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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nervous system opportunistic infections are seen in about one fifth of AIDS cases and account for over 40% of the patients with neurological manifestations. Serious infections are seen in severely immunosuppressed patients, usually with CD4 counts of 200 ml-1 or less. The commonest is CMV, which can produce acute encephalitis, sometimes with focal hemisphere or brain-stem signs, dementia, retinitis, optic neuritis and an ascending radiculomyeloencephalitis. Cryptococcal meningitis is the most frequent fungal disease; a high degree of clinical suspicion is required in patients with fever, malaise, headache or seizures. Only CSF cultures are always positive; both serum and CSF cryptococcal antigen tests are highly sensitive and specific. Treatment with amphotericin B and flucytosine is successful in at least 70% of first episodes but side-effects are common. Without maintenance therapy 50% of patients relapse; fluconazole is recommended. Cerebral toxoplasmosis can present with focal cerebral or spinal cord signs but also as a diffuse encephalopathy; negative T. gondii serology is exceptional but positive serum titres are usually unhelpful. Treatment with sulfadiazine, pyrimethamine and folinic acid achieves good results in 90% of the first episodes, but side-effects are common. Appearances on CT scan or MRI may take several weeks to improve. The value of an empirical approach to treatment is well-established; an initial cerebral biopsy is difficult to justify. Without maintenance therapy a relapse rate of 50% can be expected; therapy with sulfadiazine and pyrimethamine may also prevent pneumocystosis. HIV disease appears to increase the likelihood of neurosyphilis, and the risk of relapse after conventional penicillin doses, in patients with syphilis; at least 3-4 weeks of appropriate therapy are recommended. A number of other diseases caused by viruses, fungi, bacteria and parasites are less common; these include progressive multifocal leukoencephalopathy, herpes simplex and zoster infections and tuberculosis.
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PMID:Central nervous system opportunistic infections in HIV disease: clinical aspects. 134 47

Human immunodeficiency virus (HIV) infects cells of the monocyte/macrophage lineage in addition to lymphocytes, and infection of these cells may be responsible for viral persistence and dissemination, encephalopathy of the acquired immunodeficiency syndrome and other sequelae of HIV infection. We have developed an in vitro model utilizing peripheral-blood monocyte-derived macrophages to study HIV-1 infection of macrophages. HIV-1 isolates vary greatly in their ability to infect and replicate in macrophages, from highly restricted to highly productive infection. Productively infected macrophages undergo syncytium formation but remain viable in culture and support sustained levels of virus production for prolonged periods. Transformed monocytoid and lymphoid cell lines, however, show very different patterns of permissiveness for HIV-1 strains and do not reflect their corresponding primary cell types in studies of host cell tropism. Studies on viral entry show that the CD4 molecule, known to be the HIV receptor on lymphoid cells, is expressed at low levels on the surface of macrophages as well, where it functions as the receptor for viral entry. Therefore, differential host cell tropism does not result from the use of an alternative macrophage-specific receptor instead of CD4.
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PMID:Human immunodeficiency virus type 1 tropism for human macrophages. 138 18

A 41-year-old male homosexual with AIDS was hospitalized for temperature elevation to 40 degrees C with confusion. Neurologic evaluation found psychomotor slowing and temporospatial disorientation with no focal signs. The CD4 count was 100/mm3. CSF analysis and the CT scan were normal. Despite antiviral treatment the patient died fifteen days after admission. Gross appearance of the brain was normal. Histologic examination disclosed multiple, small foci of demyelination characteristic of progressive multifocal leukoencephalopathy. These foci were disseminated among the U fibers. In situ hybridization and immunocytochemical studies demonstrated papovavirus particles in oligodendrocytes and a few astrocytes. This case shows that papovavirus infection in AIDS patients may be responsible for a diffuse febrile encephalopathy with normal CT scan findings and a rapidly progressive course.
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PMID:[AIDS-related progressive multifocal leukoencephalopathy limited to U fibers, responsible for subacute encephalopathy with normal CT scan findings]. 144 61

This study analyzes the correlation of basic laboratory test results with clinical outcome in 94 children with perinatally acquired human immunodeficiency virus 1 infection who did not receive zidovudine during the study period of 1983 to 1988. Two life-threatening conditions highly correlated with survival, opportunistic infection and severe encephalopathy, were the end points of the study. At a median age of 25 months 30 (32%) of the 94 children had developed such conditions (Group I), and their survival at 3 years of age was 48% (95% confidence interval, 24 to 72%), contrasting with the 97% survival rate (95% confidence interval, 94 to 100%) of the remaining 64 (68%) children who had not developed such conditions by age 25 months. (Group II). Compared with children in Group II, children with life-threatening complications were more likely at the onset of symptoms to be younger and have a lower CD4 count, an impaired in vitro lymphocytic proliferation and a lack of p18 or p25 antibodies in the Western blot profile and, during the progression of the disease, a negative slope of the subsequent CD4 counts. These results highlight the need for an early diagnosis of the human immunodeficiency virus 1 infection in children and demonstrate that it is possible to determine the prognosis of their disease as early as in the first year of life.
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PMID:Natural history of human immunodeficiency virus type 1 infection in children: prognostic value of laboratory tests on the bimodal progression of the disease. 152 73

The acquired immunodeficiency syndrome (AIDS) is associated with a broad spectrum of opportunistic infections and neoplasias that differ from those occurring in the general population by their high aggressiveness, unusual location, early tendency to generalization, frequent relapse, and short survival. The severe complications of AIDS, however, represent only the last phase in a prolonged course of progressive dysfunction and destruction of the immune system set in motion by the infection with the human immunodeficiency virus (HIV). While substantial progress was achieved in the ultrastructural identification and biochemical characterization of HIV, its mode of action in the causation of AIDS is not yet fully understood. This article explores the main processes involved in the HIV infection and in its role in the origin of AIDS. It describes the phases of HIV infection, investigates the effects of HIV on the various components of the immune system, and analyzes the pathogenesis of the HIV-induced lymphadenopathies and encephalopathy, as well as the causes and mechanisms of AIDS-associated opportunistic infections and opportunistic neoplasias. The total failure of immune surveillance against a host of infectious and oncogenic agents, unprecedented in human pathology, is thus traced to the initial event of specific HIV infection of the CD4 T-lymphocytes.
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PMID:Immunopathogenesis of human immunodeficiency virus infection. 197 24

To better define the clinical and biological evolution of infants after vertical human immunodeficiency virus type 1 infection, we analyzed 94 consecutive infected patients followed up after their first clinical symptoms. The expression of clinical symptoms and biological abnormalities followed a bimodal distribution, some patients having an early and severe disease and the others having a slowly progressive one. One third of our patients suffered from early onset of opportunistic infection (OI). These patients had a significantly higher incidence of severe encephalopathy compared with patients without OI. The rate of survival at 3 years was 48% +/- 24%. In contrast, the patients without early OI or severe encephalopathy had a probability of survival at 3 years of 97% +/- 3%. This probability was not modified by the occurrence of bacterial infection or lymphoid interstitial pneumonitis. Lymphoid interstitial pneumonitis occurred at a mean age of 29 months, significantly later than OI or severe encephalopathy. Laboratory results at initial examination were correlated with clinical symptoms. Thus, when the number of CD4 lymphocytes was less than 500/mm3, children suffered more frequently from life-threatening symptoms (OI and severe encephalopathy): 15 of 22 vs 14 of 69. The same was true when the lymphocytes did not proliferate after antigenic stimulation, when anti-p18 and/or anti-p25 antibodies were absent in the serum, and when p24 antigen was detected in serum. Finally, severe encephalopathy was associated with low anti-human immunodeficiency virus cerebrospinal fluid antibody titer, whereas 88% of patients with moderate or no encephalopathy had signs of intrathecal anti-human immunodeficiency virus antibody synthesis. In conclusion, a subgroup of patients expressed very early signs of severe immunodeficiency and encephalopathy, whereas the majority of patients had a longer survival and less severe clinical symptoms during their first years of life than previously thought.
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PMID:Longitudinal study of 94 symptomatic infants with perinatally acquired human immunodeficiency virus infection. Evidence for a bimodal expression of clinical and biological symptoms. 166 56

To assess the role of complement and complement receptors in HIV-1 infection of monocytes and macrophages, we studied the infectivity of HIV-1, isolated from the peripheral blood of a patient with subacute AIDS-related encephalopathy, on the human monoblastoid cell line U937. HIV-1 and HIV-1-infected cells were capable of activating the complement system via the classical and the alternative pathways, respectively. Low concentrations of HIV-1 were able to infect U937 cells more easily in the presence than in the absence of complement. At higher virus concentrations, infectivity was no longer facilitated by the presence of complement. Infection of U937 cells was reduced in the presence of any of the monoclonal antibodies (MAbs), OKT4a (anti-CD4), OKM1 (anti-CR3), or M522 (anti-CR3). A combination of all three of these MAbs reduced the infection by an even greater amount. These data indicate that complement receptors may be a port of entry for complement-coated HIV-1.
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PMID:Complement-mediated enhancement of HIV-1 infection of the monoblastoid cell line U937. 226 Nov 26

Severe thrombocytopenia has been diagnosed in HIV seropositive patients independently of the clinical stage of disease. In view of its immunologic origin, attempts have been made to treat this condition with drugs which have proved effective in the treatment of autoimmune thrombocytopenia, though with little or no beneficial effect to these patients. This communication deals with the observation (5-22 months) of 5 HIV seropositive patients with severe thrombocytopenia who were resistant to steroids, high dose i.v. immunoglobulin and Danazol. They all responded well to splenectomy, with only one patient relapsing after 4 months. However, 2 patients showed deterioration of the immunodeficient state: in one patient the number of CD4 lymphocytes decreased and the other died of multifocal leuko-encephalopathy 4 months after splenectomy. Based on this small series, splenectomy seems to be effective in the treatment of thrombocytopenic HIV seropositive patients. However, long-term hazards still have to be assessed.
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PMID:[Thrombocytopenia and HIV: the role of splenectomy]. 246 72

Adherent human embryo brain cells have been infected with HIV. Cells replicating HIV were maintained in culture for seven sequential passes over 7 months and continued to produce HIV during that time. Human embryo brain cells displayed glial-cell morphology and expressed glial fibrillary acidic protein. Electron microscopy showed clusters of virus particles around these cells as well as budding virus. Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting. It was not possible to detect CD4 antigen on the surface of these cells by indirect immunofluorescence or alkaline phosphatase staining with CD4 monoclonal antibodies. The results of these experiments indicate that HIV replicates in non-malignant brain cells. This observation strengthens the postulated aetiological link between HIV and the encephalopathy, dementia and other neurological symptoms observed in HIV-infected patients.
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PMID:HIV replicates in cultured human brain cells. 312 70

Eight children with acquired immunodeficiency syndrome (AIDS), aged four months to 12 years, were treated with zidovudine (azidothymidine) 100 mg/m2 intravenously every six hours for 14 days, followed by oral zidovudine at the same dose for a total of six months. Of the eight, six were infected at birth and two were contaminated by blood transfusion at ages eight and nine years, respectively; seven of the eight showed specific neurologic impairment consisting of encephalopathy (six children) and myelopathy (one child). In two children, a dramatic improvement of clinical status occurred, including neurologic progress in one; in three, the improvement was dissociate or transient and in the other three, no modification was observed. A marked increase of total lymphocyte and CD4(+) cell counts occurred in four children but was transient without modification of in vitro antigen-induced lymphocyte proliferation; p24 human immunodeficiency virus serum antigens were detected in seven of eight children, then transiently disappeared in all children during intravenous therapy but reappeared progressively during the oral regimen in all but one. Progressive modification of human immunodeficiency virus serology was noted in five children, mainly characterized by the finding of anti-core antibodies. The hematologic toxicity of zidovudine was comparable with that observed in adults. These preliminary results support the need for further studies in order to delineate the optimal regimen of zidovudine in children with AIDS.
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PMID:Zidovudine therapy in children with acquired immunodeficiency syndrome. 316 4


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