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

The blood compatibility of ventricular assist devices developed by the Helmholtz Institute Aachen (HA-VAD's) was tested on calves. Seven calves received a non-coated HIA-VAD (control) and three a Bioline heparin coated device. The circulatory support of these HIA-VAD's lasted one week. Mechanical blood cell trauma estimated by hematocrit (Hct), hemoglobin (total Hb) and free plasma hemoglobin (free Hb) levels did not differ in either group. All HIA-VAD's in the control group remained thrombus free, except on one occasion when an inflow cannula was obstructed by a thrombus located in the tip. After circulatory support, the animals in this group seemed clinically healthy. However, thrombus formation was observed in the three heparin coated HIA-VAD's. One animal in this group died from complications after re-operation for pneumothorax on the fifth day of support, whereas the other two animals seemed clinically healthy. In these three animals, a strong decrease in platelet numbers was measured even after 24 hours of support which recovered after 72 hours. This decrease in platelet numbers was associated with a lower degree of platelet aggregation ability stimulated by ADP (p < 0.05). Fibrin(ogen) degradation products (FDP) increased significantly immediately after the implantation procedure (p < 0.05). Fibrinogen levels initially decreased during the implantation procedure, but increased thereafter in both groups. The FDP levels remained high in this group, although the FDP levels in both groups were decreased after the implantation procedure. The ex vivo measured circulating heparin levels were lower in the heparin coated HIV-VAD group despite the equally administrated heparin doses in both animal groups. No differences were measured in either group with regard to white blood cell (WBC) numbers and complement hemolytic activity (CH50). Despite these hemostatic changes, no mechanical trauma could be demonstrated after seven days of circulatory support.
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PMID:Blood interaction with a Bioline heparin coated HIA-VAD: a study on calves. 906 31

Interferon-gamma (IFN-gamma) has been shown to inhibit proliferation and differentiation of erythroid progenitor cells and to produce apoptosis of erythroid cells, but IFN-gamma receptors are not present on red cells and have never been demonstrated on erythroid progenitor cells. We obtained highly purified day 6 erythroid colony-forming cells (ECFCs) from human blood in sufficient quantity and purity to measure binding of radioiodinated recombinant human IFN-gamma ([125I]rhIFN-gamma). When [125I]rhIFN-gamma was incubated with day 6 ECFC, 77% of the binding was inhibited by excess unlabeled rhIFN-gamma, but no inhibition occurred with a variety of growth factors and glycoproteins. Specific binding was directly proportional to the cell concentration with a straight line passing through the origin, and equilibrium was reached at 0 degree C by 24-48 hours. Saturation of specific binding occurred at a [125I]rhIFN-gamma concentration of 1.0 nM and internalization was demonstrated with further incubation at 37 degrees C. Scatchard analysis showed a single class of binding sites and at a high ECFC cell purity of 80-89%, 1910-2070 binding sites per ECFC were present with a Kd of 0.01-0.02 nM. As day 5 ECFC developed into more mature day 7-day 12 cells, with incubation at 37 degrees C in vitro, specific binding for [125I]IFN-gamma greatly decreased. These experiments delineate specific binding sites for IFN-gamma on human erythroid progenitor cells and indicate that the enhanced sensitivity to rhIFN-gamma inhibition of mature day 3-day 6 burst-forming units-erythroid may be a result of enhanced specific binding. Human IFN-gamma is a multifunctional lymphokine, secreted by activated T lymphocytes and NK cells, which exerts antiviral, antiproliferative, and immunomodulatory activities on a wide variety of cells [1,2]. With regard to hematopoietic cells, IFN-gamma has been reported to inhibit the growth of granulocyte-macrophage colony-forming units, burst-forming units-erythroid (BFU-E) and colony-forming units-erythroid (CFU-E) in vitro [3-7]. Most recently, mature day 3 to day 6 BFU-E have been shown to be most sensitive to the inhibitory effect of recombinant human (rh) IFN-gamma, while primitive day 1 to day 2 cells and later day 7 cells were less affected [7]. Incubation of rhIFN-gamma with mature BFU-E inhibits hemoglobin accumulation and produces apoptosis of the maturing erythroid cells [7]. Moreover, since blood IFN-gamma levels are elevated and vary directly with the degree of the anemia, in patients with hematologic malignancies [8] and HIV-seropositivity [9], IFN-gamma appears to have a prominent role in producing the anemia associated with chronic disease [10,11]. Although characterization of human IFN-gamma receptors has been extensively performed for a variety of human cells including fibroblasts, lymphocytes, monocytes, granulocytes, eosinophiles, platelets, and many tumor cells [12-17], IFN-gamma receptors have not been identified on red cells [12] and the presence plus the extent of IFN-gamma receptors on progenitor cells, including human erythroid progenitor cells, remains unknown. A method has been reported from our laboratory by which human erythroid colony-forming cells (ECFC) can be highly purified, starting with peripheral blood BFU-E, in a sufficient amount for analysis of cytokine binding [18-20]. In this paper, we report the results of [125I]rhIFN-gamma binding to day 6 ECFC in vitro and demonstrate the presence of specific binding that is saturable at 1.0 nM. Scatchard analysis reveals that there are 1910-2070 rhIFN-gamma binding sites per ECFC with a Kd of 0.01-0.02 nM and, as with erythropoietin (EP) and insulin-line growth factor I (IGF-I) receptors, specific binding is highest with the earliest BFU-E studied and declines progressively as the erythroid progenitors mature.
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PMID:Specific binding of interferon-gamma to high affinity receptors on human erythroid colony-forming cells. 909 Dec 93

In tropical areas where Plasmodium falciparum malaria is endemic, concurrent HIV infection does not appear to increase malaria prevalence. To investigate the immunologic interactions between these two infections, 66 adults from Bobo Dioulasso, Burkina Faso, were enrolled in a study in May 1994. The group included 29 HIV-negative adults and 37 hospitalized HIV-positive adults with clinical AIDS and under 250 CD4+ cells per mcgl of blood. All subjects belonged to a population exposed to numerous falciparum malaria infections since birth and were thus presumed to have developed specific antimalarial protective immune mechanisms prior to HIV infection. AIDS patients had a reduced hemoglobin content and a lower number of CD3+ and CD4+ lymphocytes than healthy controls. All thick blood smears were negative for malaria parasites, but the mean level of antibodies to P. falciparum was lower and the total immunoglobulin G content of plasma was higher in AIDS patients than controls. In vitro lymphocyte proliferation and cytokine (IFN-psi, IL-2, and IL-4) production were assessed in isolated mononuclear cells (PBMC) in the presence of PHA, PPD, or 3 antimalarial agents: the baculovirus-expressed protein from P. falciparum Merozoite Surface Protein-1, a P. falciparum in vitro culture, and a crude schizont extract. AIDS patients presented with decreased levels of cell proliferation and of IFN-psi and IL-2 production compared to healthy controls in response to all antigens except the schizont extract. IL-4 production levels were similar in both groups. Mitogenic stimulation of whole blood cultures revealed similar trends in cytokine production as in PBMC cultures. These findings confirm that not all effector cells involved in the immune responses directed against malaria are affected by concurrent HIV infection and/or that important CD4+ independent mechanisms of protection against malaria are conserved. It has been proposed that HIV infection causes a selective depletion of T cell subsets that are not implicated in the antimalarial immune response.
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PMID:Selected P. falciparum specific immune responses are maintained in AIDS adults in Burkina Faso. 922 86

Open surgery in a severely anemic patient may be complicated by a substantial blood loss from a large incision and subsequent poor wound healing secondary to the anemia. We report our success in performing a splenectomy laparoscopically in a profoundly anemic patient. A 50-year-old white male Jehovah's Witness who was HIV positive was referred for splenectomy after he developed profound, worsening anemia secondary to hypersplenism that was refractory to medical management. His preoperative hemoglobin and hematocrit levels were 2.7 g/dl and 8.8%, respectively, but his religious beliefs precluded transfusion. A laparoscopic splenectomy by the posterior gastric approach was performed. The patient tolerated the surgery well and experienced no additional morbidity. On postoperative day 7, his hemoglobin and hematocrit were 6.8 g/dl and 22%, respectively. We conclude that laparoscopic splenectomy is an attractive procedure in a severely anemic patient who requires splenectomy and refuses blood transfusion.
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PMID:Laparoscopic splenectomy in a Jehovah's Witness with profound anemia. 926 51

Zidovudine is approved for administration in doses given every 4 hours. Less frequent dosing has been used in many clinical trials, but the toxicity and efficacy of such regimens have not been formally compared with the approved regimen. In this multicenter, randomized, double-blind, controlled trial, the safety, tolerance and efficacy of 600 mg of zidovudine given daily in two or six divided doses were compared. Three hundred and twenty patients with a CD4 lymphocyte count < 250 cells/mm3 (mean, 104 cells/mm3) or a prior AIDS-defining illness were treated with zidovudine 100 mg every 4 hours (regimen A) or 300 mg every 12 hours (regimen B). Eighty-eight patients (56%) and 94 patients (58%), assigned to regimens A and B, respectively, completed the planned 48 weeks of treatment. Serious anemia (hemoglobin < or = 7.5 g/dl) occurred in 13% and 7% of patients treated with regimens A and B, respectively (difference, 6%, 95% confidence interval [CI], 2, 12%; p = .13). The mean duration of treatment and the frequency of neutropenia and symptomatic complaints including nausea and headache were similar in the two treatment groups. The number of patients experiencing a new opportunistic infection (18% versus 20% for regimens A and B, respectively), and the number of deaths (five in each group) did not differ significantly between groups. The effect of treatment on CD4 lymphocyte counts and HIV p24 antigenemia also was similar for both regimens. Zidovudine given at the more convenient dose of 300 mg twice daily has similar safety, and tolerance and appears to have similar efficacy to the currently approved regimen. Use of this regimen should help simplify the treatment of HIV disease.
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PMID:A comparative trial of zidovudine administered every four versus every twelve hours for the treatment of advanced HIV disease. 929 87

The objective of this study was to identify prognostic factors for survival in patients with pretreatment CD4 < or =50 cells/mm3 treated with nucleoside analogs, and to develop and validate a mortality risk model based on these factors. The design of the study consisted of retrospective analysis of AIDS Clinical Trials Group (ACTG) protocols 116a, 116b/117, 155, and 118. The setting was the multicenter AIDS Clinical Trials Group. The patients were HIV-infected with pretreatment CD4 < or =50 cells/mm3 and various degrees of prior zidovudine (ZDV) use. Double-blind, three-arm randomized control trials ACTG 116a and ACTG 116b/117 compared ZDV with didanosine (ddI). ACTG 155 compared ZDV with zalcitabine or combination therapy. Our validation study, ACTG 118, compared the effects of three different doses of ddI on survival. The main outcome measures were survival and mortality. The three studies combined enrolled 699 patients with entry CD4 T-lymphocyte counts of < or =50 cells/mm3. Forty percent of patients died during follow-up, with a median survival of 19.7 months. Multivariate analysis showed shorter survival at p < 0.0001 with lower CD4 count (relative hazard [RH] = 0.98) and lower hemoglobin level (RH = 0.81). Other factors included older age (RH = 1.03), male gender (RH = 1.70), Hispanic ethnicity (RH = 1.68), and symptomatic disease stage (RH = 2.06). Our predictive mortality risk model differentiated well patients with differing risks of mortality. When the risk model was applied to ACTG 118, the validation data set, the identified prognostic factors could distinguish patients with varying risks of death (p < 0.001, stratified log-rank test). These results demonstrate that CD4 T-lymphocytes counts < or =50 cells/mm3 should not be considered a precursor of imminent death; considerable variability in survival exists in severely immunocompromised patients. Our identification of prognostic indicators for survival can aid clinicians and patients in management of their disease and researchers in design of future clinical trials.
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PMID:Predictors of survival in HIV-infected persons with 50 or fewer CD4 cells/mm3. 934 54

This article and the following article (Parts I and II) report the development of two clinical staging systems for HIV-infected individuals. The objective of the research reported here (Part I) was to construct a clinical staging system to predict progression to AIDS. We analyzed data from VA Cooperative Study Number 298, a multicenter, double-blind, randomized trial that compared immediate versus deferred zidovudine therapy in 338 HIV-infected individuals who did not have AIDS at enrollment. Baseline variables were tested in univariate Cox regression for their relationship to progression to AIDS, and those that appeared predictive were examined in multivariable analysis. Based on these analyses, we constructed a new clinical staging system based on CD4+ cell count, age, hemoglobin, oral hairy leukoplakia or oral thrush, and fever. The stages of the system were significant predictors of progression to AIDS (p = 0.0001, log-rank test). In conclusion, simple, valid, clinical staging systems for HIV-infected patients can be constructed using information that is readily available in clinical practice settings. Such systems provide better prognostic distinction than CD4+ cell count alone by taking into account the known prognostic effects of other variables.
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PMID:Predicting outcomes in HIV-infected veterans: I. Progression to AIDS. 939 79

To study the incidence of, the factors associated with, and the effect on survival of anemia in human immunodeficiency virus (HIV)-infected persons, we analyzed data from the longitudinal medical record reviews of 32,867 HIV-infected persons who received medical care from January 1990 through August 1996 in clinics, hospitals, and private medical practices in nine United States cities. We calculated the 1-year incidence of anemia (a hemoglobin level of <10 g/dL or a physician diagnosis of anemia); the adjusted odds ratios showing excess risk of anemia associated with demographic factors, prescribed therapies, and concurrent diseases; the risk of death for patients who developed anemia compared with risk for patients who did not develop anemia; and, of patients who did develop anemia, the risk of death for those who did not recover from anemia compared with the risk for those who did recover. The 1-year incidence of anemia was 36.9% for persons with one or more acquired immunodeficiency syndrome (AIDS)-defining opportunistic illnesses (clinical AIDS), 12.1% for patients with a CD4 count of less than 200 cells/micron or CD4 percentage of <14 but not clinical AIDS (immunologic AIDS), and 3.2% for persons without clinical or immunologic AIDS. Of anemia diagnoses, 22% were identified by physicians as drug related. Incidence of anemia was associated with clinical AIDS, immunologic AIDS, neutropenia, thrombocytopenia, bacterial septicemia, black race, female sex, prescription of zidovudine, fluconazole, and ganciclovir, and lack of prescription of trimethoprim-sulfamethoxazole. The increased risk of death associated with anemia differed by first CD4 count: for patients with a CD4 count of >/=200 cells/microL at the beginning of the survival analysis, the risk of death was 148% (99% confidence interval [CI], 114 to 188) greater for those who developed anemia; for patients whose first CD4 count was <200 cells/microL, the risk of death was 56% (99% CI, 43 to 71) greater for those in whom anemia developed. For persons in whom anemia developed, the risk of death was 170% (99% CI, 132 to 203) greater for persons who did not recover from anemia compared with those who did recover. Anemia is a frequent complication of HIV infection, and its incidence is associated with progression of HIV disease, prescription of certain chemotherapeutics, black race, and female sex. Anemia, particularly anemia that does not resolve, is associated with shorter survival of HIV-infected patients.
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PMID:Epidemiology of anemia in human immunodeficiency virus (HIV)-infected persons: results from the multistate adult and adolescent spectrum of HIV disease surveillance project. 941 98

Tuberculosis (TB) is the most often seen and serious opportunistic infection in HIV-1-infected individuals in developing countries. Infection with HIV-1 predisposes individuals to TB, both progressive primary and reactivation disease. To describe the clinical response to anti-TB therapy in HIV-1 disease, 49 HIV-1-positive Ugandan adults of mean age 29.4 years with active pulmonary TB (PTB) were studied in a trial of rifampicin containing short-course anti-TB regimens. At presentation, 18 patients were PPD skin test nonreactive, and 39 had cavitary lung disease. The mean CD4 lymphocyte count at presentation was 339/mcl. Among patients with abnormal baseline clinical values, the median time to resolution of fever, weight gain of 10%, increase of hemoglobin to 10 g/dl, and Karnofsky performance score (KPS) to 80 occurred before sputum smear and culture conversion. Short-term survival was associated with baseline lymphocytes of less than 1200/mcl, cavitary lung disease, atypical chest radiograph, and PPD nonreactivity. PPD nonreactivity and noncavitary disease were associated with significantly lower CD4 lymphocyte counts. Study findings demonstrate that the careful monitoring of clinical symptoms and simple, inexpensive, and widely available laboratory markers permit the satisfactory evaluation of early clinical response to anti-TB therapy in HIV-1-infected patients with pulmonary TB.
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PMID:Clinical course of human immunodeficiency virus type 1 associated pulmonary tuberculosis during short-course antituberculosis therapy. 948 27

Excessive production of oxygen free radicals causes the oxidation of circulating or membrane lipids, proteins, and DNA. Patients infected with HIV usually have severe malnutrition in the AIDS stage of disease. Therefore, they may be at higher risk of oxidative stress. We measured lipid hydroperoxide concentration, antioxidant status, cholesterol, triglyceride, iron, ceruloplasmin, and transferrin concentrations in the serum samples of 14 patients infected with HIV and compared our results with the results from 14 volunteers who served as controls. Lipid hydroperoxide concentrations in serum samples were measured by a colorimetric assay in which hemoglobin catalyzes the reaction of lipid hydroperoxide with a methylene blue derivative, yielding methylene blue. The total antioxidant capacity of serum was measured by the ability of serum to inhibit the formation of ferrylmyoglobin by metmyoglobin and hydrogen peroxide. Both assays were automated on the Syva-30R analyzer (Behring, San Francisco, Calif). We measured serum cholesterol and triglyceride concentrations by using the Vitro 950 analyzer (Johnson & Johnson, Rochester, NY). The lipid hydroperoxide concentrations were significantly elevated (mean, 1.44; SD, 0.95 micromol/L) in patients with HIV compared with control subjects (mean, 0.25; SD, 0.24 micromol/L). In contrast, the total antioxidant capacity was significantly lower in patients with HIV (mean, 1.04; SD, 0.13 mmol/L of trolox equivalent) compared with control subjects (mean, 1.66; SD, 0.09 mmol/L). We observed a fair correlation between serum lipid hydroperoxide concentrations and serum triglyceride concentrations in patients with AIDS. The correlation between serum hydroperoxide concentration and antioxidant status of serum was relatively poor. The lipid hydroperoxide assay was linear, from 0.1 micromol/L to 50 micromol/L. The within-run and between-run coefficients of variation were 3.5% and 4.5%, respectively, at a lipid hydroperoxide concentration of 2.5 micromol/L. The total antioxidant capacity assay was linear, from 0.1 to 2.5 mmol/L of trolox equivalent. The within-run and between-run coefficients of variation were 1.4% and 4.2% for the standard, with a target total antioxidant capacity of 1.5 mmol/L of trolox equivalent. We conclude that our automated assays for determination of total antioxidant status of serum and lipid hydroperoxide products may be helpful screening tests followed by measuring individual antioxidants, such as tocopherol, ascorbic acid, and other antioxidants for patients with severe deficiency of antioxidant status.
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PMID:Rapid automated determination of lipid hydroperoxide concentrations and total antioxidant status of serum samples from patients infected with HIV: elevated lipid hydroperoxide concentrations and depleted total antioxidant capacity of serum samples. 949 97


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