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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined 11 brains of human immunodeficiency virus (HIV) seropositive cases who died from unnatural causes (10 intravenous drug abusers who died from heroin overdose and 1 homosexual dead from a gunshot injury); 10 brains of HIV seronegative heroin addicts who died from overdose and 1 seronegative drug abuser who died from gunshot injury served as controls. Complete postmortem examination did not show evidence of acquired immune deficiency syndrome (AIDS) or AIDS related complex. Terminal changes including nerve cell ischemia, edema and diffuse vascular congestion were observed in all cases. Perivascular pigment deposition with macrophages was a constant finding in drug addicts and was probably related to chronic intravenous injection. In contrast, cerebral vasculitis was significantly more frequent and marked in HIV seropositive cases and was often associated with lymphocytic meningitis. Granular ependymitis, myelin pallor with reactive astrocytosis and microglial proliferation were also more frequent and more severe in HIV seropositive cases. Immunocytochemistry was negative for HIV antigens. Our study further supports the view that early central nervous system changes occur in HIV infection.
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PMID:Early brain changes in HIV infection: neuropathological study of 11 HIV seropositive, non-AIDS cases. 153 41

Excessive hemosiderin-laden perivascular macrophages have been described in the brains of patients with the acquired immunodeficiency syndrome (AIDS) who underwent autopsy; its meaning remains unclear. In the brains of 53 patients with AIDS who consecutively underwent autopsy, we quantified the abnormality, elucidated its relationship to the pathologic features of AIDS, and asked if there was some relationship to endogenous iron storage and transport proteins in brain macrophages and microglia. The number of perivascular siderotic macrophages was significantly increased in patients with AIDS compared with age-matched control subjects. Macrophage siderosis was strongly correlated with the presence of disseminated mycobacterial infection and vacuolar myelopathy at autopsy; a generalized wasting (cachexia) also was related significantly. Many other pathologic abnormalities were not related, including putative human immunodeficiency virus-specific neuropathologic changes such as multinucleated cells and myelin pallor. Activated macrophages and microglial cells in the central nervous system had dense intracytoplasmic accumulation of ferritin (iron storage protein) in AIDS and non-AIDS patients. These results suggest that siderosis of cerebral macrophages is related to an ill-defined nonspecific systemic imbalance associated with the breakdown of abundant stores of endogenous intracellular ferritin. Understanding chronic "secondary" effects of human immunodeficiency virus type 1 infection will become increasingly important as improved survival in patients with AIDS is realized.
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PMID:Siderotic cerebral macrophages in the acquired immunodeficiency syndrome. 158 Jul 55

Ordinarily, severe disease due to acquired cytomegalovirus (CMV) infection does not occur in immunocompetent children. We describe a previously healthy boy who acquired primary CMV infection at approximately 2 years of age and experienced a 2-year-long debilitating multisystem illness from which he ultimately recovered. Clinical features of this illness included fatigue, poor weight gain, pallor, unexplained fever, musculoskeletal complaints, drenching night sweats, lymphadenopathy, and massive hepatosplenomegaly. Laboratory abnormalities included elevated erythrocyte sedimentation rate, lymphocytosis, and elevated immune complex levels. Cellular immune function was impaired during the illness but was demonstrably normal during convalescence, and there was no other evidence for a known immunodeficiency state. Immunoblot analysis showed enhanced antibody response to a 66-kd infected cell protein after symptomatic recovery. Despite consistently normal indices of hepatic function, liver enlargement persisted after other symptoms had resolved. Liver biopsy demonstrated a mononuclear cell portal tract infiltrate with fibrosis, but CMV could not be demonstrated directly in this tissue. Primary CMV infection has not been reported previously to cause the persistent symptoms seen in this child.
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PMID:Protracted mononucleosis-like illness associated with acquired cytomegalovirus infection in a previously healthy child: transient cellular immune defects and chronic hepatopathy. 184 49

To evaluate the consequences of receiving human immunodeficiency virus type 1 (HIV-1)-seropositive blood, 90 HIV-1-seronegative recipients of HIV-1-seropositive blood (case patients) and 90 HIV-1-seronegative recipients of HIV-1-seronegative blood, matched for age, sex, number of transfusions, diagnosis, and severity of illness (controls), were followed for 12 months after transfusion at Mama Yemo Hospital in Kinshasa, Zaire. Of case patients and controls, 72% were children transfused for anemia caused by malaria. Of the 46 case patients case patients alive 6 months after transfusion and for whom HIV-1 serologic results were obtained, 44 (96%) had seroconverted. Significantly more case patients (47%) than controls (16%) died within 1 year after transfusion (P less than .001). In the first 3 months after transfusion, fatigue, diarrhea, fever, cough, pruritus, pallor, oral candidiasis, polyadenopathy, hepatosplenomegaly, and rhinorrhea were observed more often among seroconverters than controls (P less than .04). Six percent of case patients and no controls had developed clinical AIDS after 12 months of follow-up. These findings underscore the urgent need for appropriate HIV screening facilities in transfusion centers worldwide.
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PMID:Seroconversion rate, mortality, and clinical manifestations associated with the receipt of a human immunodeficiency virus-infected blood transfusion in Kinshasa, Zaire. 186 35

In chronic granulomatous disease (CGD) enzyme-deficient neutrophils and mononuclear cells lack the respiratory burst required for biocidal activity. Recurrent infections lead to granulomas in various organs but brain lesions are rare. In the present case, a 23-year-old male with numerous infections since early childhood died of overwhelming pulmonary aspergillosis. He first began to experience neurological deficits at the age of 17. Computerized tomography and magnetic resonance imaging revealed fleeting white matter lesions that were interpreted as multiple sclerosis (MS). At post mortem, three types of brain lesions were found: (1) Pigmented macrophages in perivascular spaces and the leptomeninges similar to those reported previously. They contained fine, golden-brown, lipofuscin-like material whose chemical composition included a sulfur peak by X-ray analysis. (2) Focal, well-demarcated, "burnt out" white matter lesions with loss of both myelin and axons and intense sclerosis. (3) Diffuse areas of mild pallor in the centrum ovale which spared the U fibers. The pigmented macrophages are characteristic of those seen in the periphery in CGD. The origin of the discrete, destructive white matter lesions is unclear. They may have resulted from: (i) earlier activity by CGD macrophages; (ii) previous infections due to sepsis or embolism; or (iii) possibly post-infectious encephalomyelitis. The more diffuse, mild, white matter lesions are attributed to edema. Evidence for MS, progressive multifocal leukoencephalopathy, or human immunodeficiency virus encephalitis was lacking. This case is presented to alert us to look more carefully for brain lesions in CGD, characterize them and to help determine their cause.
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PMID:Brain lesions in chronic granulomatous disease. 202 50

Early pathological abnormalities in human immunodeficiency virus (HIV-1)-related dementia have not been well documented. We report a homosexual man with fatigue and intermittent diarrhea in whom early HIV-1-related dementia was demonstrated during neurological screening in the Multicenter AIDS Cohort Study. Within 4 months he died of massive epistaxis, and the brain revealed astrocytosis of white matter and mild pallor of myelin staining in the absence of inflammation, multinucleated giant cells, and brain atrophy.
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PMID:Neuropathological changes in early HIV-1 dementia. 281 44

Aseptic meningitis, subacute encephalitis, and vacuolar myelopathy are the three diseases of the central nervous system that are specifically related to or associated with human immunodeficiency virus (HIV) infection. HIV encephalitis initially is associated with myelin pallor and gliosis of the centrum semiovale, which is found in more than 90% of brains from patients dying with the acquired immunodeficiency syndrome. With increased severity of disease, multiple glial nodules with the multinucleated cells characteristic of HIV encephalitis are present throughout the cerebral white matter, basal ganglia, and cerebral cortex, and also may be found in cerebellum, brainstem, and spinal cord. HIV has been demonstrated in monocytes and multinucleated cells by electron microscopy, immunohistochemical techniques, and in situ hybridization. Vacuolar myelopathy occurs in approximately 30% of patients and is characterized by vacuolation of the white matter of the spinal cord that is most prominent in the posterior and lateral columns at thoracic levels. The severity of the pathological lesions correlates not only with symptoms and signs of spinal cord disease but also with dementia. Although the incidence of vacuolar myelopathy is increased in patients with HIV encephalitis, its etiology is not yet established.
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PMID:Review of central nervous system pathology in human immunodeficiency virus infection. 327 4

The cause of acquired immunodeficiency syndrome (AIDS) dementia, which is a frequent late manifestation of human immunodeficiency virus (HIV) infection, is unknown but radiological and pathological studies have implicated alterations in subcortical white matter. To investigate the pathological basis of these white matter abnormalities, we performed an immunocytochemical and histological analysis of subcortical white matter from AIDS patients with and without dementia, from pre-AIDS patients (asymptomatic HIV-seropositive patients), and from HIV-seronegative control subjects. Reduced intensity of Luxol fast blue staining, designated "diffuse myelin pallor," was detected in 8 of 15 AIDS dementia patients, 3 of 13 AIDS nondemented patients, and none of the pre-AIDS patients (n = 2) or control subjects (n = 9). In contrast to Luxol fast blue staining, sections stained immunocytochemically for myelin proteins did not show decreased staining intensities in regions of diffuse myelin pallor. In addition, neither demyelinated axons nor active demyelination were detected in light and electron micrographs of subcortical white matter from brains of patients with AIDS dementia. An increase in the number of perivascular macrophages and hypertrophy of astrocytes and microglia occurred in brain sections from HIV-infected patients. These changes were not specific to dementia or regions of diffuse myelin pallor and they occurred in both gray and white matter. In contrast to the lack of myelin pathology in AIDS dementia brains, significant accumulations of serum proteins in white matter glia were detected in the brains of 12 of 12 patients with AIDS dementia and 6 of 12 AIDS patients without dementia. Serum protein-immunopositive cortical neurons were detected in the frontal cortex of 11 of 12 patients with AIDS dementia and 3 of 12 nondemented AIDS patients. Seronegative control subjects showed minimal serum protein immunoreactivity in both cortex and white matter. We conclude therefore that alterations in the blood-brain barrier and not demyelination contribute to the development of AIDS dementia.
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PMID:Cerebral white matter changes in acquired immunodeficiency syndrome dementia: alterations of the blood-brain barrier. 768 19

Vacuolar myelopathy (VM) and tract pallor are poorly understood spinal tract abnormalities in patients with the acquired immunodeficiency syndrome (AIDS). We studied the ability of magnetic resonance imaging (MRI) to detect these changes in spinal cord specimens postmortem and whether criteria could be formulated which would allow these conditions to be differentiated from other lesions of the spinal cord in AIDS, such as lymphoma, cytomegalovirus (CMV) and human immunodeficiency virus (HIV) myelitis. We imaged 38 postmortem specimens of spinal cord. The MRI studies were interpreted blind. The specimens included cases of VM myelin pallor, CMV myeloradiculitis, HIV myelitis, lymphoma as well as normal cords, both HIV+ve and HIV-ve. MRI showed abnormal signal, suggestive of tract pathology, in 10 of the 14 cases with histopathological evidence of tract changes. The findings in VM and tract pallor on proton-density and T2-weighted MRI were increased signal from the affected white-matter tracts, present on multiple contiguous slices and symmetrical in most cases. The pattern was sufficiently distinct to differentiate spinal tract pathology from other spinal cord lesions in AIDS.
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PMID:Spinal tract pathology in AIDS: postmortem MRI correlation with neuropathology. 776 Oct

It may be postulated that the encephalopathy induced by the human immunodeficiency virus HIV-1, in particular, the characteristic "myelin pallor," may result from binding of the envelope glycoprotein gp120 to galactosylceramide and/or its metabolite sulfatide in the plasma membrane of oligodendrocytes, the myelin forming cells in the central nervous system. (1) gp120 has been reported to have a high affinity for these molecules in vitro. (2) The binding of antibodies to these molecules increases intracellular free calcium levels, which may be cytotoxic. (3) The binding of gp120 to the CD4 receptor in the immune system has the same effect. We have investigated the binding of gp120 to rat oligodendrocytes in vitro by indirect immunofluorescence and have monitored changes in intracellular free calcium with the calcium-sensitive dye INDO-1, in individual oligodendrocytes exposed to the glycoprotein. Antibodies against galatosylceramide and sulfatide bound to the cell membrane, but gp120 did not. The antibodies also increased intracellular free calcium levels in the oligodendrocytes, whereas gp120 did not. It, therefore, seems highly improbable that the demyelination observed during HIV encephalopathy is a direct cytotoxic effect of gp120 on oligodendrocytes.
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PMID:HIV-1 envelope glycoprotein gp120 does not bind to galactosylceramide-expressing rat oligodendrocytes. 785 83


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