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)

Fourteen patients with AIDS were treated for 23 neurologic complications: four episodes of acute meningoencephalitis; eight episodes of subacute encephalopathy; two cases of progressive multifocal leukoencephalopathy; and nine cases of polyneuropathy. Nine patients were treated with 9-(1,3-dihydroxy-2-propoxymethyl)guanine (DHPG), one with 3'-azido-3'-deoxythymidine (AZT), and four initially with DHPG directed against cytomegalovirus (CMV) retinitis or encephalitis and subsequently with AZT against human immunodeficiency virus (HIV) encephalopathy. CMV retinitis was a helpful clinical observation indicating neurologic involvement. DHPG produced improvement in two of three cases of acute meningoencephalitis but was ineffective in cases of subacute encephalopathy or neuropathy. AZT therapy resulted in resolution in both of the two treated cases of acute confusional state and in two of the four treated cases of polyradiculoneuropathy with paraparesis but was ineffective in the late stage of subacute encephalopathy. These results suggest that CMV is important in some cases of acute meningoencephalitis, whereas HIV is a dominant pathogen in subacute dementia and polyneuropathy in patients with AIDS. DHPG may be beneficial in the former, whereas AZT appears to be effective in the latter complications.
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PMID:Responses of neurologic complications of AIDS to 3'-azido-3'-deoxythymidine and 9-(1,3-dihydroxy-2-propoxymethyl) guanine. I. Clinical features. 316 17

A fourteen-week-old boy is described who was admitted with failure to thrive and an interstitial pneumonia caused by Pneumocystis carinii infection. A late onset congenital rubella infection was diagnosed in combination with an immunodeficiency. The congenital rubella infection induced a chronic meningoencephalitis. Further investigations revealed intracerebral calcifications on computerized tomography of the skull. The clinical symptoms of early and late onset congenital rubella syndrome are described. The differential diagnosis of intracerebral calcifications are shortly reviewed.
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PMID:[Intracerebral calcification in a patient with late-onset congenital rubella]. 349 69

Diphenylhydantoin (DFH) treatment for epileptic patients has shown adverse effects such as malignant lymphadenopathy, systemic lupus erithematosus, periarteritis nodosa and recently immunological alterations such as a decreased lymphocytic response to fitohemaglutinin and serum IgA concentration, therefore we thought DFH effect on secretory IgA would be an important finding. This phenomenon might imply a defect in resistance local mechanisms for infection. Two groups of patients were studied: a) 25 children with an established diagnosis of epilepsy, "grand mal" type, that received anticonvulsive treatment with DFH for six months and b) 25 children with a diagnosis of infectious meningoencephalitis that required DFH to control convulsive crisis. Patients with a history of recurrent infections, lymphadenopathies, hepatosplenomegaly, drug allergy, collagenopathies and immunodeficiency were ruled out from this study. In all patients T and B lymphocytes, serum IgA, saliva and duodenal fluid and IgA determinations were made. Results show IgA concentration decrease in saliva and duodenal fluid of epileptic and meningoencephalitic patients (p less than 0.05), as well as lymphocyte T depression in epileptic and non epileptic patients treated with DFH (p less than 0.001).
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PMID:Effect of diphenylhydantoin in serum and secretory IgA concentrations. 677 21

A child with acute lymphocytic leukemia who was in clinical remission and developed coxsackie B4 meningoencephalitis is presented. Despite minimal evidence of immunodeficiency, the patient had progression of neurologic disease clinically, electroencephalographically and on laboratory evaluation of spinal fluid. A dramatic response to the use of intravenous immunoglobulins is reported and its rationale explained.
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PMID:A case of protracted coxsackie virus meningoencephalitis in a marginally immunodeficient child treated successfully with intravenous immunoglobulin. 760 26

Previous studies suggested that simian immunodeficiency viruses isolated from African green monkeys (SIVagm) are relatively nonpathogenic. The report describes the isolation and biologic and molecular characterization of a pathogenic SIVagm strain derived from a naturally infected African green monkey. This virus induced an AIDS-like syndrome characterized by early viremia, frequent thrombocytopenia, severe lymphoid depletion, opportunistic infections, meningoencephalitis, and death of five of eight macaques within 1 year after infection. An infectious clone derived from this isolate reproduced the immunodeficiency disease in pig-tailed (PT) macaques, providing definitive proof of the etiology of this syndrome. Although the virus was highly pathogenic in PT macaques, no disease was observed in experimentally infected rhesus macaques and African green monkeys despite reproducible infection of the last two species. Whereas infection of PT macaques was associated with a high viral load in plasma, peripheral blood mononuclear cells, and tissues, low-level viremia and infrequent expression in lymph nodes of rhesus macaques and African green monkeys suggest that differences in pathogenicity are associated with the extent of in vivo replication. The availability of a pathogenic molecular clone will provide a useful model for the study of viral and host factors that influence pathogenicity.
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PMID:Induction of AIDS by simian immunodeficiency virus from an African green monkey: species-specific variation in pathogenicity correlates with the extent of in vivo replication. 781 63

Neurocryptococcosis was a rare nervous system infection. With the rising number of patients with AIDS it became a very frequent disease. This infection is supposed to infect patients with some kind of immunodeficiency and the CSF alterations often simulate tuberculous meningitis. The purpose of this research was to compare the CSF changes in AIDS and non-AIDS patients with meningoencephalitis caused by Cr. neoformans. There were analysed 41 CSF samples from non-AIDS patients with neurocryptococcosis and 23 CSF samples from AIDS patients with neurocryptococcosis. The results of this research allowed to conclude that the inflammatory changes in the CSF from AIDS patients showed a lower intensity compared to those non-AIDS patients. These results showed as well, that the CSF samples from non-AIDS patients always revealed some changes besides the yeast cells. In some samples of AIDS patients, however the unique change was the presence of the yeast. It was demonstrated also, that the presence of Cr. neoformans in CSF, not accompanied by any other change, may suggest that is a patient with AIDS. In non-AIDS patients CSF alterations often simulates tuberculous meningitis. However these alterations were rare in AIDS patients. The yeast cells were more numerous in CSF samples from AIDS patients than in those from non-AIDS patients.
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PMID:[Comparison between CSF samples from AIDS and non AIDS patients with neurocryptococcosis]. 785 86

A wide variety of pathologies afflicting the CNS is see in patients infected with the human immunodeficiency virus. We report the case of relapsing meningoencephalitis caused by Mycobacterium avium intracellulare (MAI) in a homosexual male with the acquired immunodeficiency syndrome in whom repeated use of polymerase chain reaction was required to detect MAI-specific DNA in the cerebrospinal fluid. Successful responses to early empirical antibiotic combination treatment, including the drugs clarithromycin and rifabutin, were demonstrated by clinical, EEG, and CSF improvement during an 8-month period. To our knowledge, this study presents the first known patient with the acquired immunodeficiency syndrome effectively treated for MAI meningoencephalitis and suggests that modern antimycobacterial combination therapy may improve the poor prognosis of CNS infections with nontuberculous mycobacteria.
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PMID:Successful treatment of meningoencephalitis caused by Mycobacterium avium intracellulare in AIDS. 789 10

Cryptococcosis is an important cause of lymphocytic meningitis, especially but not necessarily in immunocompromised patients. We present the case of a 23-year-old man with a severe and rapid course of a cryptococcal meningoencephalitis, which led to visual and hearing loss, psychotic illness and radiculopathy. There was no evidence of immunodeficiency. Treatment with amphotericin B and flucytosine led to improvement of the symptoms but did not eradicate the micro-organisms from the cerebrospinal fluid (CSF). Maintenance therapy with fluconazole was necessary and led to improvement of the CSF pathology.
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PMID:Cryptococcal meningitis with severe visual and hearing loss and radiculopathy in a patient without immunodeficiency. 793 77

Infection of the central nervous system is generally a serious event due to the risk of fatality and the possibility of sequelae. In immune deficient patients, there is a relatively large range of infectious agents that may be responsible for meningoencephalitis or a cerebral lesion, and determining aetiology can be difficult. In some cases, the agent is isolated from the CSF or from a peripheral site, which permits rapid, appropriate treatment. In other cases, when a direct neurosurgical approach to the lesions is precluded, the main elements determining the best probable treatment are the nature of the immunodeficiency and especially results of imaging investigation.
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PMID:[Cerebro-meningeal infections and immune deficiencies, excluding AIDS]. 798 20

Major histocompatibility complex class II deficiency (bare lymphocyte syndrome) is a rare primary immunodeficiency disorder characterized by profound defects in human leukocyte antigen class II expression, inconsistent and incomplete expression of human leukocyte antigen class I molecules, and a complete lack of cellular and humoral immune responses to foreign antigens. To define the clinical and immunologic characteristics, outcome, and natural history of major histocompatibility complex class II deficiency, we retrospectively analyzed 30 consecutive patients. Clinical onset occurred in the first year of life, usually involving recurrent bronchopulmonary infections and chronic diarrhea. The clinical course was complicated by viral meningoencephalitis, hepatitis, cholangitis, and various autoimmune phenomena. Prognosis was very poor: the mean age at the time of death was 4 years. The main cause of death was overwhelming viral infection. Recent advances in bone marrow transplantation have raised hopes of curative treatment: 6 of 14 patients who underwent bone marrow transplantation were cured. Long-term survival after human leukocyte antigen-identical and haploidentical bone marrow transplantation seemed to depend primarily on the presence of preexisting viral infections.
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PMID:Major histocompatibility complex class II deficiency: clinical manifestations, immunologic features, and outcome. 822 25


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