Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 49-year-old man who was an HTLV-I carrier with an immunodeficiency state and intracranial pyramidal tract lesion revealed by MRI. He was born in Hokkaido and was admitted to our hospital because of fluminant hepatitis. On admission, neurologic examination revealed exaggerated deep tendon reflexes including the jaw jerk; the plantar response was flexor. Laboratory examination revealed decrease in the number of lymphocytes and CD4-positive lymphocytes in the peripheral blood and CD4/CD8 ratio was consistently low, indicating the presence of cellular immunodeficiency state. Serum anti-HTLV-I antibody was markedly increased but he did not have HTLV-I associated myelopathy (HAM). He had no underlying disease which would cause immunodeficiency state such as adult T-cell leukemia (ATL) or HIV infection. We concluded that the HTLV-I carrier state induced his immunodeficiency. During the course, he developed retrobulbar neuritis. T2 weighted cranial MRI revealed high signal lesions in the bilateral corona radiata, posterior limb of the internal capsule, and the pontine base, corresponding to the location of the pyramidal tracts. His hospital course was complicated by opportunistic infections such as Pneumocystis carinii pneumonia, cytomegalovirus infections, and meningitis, and died of multiple organ failure 7 months after the admission. Cellular immunodeficiencies in ATL patients are well known. Intracranial central nervous system (CNS) lesions in HAM patients are also mentioned. Recently coincidence of ATL and HAM in the same patients has also been reported. Asymptomatic HTLV-I carriers may have a latent immunodeficiency state and/or CNS lesions. We shall have to be alert about the presence of such carriers.
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PMID:[A patient with marked immunodeficiency in an HTLV-I carrier: a case report]. 1083 33

The prevalence of psychiatric symptoms and disorders in HIV-infected patients is high. The differential diagnosis includes psychoreactive disorders, acute psychiatric symptoms of an HIV-associated encephalopathy, and symptomatic psychotic illnesses due to secondary neurologic manifestations such as opportunistic central nervous infections and intracerebral lymphoma. Clinical aspects and psychopathological findings are not sufficient for differential diagnosis and identification of primarily psychiatric disorders. Secondary neurologic manifestations causing a symptomatic psychosis must be excluded as soon as possible by brain imaging (CT, MRI) and analysis of the cerebrospinal fluid. In emergency situations, however, German law imposes strict regulations, especially in the case of sectioned patients. These medical and medicolegal questions are illustrated by case reports and propositions for an effective strategy are made.
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PMID:[Acute psychiatric symptoms as the initial manifestation of HIV-infection: differential diagnosis, therapy and medico-legal issues]. 1084 17

We report reversible abnormalities in magnetic resonance spectra acquired from a patient with AIDS undergoing antibiotic and corticosteroid therapy for disseminated nocardiosis, a rare opportunistic infection of immunosuppressed patients which can cause cerebral abscess formation. There was no clinical, CT or MRI evidence of HIV-1 encephalitis. MR spectra were acquired before and after treatment using a two-dimensional chemical shift imaging technique (TR 1500ms, TE 130ms). Prior to treatment, a rise in the choline to creatine ratio and a reduction in the N-acetylaspartate to creatine ratio were observed in MR spectra localized to areas of the left anteromedial centrum semiovale that appeared normal on MR imaging. After 16 weeks, the patient had recovered with complete resolution of the cerebral abscesses on MRI. The MR spectral abnormalities also returned to normal. Two months later, the patient had a relapse with focal neurological signs and further abscesses were demonstrated on MRI of the brain. The patient subsequently died and histopathological and microbiological findings at autopsy confirmed the clinical picture of a recurrence of cerebral nocardiosis with no evidence of HIV-1 encephalitis. This case illustrates reversible MR-measurable metabolite changes in the brain of an HIV-seropositive patient without HIV-1 encephalitis who underwent treatment for cerebral nocardiosis.
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PMID:Reversible alterations in brain metabolites during therapy for disseminated nocardiosis using proton magnetic resonance spectroscopy. 1085 May 50

Clinical data, neuroimaging, and neuropathology of 17 patients with central nervous system tuberculosis were reported. Of this population, 12 were men, 5, women; ages ranged from 23 to 75 years (mean, 46.9). There were three HIV positive patients among them. More than a half of patients had disturbance of consciousness as initial symptom. Neurological signs were variable such as visual acuity loss, hemiparesis, paraparesis, cerebellar ataxia, and tremor, though disturbance of consciousness was the most frequent (36%). Neuroimaging (X-ray CT and MRI) revealed meningeal enhancement (53%), tuberculoma (50%), hydrocephalus, infarction or bleeding and spinal cord tuberculoma. There were three patients who showed paradoxical progression. Eleven patients were performed CSF examination, all of them revealed increased cell count (mean, 206 counts/mm3) and protein (mean, 225 mg/dl), but only 4 patients were positive on bacteriological examination including PCR. Seven patients died and 5 patients were performed autopsy. Neuropathologically, all patients showed a stage of meningitis prominent on basal brain (basal cistern and/or Sylvian fissure). Cell infiltrations including lymphocyte, monocyte, and eosinocyte were most severe around blood vessels, and observed in all cases except one which showed only fibroblast and collagen fibers indicating healed stage. In some cases, there existed epithelioid cells and Langhans giant cells, and in some cases, fibrin exudate. There were three cases having tuberculoma, one HIV case and two non-HIV cases. Center of tuberculoma in non-HIV case was formed by caseous necrosis, and tuberculoma was surrounded by granuloma constituted by epithelioid cells and Langhans giant cells with lymphocyte cell infiltration and proliferation of blood vessels. In contrast, tuberculoma of HIV case did not include granuloma, and was formed with small cells with large nucleus which surrounded arteries. Our studies, as other studies, failed to show any differences between HIV and non-HIV patients clinically, as well as on neuroimaging study. But neuropathological study suggests that mechanism of tuberculoma formation may be different between in HIV positive patients and in non-HIV patients.
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PMID:[Central nervous system tuberculosis with and without HIV infection--clinical, neuroimaging, and neuropathological study]. 1088 29

Primary CNS lymphoma, which has a strong association with Epstein-Barr virus, was increasing in incidence in patients with AIDS before the introduction and widespread use of combination antiretroviral therapy. The diagnostic strategies for primary CNS lymphoma, including contrast-enhanced CT or MRI and brain biopsy, are well established. The use of a combination of diagnostic tools to reduce the need for brain biopsy is currently being evaluated. The clinical outcome with current treatments for primary CNS lymphoma in HIV-infected persons remains relatively discouraging.
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PMID:AIDS-related primary CNS lymphoma: a brief review. 1096 10

Despite more than 15 years of extensive investigative efforts, a complete understanding of the neurological consequences of HIV-1 CNS infection remains elusive. Although the resources of numerous investigators have been focused on studies of HIV-1-associated CNS disease, the complex nature of the disease processes that underlie the clinical, pathological, and cellular manifestations of HIV-1 CNS infection have required a larger volume of studies than was initially envisioned. Several major areas remain as the focus of current research efforts. One of the more pressing issues facing researchers and clinicians alike is the search for correlates to the development of HIV-1-associated CNS neuropathology and the onset of HIVD. Although numerous parameters have been studied, none have been shown to be absolute predictors or markers of HIV-1-related CNS dysfunction. The identification of solid correlates of HIVD is an important goal that would permit clinical identification of individuals at risk for developing potentially crippling, life-threatening CNS abnormalities and would facilitate early treatment of nascent neurological problems. A more complete comprehension of the cellular foundations of CNS dysfunction and HIVD is also a fundamental part of strategies designed to treat or prevent HIV-1-associated CNS disease. Future investigations will strive to expand the body of knowledge concerning the complex interactions between infected and uninfected neuroglial cells and the roles of numerous cytokines, chemokines, and other soluble agents that are deregulated during HIV-1 CNS infection. In particular, a thorough understanding of the mechanisms of neurotoxicity may facilitate the development of new therapies that alleviate or eliminate the clinical consequences of CNS infection. Finally, investigators will continue to study HIVD within the context of single and combination drug therapies used in the treatment of HIV-1 infection and AIDS. As newer and more effective systemic treatments for HIV-1 infection and AIDS are introduced, the effects of these treatments on the onset, incidence, and severity of HIVD will also require intensive study. The impact of drug therapies on the ability of the CNS to act as an HIV-1 reservoir will also need to be addressed. Introduction of each new drug or drug combination will necessitate studies of drug penetration into the CNS and efficacy against the development of CNS abnormalities. Furthermore, as more effective treatments prolong the lifespan of individuals infected with HIV-1, the impact of extended survival on the occurrence and severity of HIVD will also require further investigations. The quest for answers to these and other questions will be complicated by the diversity of experimental systems used to study different aspects of HIV-1 CNS infection and HIVD. Each system has its own unique strengths and weaknesses. Clinical observations provide a continuous spectrum of symptomatic findings but reveal little about the underlying mechanisms of disease. In vivo imaging techniques, such as CT and MRI, also provide a continuum of observations, but the images are limited in their resolution. Neuropathological examinations of postmortem HIV-1-infected brains offer gross, cellular, and molecular views (including phenotypic and genotypic analyses of CNS viral isolates) of the diseased brain, but only provide a snapshot of the end-stage neurologic dysfunction. Studies that rely on animal surrogates for HIV-1, including SIV, simian-HIV (SHIV), feline immunodeficiency virus (FIV), visna virus, and HIV-1 SCID-hu models, permit experimental protocols that cannot be carried out in humans, but are limited by the fidelity with which each virus and animal model emulates the conditions and events observed in the human host. Finally, in vitro techniques, which include the use of primary cells and cell lines, adult or fetal human cell cultures, and BBB barrier model systems, are also convenient means by which aspe
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PMID:HIV-1-associated central nervous system dysfunction. 1101 68

The interactions among sex, HIV infection, and body fat redistribution are uncertain. We retrospectively compared total, subcutaneous, and visceral adipose tissue (TAT, SAT, VAT) contents, as determined by whole body MRI, in 85 HIV-infected persons, including 48 HIV-positive persons with self-reported changes in body shape, and matched healthy controls. The effect of sex on regional fat contents differed among HIV-infected persons with and without self-reported changes in body shape. Women without changes had significantly less SAT and TAT than did controls, while men with changes had significantly less SAT and TAT than did controls. Higher contents of VAT were found in both men and women with self-reported changes in body shape.
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PMID:Interactions among sex, HIV infection, and fat redistribution. 1106 5

Syphilitic spinal cord gumma Syphilitic gummas of the central nervous system are exceptional and are in general described in the brain. We report the case of a Brown-Sequard syndrome in a 25-year-old patient. The cervical myelography and the brain CT as well as the vertebro-occipital junction were normal. The diagnosis of multiple sclerosis was evoked and corticosteroid therapy was initiated. The patient experienced clinical improvement. Two years later, the patient was readmitted. Immunological reactions for syphilis were positive, in serum and CSF. Tests for HIV were negative. The MRI showed a cervical spinal cord process at the C3 level with adhesive spinal associated arachnoiditis. Penicillin therapy was started prior to surgery for the spinal process. The syphilitic nature was confirmed by pathology. To our knowledge, the MR appearance of a syphilitic gumma of the spinal cord has not been described previously in the scientific literature.
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PMID:[Syphilitic spinal cord gumma]. 1110 71

Neuronal injury, dendritic loss and brain atrophy are frequent complications of infection with human immunodeficiency virus (HIV) type 1. Activated brain macrophages and microglia can release quinolinic acid, a neurotoxin and NMDA (N-methyl-D-aspartate) receptor agonist, which we hypothesize contributes to neuronal injury and cerebral volume loss. In the present cross-sectional study of 94 HIV-1-infected patients, elevated CSF quinolinic acid concentrations correlated with worsening brain atrophy, quantified by MRI, in regions vulnerable to excitotoxic injury (the striatum and limbic cortex) but not in regions relatively resistant to excitotoxicity (the non-limbic cortex, thalamus and white matter). Increased CSF quinolinic acid concentrations also correlated with higher CSF HIV-1 RNA levels. In support of the specificity of these associations, blood levels of quinolinic acid were unrelated to striatal and limbic volumes, and CSF levels of beta(2)-microglobulin, a non-specific and non-excitotoxic marker of immune activation, were unrelated to regional brain volume loss. These results are consistent with the hypothesis that quinolinic acid accumulation in brain tissue contributes to atrophy in vulnerable brain regions in HIV infection and that virus replication is a significant driver of local quinolinic acid biosynthesis.
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PMID:Elevated cerebrospinal fluid quinolinic acid levels are associated with region-specific cerebral volume loss in HIV infection. 1133 5

Many studies have shown that brain infections occur early in HIV infection, usually within weeks of seroconversion. Asymptomatic seropositive persons frequently show HIV in the brain and spinal fluid. The most common presenting symptoms are memory loss, walking difficulties, mental slowing, and depressive symptoms. In patients with localized abnormalities, such as weakness, another opportunistic infection should be suspected. Most patients with HIV dementia have clear psychomotor slowing, greater than normal reflexes, and signs indicating widespread brain dysfunction. As the dementia progresses, patients develop language and attention problems, apathy, severe psychomotor slowing, and lack of insight. Delirium is a frequent side effect of the medicines used to treat dementia. Diagnosis is fairly simple, with MRI being used to rule out CMV, progressive multifocal leukoencephalopathy, and herpes. AZT and antiretrovirals offer protective effects to delay the onset and progression of AIDS dementia. The AIDS Clinical Trials Group has completed a study showing that nimodipine, a calcium-channel blocker, can lessen damage to the brain, and is safe and generally well tolerated. Combination therapies, such as antiretrovirals with cytokine blockers, will probably emerge as the treatment of choice for dementia.
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PMID:Diagnosing and treating HIV dementia. 1136 57


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