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Query: UMLS:C0019693 (HIV)
170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal function was estimated by synthetic ACTH test in 18 men with AIDS (or AIDS-related complex) and compared with that of 10 HIV positive but otherwise healthy men. According to this test none fulfilled the criteria for adrenal insufficiency defined as plasma cortisol concentration less than 500 nmol/l 30 minutes after ACTH stimulation. Seven of eighteen AIDS patients had baseline cortisol concentrations above 0.5 mumol/l compared to none in the HIV-positive group. Three of eighteen AIDS patients had a limited response to synthetic ACTH injection compared to none in the HIV-positive group. Two of these three AIDS patients had lowered serum Na+ concentration; they survived for two and three weeks, respectively. Otherwise the basal cortisol level and response to synthetic ACTH was uncorrelated with survival time, other signs of adrenal insufficiency, treatment with ketokonazole, CMV-infection, T-helper cell count or Th/Ts-ratio. The pituitary-adrenal axis was estimated by measuring the diurnal rhythm of serum ACTH and cortisol in eight patients and was found intact and normal in all of them. Thus, absolute adrenal insufficiency is uncommon in AIDS-patients. Relative adrenal insufficiency may occur in severely ill preterminal patients as a result of primary target organ failure, but the pituitary-adrenal axis generally appears to be undisturbed.
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PMID:[Adrenal cortex function in patients with AIDS and healthy HIV-positive persons]. 165 May 13

Polyclonal B-cell activation is a characteristic feature of AIDS and of the AIDS-related complex. Since the immunoregulatory cytokine interleukin-6 (IL-6) plays a major role in inducing B-cell differentiation, we examined the effects of native human immunodeficiency virus type 1 envelope glycoproteins gp120 and gp160 on IL-6 induction. In this study, we have demonstrated that both gp120 and gp160 have the ability to induce IL-6 mRNA and biologically active IL-6 protein secretion in peripheral blood mononuclear cells in vitro. The envelope protein preparations had no detectable endotoxin as tested by the Limulus amebocyte lysate assay, and hence we can rule out the effect of contaminating endotoxin, which is a potent inducer of IL-6 in monocyte/macrophage cell cultures. In addition, we have shown that the envelope glycoproteins act directly on CD4(+)-cloned T cells to induce IL-6 production in the absence of monocytes. These findings indicate that monocytes and T cells both contribute to the secretion of IL-6, which plays an important role in the pathogenesis of B-cell activation in human immunodeficiency virus infection.
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PMID:Human immunodeficiency virus type 1 envelope glycoproteins gp120 and gp160 induce interleukin-6 production in CD4+ T-cell clones. 165 94

The Association of State and Territorial Public Health Laboratory Directors (ASTPHLD), CDC, and other organizations (e.g., American Red Cross [ARC] and Consortium for Retrovirus Serology Standardization [CRSS]) have recommended for antibody testing to human immunodeficiency virus type 1 (HIV-1) that duplicate repeat reactive enzyme immunoassay (EIA) screening results be confirmed by a supplemental test. This report examines the variation in Western blot (WB) interpretive criteria reported by laboratories enrolled in CDC's Model Performance Evaluation Program (MPEP) for HIV-1-antibody testing.
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PMID:Interpretive criteria used to report western blot results for HIV-1-antibody testing--United States. 165 86

Tuftsin is an endogenous tetrapeptide that stimulates phagocytosis and is released from the Fc fragment of IgG by a splenic endocarboxypeptidase. Tuftsin activity and splenic function were measured in 21 patients with AIDS, 7 patients with AIDS-related complex (ARC), 22 patients who had undergone splenectomy, and 37 healthy volunteers. There was a significant inverse correlation between tuftsin activity and splenic function in all subjects. Tuftsin activity was significantly lower in patients with AIDS, ARC, and in those who had undergone splenectomy compared with healthy volunteers. Tuftsin deficiency may contribute to the risk of bacterial infection in symptomatic HIV-positive individuals.
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PMID:Tuftsin deficiency in AIDS. 167 Jun 48

To examine whether polyclonal activation of B lymphocytes as measured by hypergammaglobulinemia contributes to lymphadenopathy in human immunodeficiency virus (HIV) infection, correlates of adenopathy were examined in 240 homosexual men. Lymph node size was measured in 12 sites semiannually over 4 years. Both adenopathy and hyperglobulinemia developed within 1 year after seroconversion and persisted at high levels. Adenopathy declined near diagnosis of AIDS whereas serum IgG decreased 8-16 months after diagnosis. Adenopathy attributable to HIV occurred in all palpable node groups. By logistic regression, HIV-positive men were best discriminated from HIV-negative men by size of posterior cervical nodes and the number of sites with enlarged nodes. In a repeated measures model of covariance, adenopathy in HIV-positive men was associated with more CD4+ cells (P less than .002), elevated serum globulins (P less than .01), and lower platelet counts (P less than .05). Adenopathy declined over time (P less than .001) and with diagnosis of AIDS or AIDS-related complex (P less than .03). Thus, adenopathy and hypergammaglobulinemia are correlated and follow a similar course through various stages of HIV infection, suggesting that both are caused by polyclonal B cell activation.
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PMID:The evolution of lymphadenopathy and hypergammaglobulinemia are evidence for early and sustained polyclonal B lymphocyte activation during human immunodeficiency virus infection. 167 Oct 53

Zidovudine use data were examined in the Multicenter AIDS Cohort Study to determine (i) if the proportion of pre-AIDS participants (i.e., CD4+ cells less than 200/mm3 or AIDS-related complex) taking zidovudine is high enough to explain a slower than expected rise in AIDS incidence in U.S. homosexual men since mid-1987; (ii) which factors are associated with starting zidovudine and clinical trials of zidovudine; and (iii) if pre-AIDS patients, as a group, are being undertreated. Data on zidovudine use, clinical trial participation, and sociodemographic, clinical, and hematologic variables were collected every 6 months from 1,195 AIDS-free HIV-1-seropositive homosexual men from April 1987 to September 1989. Overall prevalence of zidovudine use rose from 3.6% in mid-1987 (visit 7) to 23% in mid-1989 (visit 11). Of those with less than 200 CD4+ lymphocytes/mm3, the prevalence of zidovudine use rose from 23% (24% if those taking zidovudine or placebo as part of a clinical trial are included) at visit 7 to 58% (69%) at visit 11. Of those with ARC, 20% (23%) were using zidovudine at visit 7 and 55% (65%) at visit 11. Although numbers were small, the advanced ARC participants (CD4+ cells less than 200/mm3 and two or more symptoms) reported the highest treatment rates (50, 78, 80, 60, and 74% at visits 7-11, respectively). By September 1989, 42% (31%) of those with CD4+ lymphocyte levels less than 200/mm3 were still not receiving zidovudine, suggesting that many high-risk, pre-AIDS individuals are being undertreated. To explore this finding further, we examined a range of sociodemographic, hematologic, and clinical variables to determine which factors best predicted initiation of zidovudine therapy outside of clinical trials. In multivariate analyses, CD4+ lymphocyte number was the most consistent predictor of initiation of therapy over all four study visits. For each 100 cells/mm3 deficit, the odds ratios were 2.3 (95% C.I. of 1.7-3.1) at visit 7 and 1.7% (95% C.I. of 1.4-2.0) at visit 11. Symptom status and education level were also associated with starting zidovudine, but not at all visits. The relatively low predictive power of the clinical variables raises and the possibility that nonclinical factors not measured in the MACS (drug cost, third-party insurance restrictions, and individual preferences) may play an important role in predicting zidovudine use. Finally, comparisons were made between seropositive participants starting clinical trials of zidovudine and the rest of the study population. No important differences were found in demographic or major clinical variables between clinical trial participants and zidovudine nonusers in this study.
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PMID:Zidovudine use in AIDS-free HIV-1-seropositive homosexual men in the Multicenter AIDS Cohort Study (MACS), 1987-1989. 167 11

The pathophysiology of anemia in patients with human immunodeficiency virus (HIV) infection is multifactorial. In order to determine the role of erythropoietin (EPO) response as a cause of the anemia, serum levels were determined by direct radioimmunoassay in 110 symptomatic patients with various stages of HIV infection. Symptomatic patients (ARC and AIDS) not receiving zidovudine (ZDV) therapy demonstrated a strong inverse relationship between serum EPO and hemoglobin levels (p = 0.01 and p less than 0.001, respectively). Patients with AIDS who were anemic while receiving ZDV demonstrated serum EPO levels that ranged from normal to markedly elevated (9-3,390 mU/ml). The diversity of serum EPO levels in patients with HIV infection and anemia suggests that the etiology of anemia in these patients and their potential response to recombinant human EPO may not be uniform.
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PMID:Serum erythropoietin titers in patients with human immunodeficiency virus (HIV) infection and anemia. 154 78

In a series of 646 heroin addicts anti-HIV was detected in 428 (66.2%) and HBsAg in 53 (8.2%). Forty-eight (90.5%) of the latter had concomitant chronic HDV infection. Markers of past HBV infection were found in 481 (74.4%). The prevalence of anti-HIV was significantly higher in the 534 subjects with HBV markers than in the other 112 without markers (69.8% versus 49.1%, p less than 0.001). Of the 266 anti-HIV positive subjects followed for 3-48 months (median 12), nine progressed from no disease to persistent generalized lymphadenopathy (PGL), 52 from PGL to AIDS-related complex (ARC) or AIDS (30 and 22 cases respectively), and six from ARC to AIDS. Baseline T4 + cell count was significantly lower and reduction during follow-up significantly greater in heroin addicts with disease progression than in those without.
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PMID:Prevalence of HIV infection in 646 heroin addicts and outcome of HIV-related conditions in the 266 followed up. 167 32

We enrolled 253 HIV-antibody positive heroin addicts without HIV-related disease (n = 81) or with persistent generalized lymphadenopathy (n = 172) in a prospective study to evaluate clinical progression to AIDS related complex (ARC) or AIDS and to identify factors of possible prognostic relevance. Follow-up lasted between 6 and 40 months (median 12 months). According to the non-parametric Cox's model the only significant (P less than 0.001) prognostic variable was T4+ cell count considered in three classes: greater than 800/microliters (no depletion), 400-800/microliters (moderate depletion) and less than 400/microliters (absolute depletion). Subjects with T4+ cell count of less than 400/microliters had a risk of developing ARC or AIDS that was 6.46 and 1.98 higher than those with values of greater than 800/microliters or between 400 and 800/microliters respectively. The estimated probability of progression to ARC or AIDS was 0.029, 0.056 and 0.172 at one year in subjects with T4+ cell count of greater than 800/microliters 400-800/microliters and less than 400/microliters, respectively, and 0.296, 0.501, and 0.896 at two years.
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PMID:T4+ cell depletion as a major risk factor for AIDS-related complex and AIDS. Longitudinal study of 253 HIV-antibody positive heroin addicts from northern Italy. 167 62

Sixty-eight adults and nine children infected with human immunodeficiency virus type 1 (HIV-1) were evaluated consecutively for the presence and amount of cell-free infectious virus in their plasma. Viremia was detected in 18 of 68 adults and in five of nine children; titers ranged from 10 to 100,000,000 TCID/ml plasma. Among the adults, none of 19 asymptomatic patients, 4 of 34 AIDS-related complex patients, and 14 of 15 AIDS patients had cell-free infectious virus in their plasma. None of 35 adult subjects with CD4+ lymphocyte counts greater than 400/mm3 were viremic, whereas 3 of 17 with 200-400 CD4+ lymphocytes/mm3 and 15 of 16 individuals with less than 200 CD4+ lymphocytes/mm3 were plasma viremic. In contrast to adults, each of five children infected with HIV-1 in utero or during the perinatal period were plasma viremic regardless of their CD4+ lymphocytes counts (range, 42-2227/mm3), duration of infection, or clinical stage; however, children infected by HIV-1 at older ages were less frequently plasma viremic. Therapy with zidovudine led to a 10- to 10(6)-fold decline in plasma HIV-1 TCID in all eight subjects studied before and after treatment.
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PMID:High-level viremia in adults and children infected with human immunodeficiency virus: relation to disease stage and CD4+ lymphocyte levels. 167 46


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