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)

Because little was known about the prevalence of neurological complications of human immunodeficiency virus type 1 (HIV-1) infection in Africa, we conducted a cross-sectional study among consecutive admissions to the internal medicine wards of Mama Yemo Hospital in Kinshasa, Zaire. Of the 196 patients studied, 104 (53%) were HIV-1 seropositive, of whom 50 (48%) had stage 3 and 49 (47%) had stage 4 HIV-1 infection according to the provisional WHO staging criteria for HIV infection. Neuropsychiatric abnormalities were present in 43 (41%) of 104 HIV-1-seropositive patients. Of the HIV-1-seropositive patients, 9 (8.7%; 95% confidence interval, 4-16%) were diagnosed as having possible HIV-1-associated dementia complex, 1 (1%) as having possible HIV-1 myelopathy, and 3 (2.7%) as having possible HIV-1-associated minor cognitive/motor disorder. Definitive diagnoses could not be made because there were no facilities for neuroimaging and neuropathology. Meningitis caused by cryptococcus was diagnosed in six (5.6%) and by Mycobacterium avium in two (2%) of the HIV-1 seropositive patients. Acute onset hemiplegia, believed to be due to stroke, was present in four (4%) of the HIV-1-seropositive patients. The prevalence of other central nervous system opportunistic infections and mass lesions, especially toxoplasmic encephalitis, could not be assessed. In this population of Zairian inpatients, the prevalence of neurological complications of HIV-1 infection was similar to that observed in industrialized countries among patients with advanced HIV disease.
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PMID:Neurological complications of HIV-1-seropositive internal medicine inpatients in Kinshasa, Zaire. 131 94

We describe two cases of serologically confirmed human T-lymphotropic virus type I (HTLV-I)-associated myelopathy involving North American men coinfected by the human immunodeficiency virus type 1. Our first patient suffered from a gradually progressive spastic paraparesis for 10 years prior to presenting with Kaposi's sarcoma, while our second patient developed subacutely progressive spastic paraparesis in the setting of full-blown acquired immunodeficiency syndrome. Autopsy examination of the spinal cords from these two cases revealed widespread axonal loss and demyelination principally involving the lateral columns of case no. 1 and the lateral and anterior columns of case no. 2. Vascular sclerosis and hyalinization were prominent in both cases, but in neither was there a conspicuous inflammatory component. In case no. 2, HTLV-I mRNA was not detected by in situ hybridization, but HTLV-I proviral DNA sequences were detected in this case by polymerase chain reaction. Neither case exhibited multinucleated cell (human immunodeficiency virus type 1) myelitis, vacuolar myelopathy, or evidence of HTLV-II infection by polymerase chain reaction assay.
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PMID:Human T-lymphotropic virus type I-associated myelopathy in patients with the acquired immunodeficiency syndrome. 156 47

Excessive hemosiderin-laden perivascular macrophages have been described in the brains of patients with the acquired immunodeficiency syndrome (AIDS) who underwent autopsy; its meaning remains unclear. In the brains of 53 patients with AIDS who consecutively underwent autopsy, we quantified the abnormality, elucidated its relationship to the pathologic features of AIDS, and asked if there was some relationship to endogenous iron storage and transport proteins in brain macrophages and microglia. The number of perivascular siderotic macrophages was significantly increased in patients with AIDS compared with age-matched control subjects. Macrophage siderosis was strongly correlated with the presence of disseminated mycobacterial infection and vacuolar myelopathy at autopsy; a generalized wasting (cachexia) also was related significantly. Many other pathologic abnormalities were not related, including putative human immunodeficiency virus-specific neuropathologic changes such as multinucleated cells and myelin pallor. Activated macrophages and microglial cells in the central nervous system had dense intracytoplasmic accumulation of ferritin (iron storage protein) in AIDS and non-AIDS patients. These results suggest that siderosis of cerebral macrophages is related to an ill-defined nonspecific systemic imbalance associated with the breakdown of abundant stores of endogenous intracellular ferritin. Understanding chronic "secondary" effects of human immunodeficiency virus type 1 infection will become increasingly important as improved survival in patients with AIDS is realized.
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PMID:Siderotic cerebral macrophages in the acquired immunodeficiency syndrome. 158 Jul 55

Adult T-cell leukemia (ATL), a disease entity first described by Takatsuki et al., is endemic in southwestern Japan, the Caribbean Islands, and in some parts of Africa. ATL patients are classified into four subtypes according to the clinical picture: acute, chronic, smoldering, and lymphoma type. The diagnosis of ATL is made from the characteristic clinical findings, the detection of serum antibodies to HTLV-I, and when necessary, the confirmation of monoclonal integration of HTLV-I proviral DNA in cellular DNA of ATL cells. Recently, diagnostic criteria for clinical subtypes of ATL were proposed by the Lymphoma Study Group in Japan: 1) smoldering type, normal lymphocyte level, no hypercalcemia, lactate dehydrogenase (LDH) value 1.5 times the upper limit of normal or lower, no lymphadenopathy, no involvement of liver, spleen, central nervous system (CNS), bone or gastrointestinal tract, and no ascites or pleural effusion: 2) chronic type, absolute lymphocytosis with T-lymphocytosis of greater than 3 x 10(9)/1, LDH value twice the upper limit of normal or lower, no hypercalcemia, no involvement of CNS, bone, or gastrointestinal tract, and no ascites or pleural effusion: 3) lymphoma type, no lymphocytosis, 1% or less abnormal lymphocytes, and histologically-proven lymphadenopathy: 4) acute type, remaining ATL patients who are not classified as any of the above types. Infection with HTLV-I is a direct cause of ATL. Furthermore, infection with this virus can indirectly cause many other diseases via the induction of immunodeficiency, such as chronic lung diseases, opportunistic lung infections, cancer of other organs, monoclonal gammopathy, chronic renal failure, strongyloidiasis, non-specific dermatomycosis, non-specific lymph node swelling, HTLV-I associated myelopathy (HAM/TSP), and HTLV-I uveitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Natural history of HTLV-I infection]. 163 39

The myelopathy associated with human immunodeficiency virus (HIV) infection closely resembles that in subacute combined degeneration, a disorder of vitamin B12 metabolism. To investigate whether the disorders share a pathogenetic mechanism, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) were measured in the cerebrospinal fluid (CSF) of 20 HIV-seropositive patients and 30 HIV-negative patients who were undergoing lumbar puncture for other medical reasons. The HIV-seropositive patients had significantly lower CSF concentrations of SAM (mean 77 [SD 25] vs 131 [35] nmol/l; p less than 0.001) and significantly higher concentrations of SAH (30.5 [6.8] vs 19.0 [7.1] nmol/l; p less than 0.001) than the controls. There was therefore a significant difference between the groups in the SAM/SAH (methylation) ratio (HIV 2.7 [1.0] vs control 7.6 [3.4]; p less than 0.001). There were no correlations between SAM or SAH concentrations or methylation ratio and age or sex in both groups, or serum B12 and folate concentrations, CSF folate, serum or CSF methylmalonic acid, risk factors, body mass index, specific drug treatment received, or disease stage in the HIV group. This finding suggests that HIV affects the brain from a very early stage of the infection. We suggest that, as in the pig, the CSF methylation ratio closely reflects that in the brain. In HIV-infected patients a reduced brain methylation ratio would inhibit methyltransferase enzymes, which would lead to hypomethylation in the central nervous system and ultimately to neurological lesions. In a pig model of subacute combined degeneration and in vitamin-B12-deficient human beings, the primary cause of the low methylation ratio is impaired recycling of SAH back to SAM, a process which requires vitamin-B12-dependent methionine synthase. The HIV patients in this study were vitamin B12 and folate replete, which suggests a different cause for the low methylation ratio.
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PMID:Evidence of brain methyltransferase inhibition and early brain involvement in HIV-positive patients. 167 30

A 33-year-old woman, seropositive for human immunodeficiency virus type 1 (HIV-1), presented with progressive weakness and numbness of the lower extremities, gait difficulties, and urinary frequency. Physical examination revealed bilateral lower extremity weakness, a left-sided Babinski reflex, and a thoracic sensory level to pinprick at T8. Serum rapid plasma reagin was 1:64, and fluorescent treponemal antibody-absorption (FTA-ABS) was 4+. Examination of the cerebrospinal fluid showed a mononuclear pleocytosis and reactive FTA-ABS. The myelopathy responded promptly to high-dose intravenous aqueous penicillin. Syphilis needs to be considered in the differential diagnosis of any patient who develops a myelopathy in association with HIV-1 infection. Because of the diverse nature in which syphilis may affect the spinal cord, treatment with intravenous aqueous penicillin, 12 to 24 million units daily, for a minimum of 10 days, should be considered in any HIV-1-seropositive patient with a progressive, unexplained myelopathy and positive serologic studies for syphilis.
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PMID:Spinal cord syphilis associated with human immunodeficiency virus infection: a treatable myelopathy. 173 97

An increased prevalence of vitamin B12 deficiency has been reported in patients infected by the human immunodeficiency virus (HIV). We report an unexpectedly high prevalence (20%) of such abnormal vitamin B12 metabolism in a population of HIV-infected patients referred for neurological evaluation. This abnormality was associated with both peripheral neuropathy and myelopathy. A majority of those treated with cyanocobalamin had a therapeutic response. Selected neuropathological results suggest a relationship between vitamin B12 deficiency and vacuolar myelopathy. Vitamin B12 deficiency may be a frequent and treatable cause of neurological dysfunction in patients with HIV infection.
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PMID:Abnormal vitamin B12 metabolism in human immunodeficiency virus infection. Association with neurological dysfunction. 184 71

The prevalence of neurosyphilis in human immunodeficiency virus type 1 (HIV-1)-seropositive (HIV+) persons was assessed during the course of a study of the neurological complications of HIV-1 infection. One hundred sixty-six asymptomatic HIV+ subjects, 63 neurologically symptomatic HIV+ subjects, and six at-risk HIV-1-seronegative (HIV-) control subjects underwent cerebrospinal fluid (CSF) analysis on entry into this longitudinal study. Three (1.8%) of the asymptomatic HIV+ subjects had both a reactive CSF VDRL test and a reactive CSF fluorescent treponemal antibody-absorption (FTA-ABS) test. Two of these three subjects had a history of appropriately treated early syphilis, and all had a reactive serum rapid plasma reagin test. Of the 63 neurologically symptomatic HIV+ subjects, one patient with dementia had both a reactive CSF VDRL test and a fluorescent treponemal antibody-absorption test. Subjective improvement in cognitive skills followed high-dose, intravenous penicillin therapy. Another subject had a penicillin-responsive myelopathy accompanied by a reactive CSF fluorescent treponemal antibody-absorption test result, but a nonreactive CSF VDRL. Unsuspected neurosyphilis is relatively common in our population of asymptomatic HIV+ subjects and may be responsible for neurological disease in a significant minority of neurologically symptomatic HIV+ persons. Cerebrospinal fluid examination should be performed in all HIV+ persons with a history of syphilis or serological evidence of syphilis, regardless of prior treatment. Additionally, neurosyphilis should be considered in the differential diagnosis of neurological disease in any HIV+ person.
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PMID:Neurosyphilis in human immunodeficiency virus type 1-seropositive individuals. A prospective study. 185 97

This studies have attempted human immunodeficiency virus (HIV) infection in four CD4+ or CD8+ T-cell lines derived from HTLV-I associated myelopathy virus (HAM) patients. Not only CD4+ cell line but also CD8+ cell line could be infected with HIV and CD4+ cell line showed a higher susceptibility than CD8+ cell line on HIV infection. HIV antigen in early stage after HIV inoculation was detected by using enzyme-linked immunosorbent assay (ELISA) rather than indirect immunofluorescence assay (IFA). HTLV-I producing CD4+ and CD8+ cell lines became to express two viral antigens (HTLV-I and HIV) after HIV inoculation. The results indicated that CD4-CD8+ T-cell line from patient with HAM can be infected with HIV. So that, we have found that other epitopes except for CD4 antigen may be associated with HIV infection.
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PMID:[HIV infection of CD4-CD8+ T-cell line derived from patients with HAM]. 194 69

We describe a 34-year-old man from southern Florida with a history of intravenous drug use, dually infected with human immunodeficiency virus type 1 (HIV-1) and human T-lymphotropic virus type II (HTLV-II), who developed a myelopathy clinically indistinguishable from HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). This myelopathy was characterized by spastic lower extremity weakness, distal paresthesias, sensory loss with a discrete thoracic level to pinprick, back pain, impotence, and sphincter disturbances. Nerve conduction studies revealed an associated mixed axonal and demyelinative neuropathy. Despite a lack of response to 10 months of zidovudine therapy, the myeloneuropathy improved dramatically 2 years after its onset in the absence of any therapeutic intervention.
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PMID:Tropical spastic paraparesis-like illness occurring in a patient dually infected with HIV-1 and HTLV-II. 198


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