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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo and ex vivo effects of macrophage colony-stimulating factor (M-CSF) were studied in a profoundly neutropenic rabbit model in order to determine its potential to augment pulmonary host defence against Aspergillus. M-CSF (100-600 microg/kg/d) was administered prophylactically to neutropenic rabbits with pulmonary aspergillosis starting three days pre-inoculation and then throughout neutropenia. Rabbits receiving M-CSF had significantly increased survival (P=0.01) and decreased pulmonary injury, as measured by decreased pulmonary infarction (P=0.004), when compared with untreated controls. Microscopic studies demonstrated greater numbers of activated pulmonary alveolar macrophages (PAMs) in lung tissue of rabbits receiving M-CSF, in comparison to controls (P<0.001). PAMs harvested from rabbits treated with M-CSF had a significantly greater percent phagocytosis of Aspergillus fumigatus conidia than did PAMs from controls (P=0.04). These data indicate that prophylactic administration of M-CSF augments pulmonary host defence against A. fumigatus and suggest a potential role for this cytokine as adjunctive therapy in the treatment of pulmonary aspergillosis in the setting of profound neutropenia.
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PMID:Recombinant human macrophage colony-stimulating factor augments pulmonary host defences against Aspergillus fumigatus. 1150 84

Invasive fungal infections (IFIs) have emerged as a serious threat in immunocompromised patients during the last two decades. Host defenses including appropriate cytokine responses and intact phagocytic function are necessary to combat IFIs. Several cytokines have been investigated and developed for preventive and therapeutic use. Among them, granulocyte colony-stimulating factor (G-CSF) has been mostly studied and used for various purposes, the most important being the faster recovery from neutropenia. Other cytokines with potential clinical significance in relation to IFI are granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-gamma (IFN-gamma) and macrophage colony-stimulating factor. Supported by a large number of preclinical studies but limited clinical results their potential utility against IFI has been suggested. In this review, certain questions related to this issue are discussed based on data already available and an attempt to consider future research is made.
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PMID:Granulocyte colony-stimulating factor and other cytokines in antifungal therapy. 1152 20

There are very few studies describing the preventive effect of macrophage colony-stimulating factor (M-CSF/CSF-1) on chemotherapy-induced infection. In this study, we evaluated the changes in superoxide anion production by granulocytes before and after chemotherapy in ovarian cancer patients and investigated the preventive effect of M-CSF on chemotherapy-induced febrile neutropenia. Three courses of chemotherapy [paclitaxel 180 mg/m(2) and carboplatin (area under the curve; AUC 5)] were administered to 32 ovarian cancer patients, and seven patients presented febrile neutropenia. In the 25 afebrile patients, the percentage of superoxide anion production by granulocytes was significantly decreased from 86.5 +/- 7.7 (%) to 75.1 +/- 8.8 (%) at day 7 and 71.0 +/- 6.3 (%) at day 14 without administration of CSF. However, in the patients who presented febrile neutropenia, it was more severely decreased from 86.8 +/- 6.8 (%) to 60.0 +/- 9.9 (%) at day 7 and 56.8 +/- 5.0 (%) at day 14 without administration of CSF. When M-CSF was administered to all patients in the next course with the same dose of chemotherapy, the incidence of febrile neutropenia was significantly decreased (P = 0.0195), and the duration of fever (>or= 38.0 degrees C) and high serum C-reactive protein (CRP) (>or= 2.0 mg/dl) were also significantly shortened (P = 0.0023, P = 0.0051). Moreover, in these M-CSF-treated patients, the percentage of superoxide anion production by granulocytes was maintained at the level before chemotherapy. These findings indicate that severe impairment of granulocyte function leads to febrile neutropenia, and that M-CSF reduces the incidence of febrile neutropenia by maintaining or improving granulocyte function.
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PMID:Macrophage colony-stimulating factor prevents febrile neutropenia induced by chemotherapy. 1171 51

We develop the randomized analysis for repeated binary outcomes with non-compliance. A break randomization-based semi-parametric estimation procedure for both the causal risk difference and the causal risk ratio is proposed for repeated binary data. Although we assume the simple structural models for potential outcomes, we choose to avoid making any assumptions about comparability beyond those implied by randomization at time zero. The proposed methods can incorporate non-compliance information, while preserving the validity of the test of the null hypothesis, and even in the presence of non-random non-compliance can give the estimate of the causal effect that treatment would have if all individuals complied with their assigned treatment. The methods are applied to data from a randomized clinical trial for reduction of febrile neutropenia events among acute myeloid leukaemia patients, in which a prophylactic use of macrophage colony-stimulating factor (M-CSF) was compared to placebo during the courses of intensive chemotherapies.
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PMID:Correcting for non-compliance of repeated binary outcomes in randomized clinical trials: randomized analysis approach. 1727 85

Bacterial sepsis is a major cause of neonatal morbidity and mortality. Successful management of neonatal sepsis requires early diagnosis, appropriate antimicrobial treatment, and aggressive intensive care. However, even when steps are taken appropriately, mortality rates can be high, particularly among certain subgroups, such as extremely preterm neonates and neonates with neutropenia. Multiple factors contribute to the increased susceptibility of neonates to infection, including developmental quantitative and qualitative neutrophil defects. Studies of infected animal and human neonates suggest that the use of recombinant human granulocyte colony stimulating factor (rhG-CSF) or recombinant human granulocyte macrophage colony stimulating factor (rhGM-CSF) can partially counterbalance these defects and thereby reduce morbidity and mortality. However, the body of clinical evidence is currently not sufficient to recommend rhG-CSF or rhGM-CSF administration confidently as routine adjunctive treatment for neonates with sepsis.
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PMID:Use of myeloid colony-stimulating factors in neonates with septicemia. 1188 Jul 41

A 52-year-old man was admitted for treatment of hypoplastic leukemia (M 1). After induction chemotherapy with IDR and AraC, the patient developed prolonged febrile neutropenia, and a diagnosis of invasive pulmonary aspergillosis was made. We started administration of AMPH-B and G-CSF, but the patient showed no clinical improvement. M-CSF was added to the regimen, and this led to an increase in the white blood cell count with resolution of pneumonia. It is suggested that administration of M-CSF with antibiotics and G-CSF may be beneficial for treating acute leukemia patients with prolonged febrile neutropenia after intensive chemotherapy.
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PMID:[Successful treatment of invasive pulmonary aspergillosis with G-CSF and M-CSF during long-term bone marrow suppression in hypoplastic leukemia]. 1197 51

We performed a randomized double blind study between 1992 and 1995 in which 214 patients with FIGO stage I to III ovarian cancers received administration of 10(6) units (low dose group) or 8x10(6) units (high dose group) of macrophage colony-stimulating factor (M-CSF) after cyclophosphamide/adriamycin/cisplatin (CAP) therapy. The period required to finish a set of intensive chemotherapy, which was the primary endpoint, was significantly shortened (p=0.0004), and the incidence of febrile neutropenia significantly decreased (p=0.04). In this study, we followed the patients for a prolonged period. The patients were divided into two groups: patients with complete tumor excision and those with incomplete excision, then the relapse rate and survival rate 5 years after initiation of the clinical study were compared. The relapse rate tended to be lower in the high dose group than in the low dose group in patients with no residual tumor (p=0.0750). However, there was no difference in the relapse rate between the two dose groups in patients with residual tumor. Although there were no significant differences in the survival rate between the high and low dose groups in patients with or without residual tumor, the survival rate in mucinous adenocarcinoma patients with no residual tumor was 64.3% in the low dose group (n=14) and 92.3% in the high dose group (n=14), showing a significantly higher rate (p=0.0436), and the survival rate tended to be higher in the high dose group in patients with serous adenocarcinoma (p=0.0786). Furthermore, in patients aged 40 years or younger with no residual tumor, the survival rates were 73.9 and 100% in the low and high dose groups, respectively, showing a significantly higher rate in the high dose group (p=0.0310). Our results suggest that administration of M-CSF can improve the long-term prognosis of ovarian cancer patients with no residual tumor, but further prospective randomized trials with a primary endpoint of relapse-preventing effect are needed.
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PMID:Clinical usefulness of macrophage colony-stimulating factor for ovarian cancers: Long-term prognosis after five years. 1246 57

Granulocyte-colony stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF) are being administered to patients with neutropenia. However, little is known about the endogenous levels of both factors in these patients. We measured the endogenous G-CSF levels in patients with chemotherapy-induced neutropenia (n=15, study group A), in patients who had not received chemotherapy with neutropenia caused by a number of primary diseases (n=14, study group B) and in healthy volunteers (n=15, control group). Both the study groups and the control group did not show any clinical or laboratory findings of infection. The G-CSF levels were elevated in patients following chemotherapy and in patients who had neutropenia without chemotherapy, but the mean G-CSF levels in patients with chemotherapy-induced neutropenia were significantly higher than in patients with primary diseases. The levels of endogenous G-CSF were also higher in both neutropenic groups, compared to the control group. In conclusion, endogenous G-CSF levels in chemotherapy-induced neutropenia were significantly higher than non-chemotherapy related neutropenia and controls. This may be explained as G-CSF synthesizing bone marrow stromal cells may be more affected in primary disease related neutropenia than in chemotherapy induced neutropenia.
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PMID:Endogenous granulocyte colony-stimulating factor (G-CSF) levels in chemotherapy-induced neutropenia and in neutropenia related with primary diseases. 1263 92

Immune response is the major contributor to host defense against opportunistic fungal infections such as candidiasis, aspergillosis and other rare infections. A number of cytokines have been developed and studied in vitro for activity against fungal pathogens. The most studied among them in relation to fungal infections are granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF) and interferon-gamma (IFN-gamma). The fields where these cytokines have been predominantly studied or where they may need more study are primary immunodeficiencies of the phagocytic cells, neonatal age, human immunodeficiency virus infection and cancer-related conditions such as neutropenia and hemopoietic cell transplantation. In this review, the in vitro, experimental animal and clinical data of cytokines are summarized in relation to invasive candidiasis, aspergillosis and emerging fungal infections. Cytokine administration to patients together with antifungal agents, as well as transfusion of cytokine-upgraded phagocytes, are promising immunotherapeutic modalities for further research.
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PMID:Cytokines in immunodeficient patients with invasive fungal infections: an emerging therapy. 1271 28

The purpose of this study was to clarify the effects of mirimostim (macrophage colony-stimulating factor; M-CSF) on immunological functions after chemotherapy. The percentage of natural killer (NK) cells in peripheral blood mononuclear cells (PBMCs), NK cell activity, T-helper cell 1/T-helper cell 2 (Th1/Th2) ratio, and superoxide anion production by granulocytes (granulocyte function) were measured as immunological parameters before and after chemotherapy in 44 patients with primary ovarian cancer who received at least three consecutive courses of postoperative chemotherapy. Patients were observed during the first course of chemotherapy, and 39 patients who presented grade III or IV neutropenia were entered into this study and randomly allocated to an M-CSF-administered group (group 1; 19 patients) and a non-M-CSF-administered group (group 2; 20 patients) for the second course. For the third course, a crossover trial was conducted. In the observation period, chemotherapy significantly impaired the immunological parameters. In particular, those parameters were significantly decreased at day 14 compared to the level before chemotherapy. The values of the parameters of group 1 were significantly higher than those of group 2. In the course of chemotherapy during which M-CSF was administered, 19 of the 39 patients presented grade IV neutropenia, and received granulocyte colony-stimulating factor (G-CSF) between days 7 and 14. We compared the changes of those immunological parameters in the M-CSF alone group and the M-CSF + G-CSF group, and found that the concomitant use of G-CSF did not further improve the parameters. These results indicate that chemotherapy markedly impaired the immunological functions, and that the administration of M-CSF significantly improved the impaired immunological functions.
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PMID:Mirimostim (macrophage colony-stimulating factor; M-CSF) improves chemotherapy-induced impaired natural killer cell activity, Th1/Th2 balance, and granulocyte function. 1296 81


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