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Trends in use of primary prophylactic colony stimulating factors and neutropenia-related hospitalization in commercially insured patients receiving myelosuppressive chemotherapy in the United States: 2005-2017.

PURPOSE: Describe temporal changes in use of myelosuppressive chemotherapy, primary prophylactic colony-stimulating factor, and neutropenia- … y, use of regimens with high risk for febrile neutropenia increased, as did the use of prophylactic colony-stimulating factors after 2005. Incidence of neutropenia-related hospitalization increased slightly, particularly among non-Hodgkin lymphoma patients. Further studies are required to understand this increasing trend of neutropenia-related hospitalization, changing pati …

Trends in the use of primary prophylactic colony-stimulating factors and neutropenia-related hospitalization in elderly cancer patients receiving myelosuppressive chemotherapy in the USA: 1995-2015.

PURPOSE: To assess changes in neutropenia-related hospitalization, myelosuppressive chemotherapy, and primary prophylactic colony-stimulating factor (PP-CSF) use in elderly cancer patients receiving myelosuppressive chemotherapy. METHODS: We identified annual cohorts of patients aged ≥ 66 years with breast cancer, lung cancer, or non-Hodgkin lymphoma (NHL) initiating myelosuppressive chemotherapy during 1995-2015 using Medicare 5% (1994-2008) and 20% (2007-2015) data. We described myelosuppressive chemotherapy changes by febrile neutropenia (FN) risk category (high, intermediate, unclassified

Sulodexide down-regulates the release of cytokines, chemokines, and leukocyte colony stimulating factors from human macrophages: role of glycosaminoglycans in inflammatory pathways of chronic venous disease.

Chronic venous disease (CVeD) is a debilitating condition that affects millions of individuals worldwide. The condition can result in varicose veins, or advance to severe skin changes and venous ulceration. The fundamental basis for CVeD is inflammation within the venous circulation and that it is subjected to increased hydrostatic pressure resulting in increased ambulatory venous pressure. The inflammation involves leukocytes, in particular macrophages and monocytes, inflammatory modulators and chemokines, cytokine expression, growth factors, metalloproteinase (MMP) activity, and many regulat

The relationship between introduction of American society of clinical oncology guidelines and the use of colony-stimulating factors in clinical practice in a Paris university hospital.

BACKGROUND: Clinical practice guidelines are issued periodically by professional medical societies or committees to assist practitioners in clinical decision making. However, it is unclear whether such guidelines have any lasting impact on clinical practice. OBJECTIVE: The purpose of this study was to assess the impact of the American Society of Clinical Oncology (ASCO) guidelines regarding use of hematopoietic colony-stimulating factors (CSF) on cancer care in a university hospital in Paris. METHODS: The study was performed at Hĵpital Tenon, an 830-bed university hospital in Paris, in 1996 …

Риски гематологических обледенений у пациентов, прошедших лечение от твердых опухолей, связанных с использованием пегилизованных гранулоцитов-стимулирующих факторов: 2005.

Широкое применение пегилизованных гранулоцитов (PGCS), в частности pegfilgrastim и липегфилграстим, в целях сокращения числа случаев нейтрализации женских половых органов у пациентов, проходящих химиотерапию. Вместе с тем по-прежнему сохраняется озабоченность по поводу долгосрочной безопасности ПХГФ, в частности по поводу риска вторичных гематологических заболеваний. Цель настоящего исследования заключалась в оценке распространенности вторичных гематологических заболеваний у пациентов, которые лечились от твердых опухолей с помощью PGCSF в одном учреждении 2005 в адрес 2019. Ретроспективный ан

Совпадение в аннотации оригинала
The use of pegylated granulocyte colony-stimulating factors (PGCSFs), specifically pegfilgrastim and lipegfilgrastim, has been widely adopted to reduce the incidence of febrile neutropenia in patients undergoing chemotherapy. However, concerns regarding the long-term safety of PGCSFs, particularly the risk of secondary haematological malignancies, remain. Th…

Long-acting versus short-acting granulocyte colony-stimulating factors among cancer patients after chemotherapy in China: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Granulocyte colony-stimulating factors (G-CSFs) include long-acting ones and short-acting ones. They have been mainly applied in Chinese clinical practice for years to prevent neutropenia. However, which type of G-CSF is more superior has not been conclusively determined. METHODS: A systematic literature search was conducted using the PubMed, Embase, Cochrane Library, clinical trials.gov, China National Knowledge Infrastructure, and WAN FANG databases for related studies published till August 2021. Revman 5.3 software was used to assess the effectiveness and safety of these 2 type…

Accumulation of T-cell clones producing high levels of both granulocyte-macrophage and macrophage colony-stimulating factors (CSF-1) in lymph nodes involved by Hodgkin's disease.

We have previously shown that total T cells derived from lymph nodes (LN) involved by Hodgkin's disease (HD) secrete higher levels of colony-stimulating activity than total T cells present within benign hyperplastic (BH) LN and B-non-Hodgkin's lymphoma (B-NHL) LN, suggesting that T cells with particular properties accumulate in HD LN. To further characterize this T-cell population, we have quantified production of both granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) production in a total of 98 T-cell clones (TCC) derived from CD25+ act

Divergent effects of interleukin-4 (IL-4) on the granulocyte colony-stimulating factor and IL-3-supported myeloid colony formation from normal and leukemic bone marrow cells.

Human recombinant interleukin-4 (IL-4) was studied for its effects on myeloid progenitor cells from normal and leukemic bone marrow cells in the presence and absence of additional growth factors. IL-4 itself did not support myeloid cluster or colony formation (CFU-GM). However, cultures supplied with IL-4 (300 U/mL) and IL-3 demonstrated a significant decline in myeloid colony numbers (CFU-GM) compared with the effects of IL-3 alone: (48 +/- 27 v 88 +/- 27 CFU-GM/10(5) MNC). In contrast, IL-4 augmented the G-CSF-supported CFU-GM: (80 +/- 31 v 148 +/- 52 CFU-GM/10(5) MNC). The effects of IL-4 w

Increased urinary excretion of macrophage-colony-stimulating factor (M-CSF) in patients with IgA nephropathy: tonsil stimulation enhances urinary M-CSF excretion.

Upper respiratory tract infection including chronic tonsillitis is considered to be involved in the onset and/or the progression of IgA nephropathy. It is well known that deterioration of urinary findings occurs after episodes of upper respiratory tract infection in patients with IgA nephropathy. We previously showed that the expression of macrophage-colony-stimulating factor (M-CSF) is increased in the glomeruli of patients with IgA nephropathy and correlated with glomerular mesangial proliferation, suggesting that M-CSF plays an important role in the progression of IgA nephropathy. In the pr

Stem cell factor and granulocyte colony-stimulating factor promote brain repair and improve cognitive function through VEGF-A in a mouse model of CADASIL.

Cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL) is a cerebral small vascular disease caused by NOTCH3 gene mutation in vascular smooth muscle cells (VSMCs), leading to ischemic stroke and vascular dementia. To date, the pathogenesis of CADASIL remains poorly understood, and there is no treatment that can slow the progression of CADASIL. Using a transgenic mouse model of CADASIL (TgNotch3R90C), this study reveals novel findings for understanding CADASIL pathogenesis that decreased cerebral vascular endothelial growth factor (VEGF/VEGF-A) is li

Anti-granulocyte-macrophage colony-stimulating factor autoantibodies are a risk factor for central nervous system infection by Cryptococcus gattii in otherwise immunocompetent patients.

Cryptococcosis is caused by either Cryptococcus neoformans or C. gattii. While cryptococcal meningoencephalitis is caused mostly by C. neoformans in immunocompromised patients, the risk factors remain unclear for patients with no known immune defect. Recently, anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibodies were detected in the plasma of seven "immunocompetent" cryptococcosis patients, and the cryptococcal strains from these patients were reported as C. neoformans (three strains), C. gattii (one strain), and Cryptococcus (three strains not identified to the specie

Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha.

Pretreatment with recombinant human granulocyte CSF (G-CSF) protected mice in two different models of septic shock. Intravenous injection of 250 micrograms/kg G-CSF to mice prevented lethality induced by 5 mg/kg LPS. Injection of 50 micrograms/kg G-CSF protected galactosamine-sensitized mice against LPS-induced hepatitis. In either case, this protection was accompanied by a suppression of LPS-induced serum TNF activity. In contrast, when galactosamine-sensitized mice were pretreated with 50 micrograms/kg murine recombinant granulocyte/macrophage CSF instead of G-CSF and subsequently challenged

Effects of indirect and additional direct costs on the risk threshold for prophylaxis with colony-stimulating factors in patients at risk for severe neutropenia from cancer chemotherapy.

STUDY OBJECTIVES: Previous studies have used direct hospital costs to determine the threshold at which the cost of prophylactic use of colony-stimulating factor (CSF) is offset by savings from the lower risk of hospitalization for febrile neutropenia. By conducting a survey of patients in whom febrile neutropenia had developed during treatment with chemotherapy, we sought to reassess these costs by including estimates of indirect costs associated with febrile neutropenia as well as new categories of direct costs that were not previously available. Costs were included in an existing cost-minimi

Treatment Modalities and the Impact of Granulocyte Colony-Stimulating Factor in AML Patients Treated With Venetoclax and Azacitidine: A DATAML Registry Study.

INTRODUCTION: Azacitidine-venetoclax (AZA-VEN) has become a standard treatment in older or chemotherapy-ineligible AML patients. While the registration trial showed a median overall survival (OS) of 14.7 months, most real-world studies have not reproduced this result. PATIENTS AND METHODS: We analyzed treatment patterns, adverse events, responses and outcomes in 199 patients treated with AZA-VEN in the DATAML registry. RESULTS: The median age was 75.6 years, 48.7% had secondary AML (11% post-MPN); 11.7% had another cancer, and 9% had received AZA for prior myelodysplastic syndrome. Cytogenet

Effect of Granulocyte Colony-Stimulating Factor (G-CSF) and Botulinum Toxin Type A on Fat Graft Retention in a Rat Model.

BACKGROUND: Autologous fat grafting is widely used in reconstructive and aesthetic surgery; however, unpredictable graft survival remains a major limitation. Various biological modifiers have been proposed to improve graft retention. This study aimed to evaluate the effects of Granulocyte Colony-Stimulating Factor (G-CSF) and Botulinum Toxin Type A (BoNT-A), alone and in combination, on fat graft survival in a rat model. METHODS: In this experimental animal study, 20 Wistar rats were randomly allocated into four groups: Group 1 (BoNT-A + G-CSF), Group 2 (BoNT-A), Group 3 (G-CSF), and Group 4

Expression of Macrophage Colony-Stimulating Factor 1 (CSF-1) by Spinal Cord Astrocytes in Mice with Experimental Autoimmune Encephalomyelitis.

Immunofluorescence analysis was used to study the expression pattern of macrophage colony-stimulating factor 1 (CSF-1) in spinal cord cells in a murine model of multiple sclerosis (experimental autoimmune encephalomyelitis). Marked upregulation of CSF-1+ signal was observed in spinal cord astrocytes in both acute and chronic stages of the disease. These findings suggest a potential role for CSF-1 in the pathogenesis and progression of experimental autoimmune encephalomyelitis/multiple sclerosis.

Granulocyte colony-stimulating factor protects against acute systemic alphavirus disease in a type I IFN-dependent manner.

INTRODUCTION: Arthritogenic alphaviruses, including chikungunya (CHIKV) and Mayaro virus (MAYV), cause disease characterized by fever, rash, and incapacitating joint pain. Alphavirus arthritis is associated with infiltration of myeloid cells and increases in several cytokines systemically, including granulocyte colony-stimulating factor (G-CSF). G-CSF is secreted by endothelial cells, fibroblasts, macrophages, and monocytes and binds to colony-stimulating factor 3 receptor (CSF3R, also known as G-CSFR) on the surface of myeloid cells. G-CSFR signaling initiates the proliferation, differentiati

Impact of Granulocyte Colony Stimulating Factor Use Following CD-19 Chimeric Antigen Receptor T-Cell Therapy.

CD-19 chimeric antigen receptor T-cell therapy (CAR-T) has improved outcomes in relapsed/refractory B-cell malignancies but is associated with cytokine-mediated toxicities such as cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), hematologic toxicities, and infection. Neutropenia is common following CAR-T and varies in duration. Granulocyte colony-stimulating factor (G-CSF) is used to support neutropenia following CAR-T. However, its use within 14 d post-CAR-T is debated due to concerns it may contribute to CRS and ICANS. Data on the efficacy and

Autochthonous Cryptococcus gattii genotype VGIIb infection in a Japanese patient with anti-granulocyte-macrophage colony-stimulating factor antibodies.

A 31-year-old Japanese man presented with cerebral and pulmonary cryptococcosis. Cryptococcus gattii (C. gattii) genotype VGIIb was detected in the patient's sputum and cerebrospinal fluid specimens. The serum levels of anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibodies were elevated in this patient, which has been associated with pulmonary alveolar proteinosis and is considered a risk factor for C. gattii infection. After undergoing >12 months of antifungal treatments, the patient showed improvements in symptoms and findings on brain and lung imaging. Several Japanese p