocortical neuropil reveal a loss of synaptic density and vacuolation of dendritic processes. Failure to demonstrate an association of these changes with the presence of HIV antigens suggests that neocortical damage may be an indirect effect of HIV infection of the CNS.
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PMID:Neocortical damage during HIV infection. 190 52


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