Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autopsy or biopsy findings in 10 human immunodeficiency virus (HIV)-positive persons from Bangalore, India, revealed a wide spectrum of pathological changes. Patients' mean age was 33.4 years and the mean duration between symptom onset and death was 27.13 days. Nine patients had evidence of neuro-acquired immunodeficiency syndrome (AIDS) and 8 of them succumbed to various opportunistic infections. Histologic examination showed diffuse cryptococcal meningitis in 5 cases; 2 cases showed disseminated systemic cryptococcosis. Pulmonary tuberculosis was present in 3 patients. Despite no signs of associated neurotuberculosis in any patient, 4 autopsied and 1 biopsied case showed evidence of systemic tuberculosis. Toxoplasma encephalitis was present in 2 cases; observed in this series was the first case, in India, of co-existent toxoplasma and acanthamoeba. Other bacterial infections such as meningococcal meningitis and psudomonas septicemia were found in 3 cases; pneumocystis carinii pneumonia was present in 1 case. Evidence of early HIV leukoencephalopathy was observed in the only asymptomatic HIV-positive individual (who died in a traffic accident). AIDS-associated bacterial infections caused by organisms other than Mycobacterium tuberculosis are often underdiagnosed and should be considered in developing countries. In cases of cryptococcal and tuberculosis meningitis or multiple parasitic infections, patients should be screened for associated HIV infection.
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PMID:Pathological lesions in HIV positive patients. 775 Oct 41

The intrathecal synthesis of interleukin 10 (IL-10) was investigated in 120 paired cerebrospinal fluid (CSF) and serum specimens from patients with various inflammatory and non-inflammatory diseases of the central nervous system (CNS). IL-10 was not demonstrated in the sera, but detectable levels were found in the CSF from: patients with acute viral ("aseptic") meningitis, but only within 48-72 h of symptom onset; human immunodeficiency virus type 1 (HIV)-infected patients with HIV-related encephalitis/leukoencephalopathy or cryptococcal meningitis; a patient with primary B cell lymphoma of the CNS, and a patient with encephalomeningeal sarcoidosis (in whom IL-10 was demonstrated in all CSF collected over a period of 6-months). In chronic meningeal infections/inflammations, IL-10 seems to be continuously produced within the CSF. Our findings suggest that IL-10, a cytokine which exerts many immunosuppressive actions, may play different immunomodulatory roles in CNS diseases; in particular, its intrathecal synthesis may explain why some infectious and inflammatory meningeal diseases may have slow development and chronic evolution.
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PMID:Intrathecal synthesis of interleukin-10 (IL-10) in viral and inflammatory diseases of the central nervous system. 783 46

Using polymerase chain reaction (PCR), 34 cerebrospinal fluid (CSF) samples from 28 patients with progressive multifocal leukoencephalopathy (PML) were analyzed. As controls, 116 samples were evaluated from 82 human immunodeficiency virus type 1 (HIV-1)-infected patients and 1 HIV-1-negative patient. Of the HIV-1-positive patients, 23 had cerebral toxoplasmosis, 10 had HIV leukoencephalopathy, and 49 had other neurologic complications. Detection of JC virus (JCV) DNA in CSF was increased 10-fold by the addition of carrier DNA before phenol-chloroform-isoamyl alcohol extraction. The primer pair JC 26/29, from the VP1/large T region, had a limit of detection of 10(5) JCV DNA molecules/100 microL. The primer pair JC 36/39, located in the large T gene region, had a 100-fold lower limit of detection. With JC 26/29, the sensitivity was 43% (12/28) and specificity was 100%. Using JC 36/39, sensitivity increased to 82% (23/28), and false-positive results were not observed. Diagnosis of PML is greatly aided by PCR analysis of CSF.
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PMID:Specific diagnosis of progressive multifocal leukoencephalopathy by polymerase chain reaction. 816 9

Based on a consecutive autopsy series of 184 patients with AIDS, a critical review of the pathology of the central nervous system (CNS) is given. The lesions can be divided into three groups: 1. opportunistic/non-opportunistic infections, 2. changes due to the human immunodeficiency virus (HIV), and 3. neoplasms. The frequency and morphology of CNS lesions in our cohort are compared with those in other series. Marked lesions of the CNS were found in 111 patients (60%), while mild/nonspecific changes were seen in 52 cases (28%). Toxoplasmosis (23%) was the most frequent CNS infection, followed by cytomegalovirus (17%), and papovirus (5%). HIV giant cell encephalitis, HIV leukoencephalopathy, vacuolar myelopathy and leukoencephalopathy were observed in 11%. Primary CNS lymphomas were present in 6%, while secondary involvement of the CNS in systemic lymphomas was seen in only two cases (1%). Lesions due to CNS infections in patients with AIDS often show atypical patterns, and frequently, there are multiple infections with simultaneous involvement of the CNS by lesions of different etiology. The present study confirms the frequent involvement of the CNS in AIDS, although there are differences in the incidence and pattern of lesions related to geographic and/or demographic factors.
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PMID:[Pathology of the central nervous system in AIDS. An overview of 184 patients]. 821 4

Histopathologic lesions in the central nervous system (CNS) of 400 autopsy cases of the acquired immunodeficiency syndrome (AIDS) collected from 1982 to 1990 were studied. Lesions most closely associated with human immunodeficiency virus (HIV) infection in the CNS (perivascular macrophages, nodular encephalomyelitis, diffuse leukoencephalopathy, necrotizing encephalitis, and long-tract degeneration) were found in 20% of the cases. The group of vascular and inflammatory lesions and of opportunistic infections was seen in 25% of cases. These two lesion groups were found together in 32% of cases, and none of these lesions was present in 23% of cases (most of the latter having no significant CNS lesions). Length of survival increased in the last group of 100 cases compared with the first 300 cases. The homosexual and bisexual risk groups showed continuously increasing lengths of survival for each category of HIV-associated CNS lesions throughout the study, while the lengths of survival in the other risk groups varied. Patients in the last group of 100 autopsy cases with any HIV-associated lesion survived longer than patients without these lesions. The AIDS patients with no CNS lesions had the shortest mean length of survival. The results suggest that although survival is prolonged as specific therapy is given, there is an increase in CNS lesions in AIDS patients with longer survival. This may indicate that CNS lesions in AIDS are generally dependent on systemic disease progression over many months as immune function decreases.
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PMID:Histopathologic features in the central nervous system of 400 acquired immunodeficiency syndrome cases: implications of rates of occurrence. 824 20

True demyelination, or at least a leukoencephalopathy with predominant involvement of myelin, may occur in many neurological complications of human immunodeficiency virus (HIV)-infection, resulting from various mechanisms which are not all well understood. These include lesions directly related to infection of the nervous tissue by HIV, opportunistic infections and lymphomas secondary to the cell-mediated immunodeficiency, and changes due to other general or systemic complications of acquired immunodeficiency syndrome (AIDS). HIV-induced pathology of the nervous system includes HIV-specific disease, due to direct infection of the nervous system by the virus. This is characterized by the presence of distinctive multinucleated giant cells and white matter changes, HIV encephalitis and HIV leukoencephalopathy, which may overlap in one third of cases. The pathogenesis of myelin destruction is unclear. Direct infection of neurons or glial cells has never been demonstrated. Indirect immunopathologic, toxic, metabolic, or vascular mechanisms secondary to infection of monocytes/macrophages are more likely. Less specific HIV-associated central nervous system (CNS) pathology including vacuolar myelopathy, and vacuolar leukoencephalopathy are characterized by numerous vacuolar myelin swellings in spinal or cerebral white matter. The exact aetiopathological relationship of these changes to HIV infection is uncertain. It seems likely that factors other than, or additional to, HIV infection play a role in their causation. Apart from these changes which usually occur at the late stages of the disease, acute perivenous inflammatory leukoencephalopathy, presenting either as acute haemorrhagic leukoencephalopathy, acute demyelinating perivenous encephalitis, or acute multiple sclerosis-like leukoencephalopathy revealing HIV-infection occur in rare cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HIV-related demyelinating disease. 825 24

Using stereological methods, two cerebral cortical areas from AIDS brains were investigated. Neuronal density, profile area of neurons, and perikaryon volume fraction were measured and compared to age-matched control brains. In the fronto-orbital cortex (area 11) of AIDS brains, a significant loss of neurons was seen. The perikaryon volume fraction was likewise decreased. The size of neurons did not differ between control and AIDS brains. In patients with clinical signs of progressive dementia and in brains with human immunodeficiency virus (HIV)-specific neuropathology (HIV-leukoencephalopathy and/or HIV-encephalitis) as compared to patients lacking these features, a small decrease in neuronal density was noted but this difference did not reach the level of statistical significance (P = 0.16). In the superior parietal lobule (area 7) of AIDS brains, no loss of nerve cells was noted. AIDS patients with progressive dementia and brains with HIV-specific neuropathology showed no difference in neuronal densities as compared to those without such features. We conclude that the fronto-orbital cortex, in contrast to the parietal cortex, is mainly damaged in AIDS brains. Neuronal loss was not significantly correlated with development of dementing symptoms and of HIV-specific neuropathology.
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PMID:Neuronal damage in the cerebral cortex of AIDS brains: a morphometric study. 844 9

Two magnetization transfer (MT) contrast effects, a T2-like effect and the improved contrast observed when gadolinium is used with MT, are combined in a single sequence. Forty patients (22 males:18 females; mean age, 45 years (23-87)) with suspected intracranial pathology underwent MRI on a 1.5 Tesla system. Of 46 lesions; seven were ischemic, five infective, seven neoplastic, four hemorrhagic, four multiple sclerosis, seven human immunodeficiency virus (HIV) leukoencephalopathy, nine normal/miscellaneous, and three gliosis. A conventional spin-echo sequence (TR 900 TE 15) was used with on-resonance binomial MT pulses. The sequence was performed postgadolinium +/- MT. The signal intensity ratios +/- MT were: white matter, 0.62 +/- 0.03; gray matter, 0.75 +/- 0.04; ischemia, edema, and demyelination, 0.75 (0.57-0.86); and gadolinium/methemoglobin, 0.85 (0.81-0.98). Areas which exhibited MT had T2-like contrast and those that did not maintained expected contrast for the given parameters. The result was a combination of T2-like contrast, gadolinium enhancement, and dark cerebrospinal fluid (CSF) providing both increased sensitivity to lesions which exhibited both contrast features and improved delineation of periventricular lesions. Furthermore, the differential signal between T2-like contrast of edema and gadolinium enhancement in neoplastic or infective lesions was maintained.
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PMID:Clinical utility of a new contrast option from magnetization transfer contrast. 857 39

Seventeen asymptomatic individuals positive for human immunodeficiency virus type 1 (HIV-1) and 16 patients with acquired immunodeficiency syndrome (AIDS), all with polymerase chain reaction evidence of HIV-1 DNA, were selected for quantitative analysis to correlate the levels of HIV-1 DNA in brain tissue with the stage of infection. The AIDS patients either were clinically asymptomatic or presented various abnormalities. Neuropathological lesions were assessed by morphological and immunohistochemical methods. To determine the level of HIV-1 DNA, semiquantitative nested polymerase chain reaction was applied using a digoxigenin-labeled primer and chemiluminescence. Serial dilutions of standard HIV DNA were run in parallel with brain DNA samples. Among the 16 AIDS brains studied, 9 showed changes characteristic of HIV encephalitis/leukoencephalopathy while 1 showed focal pontine leukoencephalopathy and 6 showed no obvious neuropathological lesions. Abnormalities in pre-AIDS individuals included meningitis, microgliosis, and astrogliosis. Copy numbers of HIV-1 DNA in the brains of AIDS patients were higher than those in asymptomatic individuals (median, 135 vs 45 copies/150,000 cells). However, there was some degree of overlapping between the two groups, with some AIDS patients showing low figures while 3 asymptomatic individuals had high copy numbers. This suggests that the use of HIV-1 DNA load in the central nervous system as an indicator of progression of the disease should be restricted to large series and not single patients.
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PMID:HIV-1 DNA in brains in AIDS and pre-AIDS: correlation with the stage of disease. 887 81

To determine the onsets and specificities of neuropathological features observed after simian immunodeficiency virus (SIV) infection of macaques, brains of 19 clinically unaffected rhesus monkeys (group A) were examined after intervals ranging from 1 to 48 weeks post-infection and compared to 8 animals with AIDS (group B) as well as to 8 uninfected controls. Based on morphological and virological parameters, seven patterns specific for SIV infection of the central nervous system (CNS) were discerned. In both groups of infected but not control animals, we found mononuclear aggregates in meninges, perivascular space, and choroid plexus stroma (designated pattern 1), isolated infected cells within CNS parenchyma (pattern 2), axonal degeneration (pattern 3), spongy change (pattern 4), microglial proliferation (pattern 5), and small vessel proliferation (pattern 6). SIV encephalitis (pattern 7) was only evident in animals with clinically evident disease. Changes characteristic of patterns 3, 5 and 6 appeared to be chronic and non-progressive, whereas lesions of patterns 1, 2 and 4 appeared to have progressed in animals with AIDS. The main component of mononuclear aggregates in animals of group A were lymphocytes, in contrast to animals of group B, in which macrophages dominated the inflammatory infiltrates. Altogether, our results demonstrate that subtle leukoencephalopathy was a specific feature of clinically silent as well as clinically evident phases of SIV infection. This might explain the neurological impairment of HIV-positive non-AIDS individuals.
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PMID:Nature and sequence of simian immunodeficiency virus-induced central nervous system lesions: a kinetic study. 892 61


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