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

Hematopoietic growth factors are well known to increase neutrophil counts and support the administration of myelotoxic and myelosuppressive therapies, especially chemotherapies. Filgrastim (r-metHuG-CSF) has been used in the setting of HIV disease to treat neutropenia and HIV-associated neutrophil defects. This article reviews the biology, product characteristics, and preclinical and clinical development of Filgrastim. Emphasis is given on the use of Filgrastim in the setting of HIV infection and AIDS.
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PMID:Biopharmaceutical drug development: Filgrastim (r-metHuG-CSF) use in patients with HIV infection. 1059 29

Neutropenic individuals are at high risk for bacterial and fungal infections. Filgrastim (r-metHuG-CSF, NEUPOGEN) has been shown to improve chemotherapy-induced neutropenia significantly. Because a high incidence of HIV-infected patients have neutropenia, often associated with myelosuppressive antiretroviral medication, Filgrastim is frequently used as a treatment strategy for this HIV-associated neutropenia. This review summarizes published work related to the use of Filgrastim in HIV-infected patients. Literature bases (EMBASE, MEDLINE, Int. Pharm. Abs., SciSearch, and Aidsline) from 1970 to 1998 were searched for articles describing the relationship of Filgrastim and ANC to bacterial infection rates, bacterial infection outcome, and overall survival. Thirty-five related articles were identified during this search. Filgrastim appears to have a significant role in increasing peripheral ANC and enhancing neutrophil function in patients with HIV infection and AIDS. This may translate into a clinical benefit of delivery of full-dose myelosuppressive antiretroviral therapy and decreased susceptibility to infections and increased survival in this patient population.
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PMID:The use of Filgrastim in AIDS-related neutropenia. 1059 30

Data have shown that neutropenia is a risk factor for severe bacterial infections. Two trials were done in HIV-infected patients to study the effect of Filgrastim on neutropenia and the incidence of severe bacterial infections. The incidence of Mycobacterium avium complex (MAC) infection in this setting was also evaluated. This paper reviews the results of these two studies, which suggest that Filgrastim is safe and effective in preventing severe neutropenia in patients with advanced HIV infection.
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PMID:Clinical experience with Filgrastim in AIDS. 1059 31

G-CSF has immunomodulatory effects of neutrophilic granulocytes and monocytes/macrophages. Two studies were done: one in normal volunteers and the other in HIV-infected patients plus their respective control donors to evaluate the effect of Filgrastim on cytokine responses. Filgrastim treatment of volunteers resulted in an anti-inflammatory cytokine response, when blood was stimulated ex vivo with the endotoxin lipopolysaccharide (LPS). Similarly, in the presence of Filgrastim in vitro, the LPS-inducible release of proinflammatory cytokines was attenuated. Blood from HIV-infected patients at advanced stages of disease showed reduced interleukin (IL)-2 formation in response to staphylococcal exotoxin B (SEB), which was restored in the presence of Filgrastim.
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PMID:Anti-inflammatory aspects of Filgrastim and impact on IL-2 release. 1059 32

In a study of 258 moderately neutropenic HIV-infected patients, Filgrastim (recombinant methionyl human granulocyte colony-stimulating factor) treatment significantly reduced the incidence of severe neutropenia and bacterial infections. Filgrastim-treated patients also had 54% fewer severe bacterial infections and 45% fewer days in hospital for any bacterial infections. No unexpected or new adverse events were observed and there were no differences in plasma HIV-1 RNA levels between the groups.
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PMID:Prevention of bacterial infections in patients with advanced HIV infection. 1059 77

The effect of Filgrastim (recombinant methionyl human granulocyte colony-stimulating factor) treatment on neutrophil function was studied in HIV-infected patients. Filgrastim therapy significantly increased oxidative capacity of neutrophils, increased bacterial killing, and reduced accelerated apoptosis of neutrophils observed in this patient population.
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PMID:Filgrastim treatment of HIV-infected patients improves neutrophil function. 1059 78

Genetic modification of hemopoietic progenitor cells ex vivo, followed by the infusion of the genetically modified cells into the human immunodeficiency virus-1 (HIV-1) infected donor, has been proposed as a treatment for HIV-1 infection. The current study was undertaken to evaluate the effect of hemopoietic stem cell mobilization and harvesting on HIV-1 replication in persons with HIV-1 infection. Eighteen HIV-1-infected persons received recombinant granulocyte colony-stimulating factor (G-CSF; Filgrastim) 10 microg/kg per day, for 7 days. On days 4 and 5, peripheral blood mononuclear cells were harvested by leukapheresis. The CD4+ lymphocyte count at entry was >500/microL for 6 subjects, 200 to 500/microL for 6 subjects, and <200/microL for 6 subjects. For 9 of 18 subjects, plasma HIV-1 RNA levels increased 4- to 100-fold (>0.6 log(10)) above baseline between days 4 and 7 and returned to baseline by day 27. Significant increases of plasma HIV-1 RNA levels occurred in 5 subjects despite 3-drug antiretroviral therapy. Changes in CD4+ and CD34+ cells during mobilization and harvesting were similar in all subjects whether they had or did not have increased plasma HIV-1 RNA levels. Thus, mobilization and harvesting of bone marrow progenitor cells from persons infected with HIV-1 induced a transient increase in viral replication in some patients but was not associated with adverse effects. (Blood. 2000;95: 48-55)
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PMID:Changes in human immunodeficiency virus type 1 virus load during mobilization and harvesting of hemopoietic progenitor cells. Adult AIDS Clinical Trials Group 285 Study Team. 1060 83

Granulocyte colony-stimulating factor (r-met Hu G-CSF; filgrastim; 10 microgram/kg/day for 7 days) was used to mobilize CD34+stem cells into the peripheral blood of human immunodeficiency virus type 1 (HIV-1)-infected individuals and a group of HIV-1-uninfected donors as a measure of immunologic reserve in HIV-1-infected people. G-CSF mobilized CD34+ cells of HIV-1-infected individuals with cell counts >500 CD4+ cells/mm3, as well as in HIV-1-uninfected donors. In contrast, CD34 cell mobilization was significantly blunted in HIV-1-infected individuals with cell counts <500 CD4+ cells/mm3 (<200 cell days vs. >650 cell days, P<.0005, compared with the >500 CD4+ cell cohort). At least 1.75x10(7) CD34 cells were harvested by leukapheresis from patients in each study cohort. CD34+ cell viability and the ability to differentiate precursor cells into myeloid and erythroid progenitor cells were not affected by HIV-1 infection.
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PMID:Reduced mobilization of CD34+ stem cells in advanced human immunodeficiency virus type 1 disease. 1060 61

Neutropenia frequently complicates infection due to human immunodeficiency virus (HIV). The etiology of neutropenia in this setting includes bone marrow infection or infiltration, myelosuppressive therapies, the presence of antibodies to HIV, and accelerated apoptosis. Protection against microbial invaders by neutrophils is further compromised by impaired chemotaxis and phagocytosis, production of toxic oxygen species, and expression of cellular adhesion molecules. Neutropenia is a significant risk factor for bacterial infection in HIV-infected patients. Endogenous cytokines, such as granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor, regulate neutrophil count and function. Treatment with recombinant human methionyl G-CSF (filgrastim) has lessened neutropenia in patients with HIV infection. Clinical trials have shown that the incidence of bacterial infections and the number of consequent days of hospitalization for HIV-infected patients receiving filgrastim therapy are lower. Filgrastim treatment also allows administration of larger doses of myelosuppressive agents.
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PMID:Neutropenia, neutrophil dysfunction, and bacterial infection in patients with human immunodeficiency virus disease: the role of granulocyte colony-stimulating factor. 1067 24

Studies have indicated that professional APCs in the periphery, such as dendritic cells and macrophages, play an important role in initiating DNA vaccine-specific immune responses. To engineer the immune response induced by DNA vaccines in vivo we investigated the modulatory effects of codelivering growth factor genes for the hematopoietic APCs along with DNA vaccines. Specifically, we examined the effects on the antigen-specific immune responses following the codelivery of the gene expression cassettes for M-CSF, G-CSF, and GM-CSF along with HIV-1 DNA immunogen constructs. We observed that coimmunization with GM-CSF increased the antibody response and resulted in a significant enhancement of lymphoproliferative response. Furthermore, among all coinjection combinations, we found that M-CSF coinjections resulted in a high level of CTL enhancement. This enhancement of CTL responses observed from the coinjection with M-CSF was CD8+ T cell dependent and was associated with the presence of CD11c+ cells at the site of injection and with the antigen-specific induction of the beta-chemokine MIP-1beta, suggesting a role for this chemokine in CTL induction. These results suggest that hematopoietic growth factors should be further studied as potential adjuvants for in vivo modulators of immune responses.
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PMID:Macrophage colony-stimulating factor can modulate immune responses and attract dendritic cells in vivo. 1068 Aug 44


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