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)

Anthropometric measurements and dietary intakes of male drug addicts (n = 62), infected (n = 23) or not infected (n = 39) with human immunodeficiency virus (HIV), who underwent two phases of detoxification (P1:15 d to 1 mo and P2: 5-6 mo) were assessed. Body weight, weight gain during detoxification, height, body mass index, and ideal body weight were measured. A prospective food-record questionnaire was compiled and energy and nutrient contents of ingested food were determined. Food intakes were compared with dietary recommendations for the Spanish population. At the time of the study, all patients had substantial weight gains, mostly in P1. Nutrient consumption was lower in P2 (energy, protein, and lipids) and in groups not infected with HIV. In P2, lipid intake was higher in the HIV-positive than in the HIV-negative group (P < 0.05, Student's t test). Moreover, an interactive effect of HIV by phase was shown for lipid intake (P = 0.04, two-way analysis of variance). Magnesium, folate, and vitamin E intakes were lower than recommended in nearly all patients. Energy, zinc, riboflavin, and vitamin B-6 intakes were lower than recommended or were borderline. HIV infection did not have a negative effect on anthropometric measurements or on nutrient intakes. The anthropometric assessment may suggest an adequate recovery of the indexes measured in all patients, which principally took place during P1. Measurement of nutrient intakes showed certain imbalances and deficits that should be corrected.
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PMID:Effects of human immunodeficiency virus infection and detoxification time on anthropometric measurements and dietary intake of male drug addicts. 925 Jan 40

Based on previous studies from our group, we hypothesized that enhanced oxidative stress in association with a persistent immune activation may be important in both the immunopathogenesis and certain clinical manifestations in a subgroup of patients with common variable immunodeficiency (CVI). To explore this hypothesis further, we examined plasma levels of lipid peroxidation, antioxidant vitamins and redox status of various thiol species in 20 CVI patients and 16 healthy control subjects. We found significantly higher malondialdehyde (MDA) levels in plasma from CVI patients than in healthy control subjects. Furthermore, in a subgroup of CVI patients characterized by persistent immune activation in vivo (CVIHyper), we found significantly decreased levels of vitamin E and beta-carotene. In the CVI patients, there was a significant inverse correlation between MDA levels and levels of vitamin E and beta-carotene. Finally, we found a marked elevation in plasma levels of reduced homocysteine in the CVI group, but no corresponding rise in plasma levels of total homocysteine. In the CVI group, the high plasma levels of reduced homocysteine were significantly correlated with enhanced lipid peroxidation and low levels of vitamin E. The results of the present study further support a role for enhanced oxidative stress in the immunopathogenesis of CVI. Furthermore, our finding of markedly elevated plasma levels of reduced homocysteine in CVI patients without simultaneous elevation of other homocysteine species suggests that this disturbance in homocysteine metabolism may be related to enhanced oxidative stress.
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PMID:Elevated plasma levels of reduced homocysteine in common variable immunodeficiency--a marker of enhanced oxidative stress. 935 42

Individuals with acquired immunodeficiency virus (HIV) and patients with acquired immunodeficiency syndrome (AIDS) present a variety of pathologic alterations that influence their nutritional status during various stages of the disease. Previous studies have reported a reduction in plasma vitamin E levels in these patients associated with a higher production of free radicals. Individuals with infection, fever, or acute diarrhea excrete considerable amounts of vitamin A in urine. This observation raised the hypothesis that this may also be the case for vitamin E and that its urinary excretion may play a significant role in the reduction of plasma vitamin E levels. In the present investigation, 28 serologically positive HIV-1 (HIV group) divided into a group of 16 patients with AIDS (< 200/mm3 CD4+ T lymphocytes) were studied. The control group consisted of 11 healthy individuals. Urinary and plasma vitamin E levels were determined by high-performance liquid chromatography. Patients with AIDS presented reduced plasma vitamin E levels (15.25 +/- 12.19 mumol/L) compared with the HIV (26.40 +/- 17.01 mumol/L) and control (40.03 +/- 31.80 mumol/L) groups. On the other hand, urinary excretion was higher in the AIDS group (0.86 +/- 0.99 mumol/24 h) than in the HIV group (0.62 +/- 0.46 mumol/24 h) and considerably higher than in the control group (0.05 +/- 0.13 mumol/24 h). These results indicate elevated vitamin E excretion in the urine of both patients with AIDS and patients with HIV-1, levels is recommended for patients with HIV and patients with AIDS and, if necessary, the combination of existing medical therapy with vitamin supplementation to maintain the nutritional status related to vitamin E.
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PMID:Urinary excretion and plasma vitamin E levels in patients with AIDS. 961 5

We investigated the effect of EPC-K1, which is a phosphodiester compound of vitamin E and vitamin C, on NF-kappaB activity in human cultured astrocytoma cells T98G. In TNFalpha-stimulated T98G cells, treatment with EPC-K1 inhibited both DNA binding activity and transactivation of NF-kappaB in a dose-dependent manner, and the suppressive effect of EPC-K1 was stronger than either that of vitamin E or vitamin C. Moreover, we showed that in TNFalpha-stimulated T98G cells treatment with EPC-K1 repressed NF-kappaB-dependent activation of the human immunodeficiency virus 1 promoter. In contrast, TNFalpha-induced activation of the human immunodeficiency virus 1 promoter was not completely inhibited by either treatment with vitamin E or vitamin C. We, thus, suggest that EPC-K1 is considered to be one of the inhibitory agents of NF-kappaB.
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PMID:Inhibition of NF-kappaB-dependent transcription of human immunodeficiency virus 1 promoter by a phosphodiester compound of vitamin C and vitamin E, EPC-K1. 966 21

Apoptosis is the main cause of CD4+ T-lymphocyte depletion in acquired immune deficiency syndrome (AIDS). Various agents appear to be able to trigger apoptosis in CD4+ T cells, including viral proteins (i.e. gp120, Tat), inappropriate secretion of inflammatory cytokines by activated macrophages (i.e. tumor necrosis factor alpha) and toxins produced by opportunistic micro-organisms. Since oxidative stress can also induce apoptosis, it can be hypothesized that such a mechanism could participate in CD4+ T-cell apoptosis observed in AIDS. This correlates strongly with the observation that AIDS patients present low levels of antioxidants (i.e. superoxide dismutase-Mn, vitamin E, selenium and glutathion) most likely due to inappropriate nutrition (i.e. diets poor in antioxidants), alcohol and drug consumption, and digestive problems associated with the disease. Furthermore, the coadministration of the antiviral drug zidovudine with antioxidants increases its therapeutic potential. Finally, the following additional observations support the hypothesis that oxidative stress is involved in cell apoptosis in AIDS: (1) The depletion of the anti-apoptotic/antioxidant protein Bcl-2 in human immunodeficiency virus (HIV)-infected CD4+ cells; (2) a decrease of apoptosis in HIV-infected cells treated with antioxidants and; (3) the presence of the pro-apoptotic/pro-oxidant cytokines secreted by activated macrophages in AIDS patients. Therefore, anti-apoptotic/antioxidant strategies should be considered, alongside antiviral strategies, in order to design a more efficient therapy for AIDS in the near future.
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PMID:The keys of oxidative stress in acquired immune deficiency syndrome apoptosis. 988 26

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by the human immunodeficiency virus (HIV) after development of severe immunosuppressive changes. Chronic ethanol (EtOH) consumption accentuates the severity of murine AIDS (MAIDS). Because hormone production is often suppressed by chronic EtOH intake, as well as retrovirus infection, we investigated whether hormone supplementation during chronic EtOH consumption contributes to slowing immune dysfunction caused by LP-BM5 infection and/or EtOH use. Because dehydroepiandrosterone sulfate (DHEAS) was previously shown to have immune-enhancing properties during MAIDS, we determined whether DHEAS reduced cytokine dysregulation otherwise exacerbated by chronic EtOH intake during MAIDS. Adult female C57BL/6 mice were infected with LP-BM5 murine retrovirus. Some were fed 40% EtOH in drinking water and agar gel for 16 weeks postinfection. EtOH consumption further inhibited T- and B-cell proliferation beyond suppression due to retrovirus infection. Interleukin (IL)-2 release produced by concanavalin A-stimulated splenocytes was reduced by EtOH use by infected and uninfected mice. DHEAS overcame much of the effects induced by retrovirus infection and/or EtOH use. IL-4 secretion and IL-6 secretion were enhanced. Hepatic vitamin E levels were decreased by murine retrovirus infection, as well as by EtOH use in both uninfected and infected mice. In addition, DHEAS (0.01%) supplementation during MAIDS prevented the further dysregulation of cytokines and hepatic lipid peroxidation due to EtOH intake, partially restored T- and B-cell proliferation, and maintained hepatic vitamin E levels to near normal levels.
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PMID:Immune dysfunction during alcohol consumption and murine AIDS: the protective role of dehydroepiandrosterone sulfate. 1037 6

We assessed oxidative stress in three different clinical conditions: smoking, human immunodeficiency virus (HIV) infection, and inflammatory bowel disease, using breath alkane output and other lipid peroxidation parameters such as plasma lipid peroxides (LPO) and malondialdehyde (MDA). Antioxidant micronutrients such as selenium, vitamin E, C, beta-carotene and carotenoids were also measured. Lipid peroxidation was significantly higher and antioxidant vitamins significantly lower in smokers compared to nonsmokers. Beta-carotene or vitamin E supplementation significantly reduced lipid peroxidation in that population. However, vitamin C supplementation had no effect. In HIV-infected subjects, lipid peroxidation parameters were also elevated and antioxidant vitamins reduced compared to seronegative controls. Vitamin E and C supplementation resulted in a significant decrease in lipid peroxidation with a trend toward a reduction in viral load. In patients with inflammatory bowel disease, breath alkane output was also significantly elevated when compared to healthy controls. A trial with vitamin E and C is underway. In conclusion, breath alkane output, plasma LPO and MDA are elevated in certain clinical conditions such as smoking, HIV infection, and inflammatory bowel disease. This is associated with lower levels of antioxidant micronutrients. Supplementation with antioxidant vitamins significantly reduced these lipid peroxidation parameters. The results suggest that these measures are good markers for lipid peroxidation.
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PMID:Breath alkanes as a marker of oxidative stress in different clinical conditions. 1080 18

Although growth failure is common during pediatric infection with human immunodeficiency virus (HIV) and associated with increased mortality, the relation of specific nutrition factors with growth and mortality has not been well characterized. A longitudinal study was conducted with 194 HIV-infected infants in Kampala, Uganda. Plasma vitamin A, carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lycopene, and lutein/zeaxanthin), and vitamin E were measured at age 14 wk, and weight and height were followed up to age 12 mo. Vitamin A and low plasma carotenoid concentrations were predictive of decreased weight and height velocity. Between ages 14 wk and 12 mo, 32% of infants died. Underweight, stunting, and low concentrations of plasma carotenoids were associated with increased risk of death in univariate analyses. Plasma vitamin A concentrations were not associated with risk of death. In a final multivariate model adjusting for weight-for-age, plasma beta-carotene was significantly associated with increased mortality (odds ratio: 3.16, 95% confidence interval: 1.38 to 7.21, P < 0.006). These data suggest that low concentrations of plasma carotenoids are associated with increased risk of death during HIV infection among infants in Uganda.
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PMID:Relation of vitamin A and carotenoid status to growth failure and mortality among Ugandan infants with human immunodeficiency virus. 1144 74

Chronic renal failure induces a clinical state of immunodefi ciency that also depends upon a wide spectrum of dialysis membranes used during hemodialysis. Previous studies have shown that cellular immunodeficiency is caused by malfunc tion of the antigen presenting cells (monocytes or granulocytes). Subsequent activation of rolling mononuclear leuko cytes results in up-regulated expression of CD11b/CD18 (Mac-1) on endothelial cells. It is postulated that a VitE coated dialysis membrane might minimize the membrane biocompatibility, thereby generating a smaller amount of re active oxygen species (ROS). The purpose of this study was to evaluate the expression of the CD11b/CD18 adhesion mole cule on lymphocytes, monocytes, and granulocytes during HD in 10 patients, using flow cytometric analysis. The study protocol included the measurement of molecule expression using cellulose membrane (Clirans RS15, TERUMO Corp. Japan), and the same membrane coated by vitamin E (Exce brane, Clirans E15, TERUMO Corp., Japan) during 20 dialysi sessions each. Lymphocyte CD11 b/CD1 8 (Mac-1) expression did not change with either dialyzer type. However, monocyt (p = 0.046) and granulocyte (p = 0.018) CD11b/CD18 ex pression in the post HD period was significantly lower using the vitamin E coated membrane compared with the contro cellulose membrane. Our findings suggest a significant de crease in activation and migration of monocytes and granu locytes when using a vitamin E coated cellulose membrane.
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PMID:Effect of vitamin E modified cellulose membrane on human lymphocyte, monocyte, and granulocyte CD11b/CD18 adhesion molecule expression during hemodialysis. 1173 Jan 99

Human immunodeficiency virus infection is often followed by neurodegeneration, the cause of motor and cognitive impairment in some patients affected by acquired immunodeficiency. Several in vitro data indicate glycoprotein (gp) 120 as one of the substances responsible for the neurodegenerative event that takes place only if non-neuronal cells (glial cells) are present. Our purpose was to investigate the molecular mechanisms through which glial cells could affect neuron viability after exposure to gp120 protein. We used a sandwich co-culture of primary hippocampal neurons and primary glial cells, where the two cell populations face each other but are separable. Exposure of 1-week-old rat hippocampal neurons in co-culture with glia to 600 pM gp120 protein resulted in the death of 30% of neurons after 6 days of treatment. A significant increase of intracellular calcium ([Ca2+]i), evident 72 h after gp120 exposure (control 45.8+/-7.6 nM, gp120 176.5+/-43.6 nM), preceded neuron death. The gp120 protein affected neither the viability nor the morphology or [Ca2+]i of glial cells. However, a significant amount of reactive oxygen species as well as of interleukin-1beta was produced. Treatment of the co-culture with an antibody against interleukin-1beta prevented neuron increase of [Ca2+]i and cell death but not glial production of reactive oxygen species, whereas prior incubation of glial cells with Trolox, an antioxidant analog of vitamin E, down-regulated interleukin-1beta expression and completely prevented neuron cell death. Our results indicate that reactive oxygen species produced in glial cells by gp120 exposure cause neurodegeneration by inducing the synthesis of interleukin-1beta.
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PMID:Reactive oxygen species generated by glia are responsible for neuron death induced by human immunodeficiency virus-glycoprotein 120 in vitro. 1174 46


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