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

Encephalitis occupies a large part in the neurological complications of HIV infection. It is frequent and in most cases of poor prognosis. Some cases of encephalitis are directly related to HIV while others are caused by an opportunistic infection. Among the former is the acute encephalitis coincident with seroconversion, which is exceptional and spontaneously regressive, and the subacute encephalitis better known as HIV encephalopathy which has a constantly pernicious course ending in subcortical dementia lethal within a few months. Some cases of opportunistic encephalitis are associated with a virus: a Papovavirus is responsible for progressive multifocal leucoencephalopathy where mental deterioration is combined with focal symptoms, both resulting in death in less than 6 months. Cytomegalovirus is responsible for an encephalitis that is frequently found on pathological examination but is usually subclinical. Anecdotic cases of toxoplasmic encephalitis have been reported. Finally, emphasis should be placed on the frequency of encephalitis-associated pathologies with all possible combinations, the most common being HIV encephalitis with another encephalitis and/or focal ou multifocal infectious or tumoral processes.
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PMID:[Encephalopathies in infection by human immunodeficiency virus]. 131 16

In a recent workshop held on Sanibel Island, Florida (18-21 January 1992), the two most common neuroimmunologic diseases of young adults, multiple sclerosis (MS) and HIV encephalopathy, were jointly discussed. The logic of assembling investigators from these two fields was based not on an assumed etiologic connection between MS and retroviral infection of the central nervous system (CNS), but rather in the hope of uncovering potential common pathogenic mechanisms, particularly as might relate to trafficking of mononuclear cells into the central nervous system, the distribution and function of macrophages and microglia, the structure and function of the blood-brain barrier, and the role of cytokines released by activated cells. Multiple sclerosis is a disease without a known etiologic agent or pathogenesis. While the causative agent for HIV leukoencephalopathy is known, the pathogenesis of the disease remains entirely enigmatic (a topic covered by R. Johnson). This meeting brought together two different groups of investigators to compare and contrast the diseases and to share perspectives, paradigms, and data with the aim of cross-fertilizing the disciplines and generating healthy hybrids.
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PMID:Neurological consequences of immune dysfunction: lessons from HIV infection and multiple sclerosis. 135 91

There is little published data on concomitant use of zidovudine and intravenous immunoglobulin (IV IgG). In this paper we review our experience of four HIV-1 infected children treated with zidovudine for periods of 19-33 months (mean 26.5 months) subsequent to starting IV IgG for period of 18-20 months (mean 19 months). In these children the only clear benefit we found was in one child who had developed HIV encephalopathy which resolved after starting zidovudine. The respective roles of zidovudine and intravenous immunoglobulin in HIV-1 infected children need to be clarified in larger comparative trials.
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PMID:Zidovudine therapy in combination with intravenous immunoglobulin in HIV infected children. 136 18

Didanosine is a dideoxynucleoside analogue which undergoes intracellular conversion to the putative active triphosphate metabolite. The active metabolite appears to inhibit viral reverse transcriptase and terminate the proviral DNA, and produces virustatic inhibition of actively replicating human immunodeficiency virus (HIV) at clinically relevant concentrations. In phase I studies didanosine had beneficial effects on various surrogate markers of clinical efficacy and also improved clinical manifestations of HIV infection, with a 21-month survival rate of 80% in patients with acquired immune deficiency syndrome (AIDS) and 93% in patients with AIDS-related complex (ARC) in 1 study. Didanosine also improved CD4+ cell counts in a phase II/III trial in patients previously treated with zidovudine, whereas cell counts declined in patients continuing zidovudine therapy. However, the effects of didanosine on clinical end-points (disease progression, survival, HIV encephalopathy) remain to be established. Peripheral neuropathy and pancreatitis are the predominant dose-limiting adverse events and didanosine therapy should be withdrawn in patients developing signs or symptoms of pancreatitis and during acute treatment of Pneumocystis carinii pneumonia. However, at currently recommended clinical dosages didanosine is generally well tolerated with minimal haematological toxicity. Thus, in a therapeutic area with few treatment options, didanosine offers a welcome alternative for patients intolerant of, or resistant to, zidovudine. There are a number of clinical trials in progress evaluating didanosine alone or in combination with other antiviral agents, and these results are awaited with considerable interest.
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PMID:Didanosine. A review of its antiviral activity, pharmacokinetic properties and therapeutic potential in human immunodeficiency virus infection. 137 14

Elevated cerebrospinal fluid (CSF) levels of neopterin and beta 2-microglobulin (beta 2MG) reflect activation of the cellular immune response in the central nervous system (CNS). In 118 consecutive subjects [15 controls and 103 patients with human immunodeficiency virus (HIV) infection classified according to the Walter Reed staging system (WR)], neopterin and beta 2MG were determined in paired samples of CSF and serum. The permeability of the blood-CSF barrier and local release of neopterin and beta 2MG were taken into account: The molecular weight and diameter were used to determine filtration at the blood-CSF barrier. CSF neopterin levels were increased in all stages of HIV infection. beta 2MG levels were elevated in WR2 and later stages. Neopterin, beta 2MG, and cell counts similarly showed peaks in WR2, as did neopterin and beta 2MG also in the later stages WR5 and WR6. Neurologically asymptomatic patients exhibited higher neopterin CSF levels than did controls (12.67 +/- 11.6 vs. 2.34 +/- 1.05 nmol/l, P less than 0.001) and higher CSF beta 2MG (2.12 +/- 1.25 vs. 1.3 +/- 0.37 mg/l, P = 0.001). Patients with HIV encephalopathy had higher levels of beta 2MG (3.75 +/- 1.83 mg/l) than asymptomatic patients (P less than 0.01). CSF levels of neopterin were markedly different in patients with HIV encephalopathy and toxoplasmosis (P less than 0.01). A high quantity of local release of the markers neopterin and beta 2MG may reflect HIV infection of the CNS in early and late stages and additional release upon opportunistic infections.
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PMID:Expansion of neopterin and beta 2-microglobulin in cerebrospinal fluid reaches maximum levels early and late in the course of human immunodeficiency virus infection. 139 42

Endogenous event-related potentials (and especially the P300 component) have delayed latencies relative to normal controls in patients with dementias of diverse aetiologies. Moreover, the subcortical varieties of dementia tend to affect also the early-stage N1 and P2 components whereas both types of dementias affect the later-stage N2 and P3 components. However it has become obvious that patients with HIV infection are susceptible to develop progressive, AIDS-related dementia, renamed 'HIV encephalopathy' by the Center for Disease Control. Several studies have shown that endogenous, but also early, components of long latency auditory evoked potentials are prolonged in latency in HIV-demented patients. However, these changes may also be present in class II and III patients and may permit the early recognition of HIV encephalopathy.
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PMID:[Cognitive evoked potentials and HIV infection]. 148 19

We followed prospectively all patients with HIV infection admitted to the infectious diseases ward at Auckland Hospital over a seven month period. Neurological manifestations of HIV infection were the primary reason for admission in 18 of the 55 patients (33%). Diagnoses were usually presumptive, based on history, clinical findings, radiological appearances and response to empirical therapy. Eight patients had cerebral toxoplasmosis, three primary cerebral lymphoma, two cytomegalovirus retinitis, two HIV neuropathy, one cryptococcal meningitis, one HIV encephalopathy, and one HIV meningitis. Another patient with HIV infection was admitted to the neurology ward at Auckland Hospital with HIV myelopathy during the same seven month period. The median survival of the patients treated for presumptive toxoplasmosis was 7.5 months. Only two patients had not developed AIDS, one having HIV meningitis and the other HIV myelopathy, and in both, symptoms resolved spontaneously with no relapse at one year follow up. The spectrum of neurological manifestations of HIV infection is wide. Investigations to determine the most likely diagnosis are indicated and specific therapy may lead to both excellent palliation and prolonged survival.
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PMID:Neurological disease in patients with human immunodeficiency virus infection. 154 70

We describe the clinical and epidemiological characteristics of human immunodeficiency virus (HIV) infection in patients greater than 55 years of age at the time of diagnosis and make comparisons with younger HIV-infected patients. Patients were selected by stratification according to age (greater than 55 years and less than 40 years) from a large cohort, and information was obtained by review of charts. Three samples of younger patients were used for general comparison (sample 1), for analysis of progression to acquired immunodeficiency syndrome (AIDS) (sample 2), and for analysis of survival after AIDS (sample 3). We identified 33 patients greater than 55 years of age (30 men and 3 women). The mean age was 60.1 years (range, 55-72). Risk factors included homosexual/bisexual, 22 (67%); blood products, seven (21%); heterosexual, two (6%); and unknown risk, two (6%). HIV encephalopathy tended to be more common in the older group, while Kaposi's sarcoma was more common in younger controls. Older patients more frequently acquired HIV infection via transfusion of blood or blood products (p less than 0.005), were more likely to have AIDS at presentation (p less than 0.001), progressed to AIDS more rapidly (p less than 0.002), and had higher mortality rates (p less than 0.001). Transfusion of blood or blood products is an important mode of acquisition of HIV in patients greater than 55 years of age. HIV infection has a more rapid and aggressive course in older patients.
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PMID:HIV infection in patients over 55 years of age. 154 71

We report a four-year-old boy with HIV encephalopathy after vertical HIV infection. On the first admission to our hospital he showed ataxia, loose of expressive language and interstitial pneumonia. After treatment of the pneumonia the patient was started on oral zidovudine with 6 x 6 mg/kg bw/day, because of persisting neurologic symptoms and deep white matter lesions in the MR tomogram of the brain. Two months later he showed an improvement of the gait and the reappearance of the expressive language. Seven months after the start with zidovudine the MR tomogram of the brain revealed the disappearance of white matter lesions with exception of little areas of demyelinisation. No side effects of treatment were observed. The only persisting pathological clinical signs were developmental delay of about a half year and moderately hyperactive tendon reflexes of the lower extremities. Our case suggests that even oral treatment with zidovudine can have a beneficial effect on the HIV encephalopathy in infants.
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PMID:[The effect of high-dose peroral zidovudine treatment in a 4-year-old child with HIV encephalopathy]. 156 Sep 90

The nervous system is frequently affected in patients with the acquired immune deficiency syndrome (AIDS). In addition to opportunistic CNS infections and cerebral lymphomas, approx. 20% of the patients develop HIV-associated encephalopathies. Two major histopathological manifestations are observed. HIV leukoencephalopathy (progressive diffuse leukoencephalopathy) is characterized by a diffuse loss of myelin in the deep white matter of the cerebral and cerebellar hemispheres, with scattered multinucleated giant cells and microglia but scarce or absent inflammatory reaction. HIV encephalitis (multinucleated giant cell encephalitis) is associated with accumulations of multinucleated giant cells, inflammatory reaction and often focal necroses. In some patients, both patterns may overlap. In order to identify the HIV genome in the CNS, brain tissue from 27 patients was analyzed for the presence of HIV gag sequences using the polymerase chain reaction (PCR) and primers encoding a 109 base pair segment of the gag gene. Amplification of HIV gag succeeded in all 5 patients with clinical and histopathological evidence for HIV encephalopathy but was negative in the 20 AIDS patients with opportunistic bacterial, parasitic and/or viral infections or with cerebral lymphomas. These results strongly suggest that the evolution of histopathologically recognizable HIV-encephalopathies closely correlates with the presence and/or tissue concentration of HIV. Since there were no cases with amplified HIV DNA in the absence of HIV-associated tissue lesions, we conclude that harboring and replication of HIV in the CNS rapidly causes corresponding clinical and morphological changes of HIV-associated encephalopathies. In two children with severe HIV encephalomyelitis, large amounts of HIV gag and env transcripts were detected in affected areas of the brain and spinal cord by in situ hybridization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuropathology and pathogenesis of HIV encephalopathies. 158 55


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