Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prednisone test revealed normal bone marrow reserve of neutrophils (BMR) in subjects with innocent neutropenias e.g. neutropenias not associated with any other disturbances in haemopoiesis or with increased incidence of infections, assumed to be an individual anomaly of the subject. On the other hand, diminution or absence of MBR in chronic hypoplastic neutropenias, transient post-chemotherapeutic neutropenias and neutropenias with increased destruction of neutrophils were observed. The magnitude of that diminution was not dependent of the cause of neutropenia. It is suggested, that the prednisone test (and probably tests with other BMR mobilizing agents) may serve as screening tests for exclusion (or confirmation) of relative granulopoietic insufficiency as the cause of neutropenia. Only after confirmation of reduced BMR another explanations of neutropenia should be sought using other method as muramidase level, adrenaline test or granulocyte kinetics with DF32P, 3HDFP, or 51Cr.
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PMID:Assessment of the value of prednisone test in differential diagnosis of neutropenic state. 116 68

Granulopoiesis was studied simultaneously by three methods in normal subjects and in subjects with neutropenia of various aetiologies: in vitro labelling of autologous and homologous granulocytes for the study of peripheral kinetics, in vivo labelling with DF32P (di-isopropyl-flourophosphate 32P) or 75Se-selenomethionine, and bone marrow autoradiography after in vitro labelling with 3H-thymidine for the study of bone marrow granulopoiesis. Three main mechanisms of neutropenia can be distinguished: a) peripheral hyperdestruction, corpuscular or extra-corpuscular, and false leukopenias (change in the distribution of peripheral granulocytes from the circulating to the marginal granulocyte pool; b) quantitative bone marrow insufficiency without qualitative abnormality; c) qualitative abnormality in bone marrow granulopoiesis with cell death in either the maturation stage or the proliferative stage. There is no exact correlation between clinical and kinetic classifications, but most cases of post-infection chronic neutropenias and idiopathic neutropenias fall into the first two categories, and most cases of benzol intoxication and bone marrow insufficiency due to X-irradiation fall into the last category. Some of these last patients developed an acute myeloblastic leukaemia in the two following years and can be considered as preleukaemic states.
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PMID:Studies of granulocyte kinetics in normal and granulocytopenic subjects. 121 98

The results of erythropoietin (ESF) studies in dogs with cyclic haematopoiesis are presented. Even though the dogs were exposed to a constant stimulus of hypoxia, cycles in the plasma ESF levels occurred at 11 to 12 day intervals. In some dogs, minor midcycle peaks were observed and the amount of ESF produced varied with the different animals. The peaks of ESF characteristically appeared approximately five days after onset of neutropenia. A hypothesis is presented to explain the known facts concerning canine cyclic haematopoiesis. It suggests that a poietin controlling factor is produced and that this assumed factor then stimulates the production of specific factors leading to increases of reticulocytes, platelets, and monocytes. The monocytes in turn produce more colony stimulating factor (CSF) leading to the formation of granulocytes. Such a sequence of events would explain the apogee of reticulocyte, platelet, and monocyte counts at a time when the nadir of granulocyte counts is reached.
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PMID:Hormonal control of erythropoiesis in canine cyclic haematopoiesis. 125 Nov 40

Myelopoiesis in healthy subjects and in 8 cases of refractory anaemia or preleukemia states was studied by the combined cytophotometric-autoradirgraphic method. Granulocytopenia was present in 7 of 8 cases. The results can be summarized as follows: 1. Mature myelocytes of healthy persons are a mainly differentiating cell population with a low labelling index (3-10%) and a high incidence in G1-Phase. 2. The proliferating immature granulopoietic cells of the patients with neutropenia showed a reduced labelling index with 3H-thymidine as a result of an arrest of these cells in G1 (6 of 8 cases). 3. A similar result was obtained in the study of the hyperplastic myelopoiesis of an other patient with preleukemia and normal granulocyte count in peripheral blood, with the disturbance of cell proliferation preceding the symptom neutropenia. 4. Finally in only one case an increased frequency of myelopoietic cells in G2-phase was found suggesting an arrest of cell proliferation in the premitotic phase.
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PMID:Myelopoietic cell proliferation in granulocytopenia of refractory anaemia and preleukemia states with hyper-plastic bone marrow. 125 7

The effects of endotoxin administration on in vitro granulocyte function were studied in normal man. Four healthy volunteers received an intravenous injection of Pseudomonas endotoxin, 0.1 mug/kg. Endotoxemia resulted in transient neutropenia followed by a rebound neutrophilia. The nadir of the granulocyte count occurred at about 1 hr and maximal neutrophilia 2-4 hr after endotoxin administration. Throughout this time period, neutrophil phagocytosis and killing of Candida albicans were normal, as were resting and postphagocytic glucose metabolism and leukocyte random migration. However, postendotoxin neutrophils demonstrated a markedly decreased chemotactic response in Boyden chambers. The defect was maximal 1 hr after endotoxin administration and persisted 3-4 hr. These observations suggest that, in addition to neutropenia, endotoxin can transiently cause a chemotactic defect or select for a population of circulating neutrophils with an impairment of chemotactic activity.
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PMID:Granulocyte function in experimental human endotoxemia. 126 Jan 18

In paroxysmal nocturnal hemoglobinuria (PNH), infection, both viral and bacterial, disproportionate to the mild neutropenia seen in many such patients is responsible for significant morbidity. We report impaired granulocyte chemotaxis efficiency which may contribute to the problems induced by bacterial infections. PNH (but not normal) granulocytes, after exposure to very small concentrations of activated serum complement components, migrate poorly, as documented by their inhibited chemotaxis toward bacterial products or activated complement components in Boyden chambers. The granulocytes remain intact, excluding trypan blue, phagocytosing, and killing bacteria, despite this activated complement exposure. It is also suggested that this chemotactic defect may involve only a clone of cells, analogous to the clonal lysis of PNH erythrocytes; those few granulocytes capable of migration after exposure to activated complement contain normal quantities of leukocyte alkaline phosphatase (LAP), in contrast to the LAP deficiency of the overall PNH granulocyte population. Since bacterial infection may initiate or potentiate hemolysis, one of the major symptoms of the disease, these results could explain much of the morbidity of PNH.
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PMID:Complement-mediated granulocyte dysfunction in paroxysmal nocturnal hemoglobinuria. 127 74

Colony stimulating factors (CSFs) are glycoprotein hormones that regulate growth and differentiation of hematopoietic progenitor cells. Their use to stimulate granulocyte precursors during periods of neutropenia in patients with acute myeloid leukemia (AML) is limited by their concomitant stimulation of the proliferation of myeloblasts. The effects of these agents on leukemic lymphoblasts is not entirely known. We have investigated the in vitro effects of granulocyte-CSF (G-CSF) and granulocyte/macrophage-CSF (GM-CSF) on leukemic cells from children with acute lymphoblastic leukemia (ALL). DNA synthesis of bone marrow cells from 22 children with ALL, either at diagnosis or in relapse, was examined with and without CSFs. Proliferative potential was also tested in a clonogenic assay with 13 bone marrow specimens. These factors did not stimulate the growth of ALL cells in either assay. Our results indicate that G-CSF and GM-CSF should be able to stimulate granulocyte proliferation without enhancing leukemic proliferation during periods of neutropenia in children with ALL.
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PMID:The effect of recombinant GM-CSF and G-CSF on the bone marrow cells of children with acute lymphoblastic leukemia. 127 25

Frequent complications of human immunodeficiency virus infection are hematopoietic failure and poor tolerance of myelosuppressive drugs. Reasons for neutropenia resulting from hematopoietic failure are infection of the bone marrow and hematotoxicity of treatment with zidovudine, ganciclovir, sulfonamides, and interferons. Moreover, tumor necrosis factor-alpha, transforming growth factor-beta and interferon-gamma have been shown to suppress proliferation of bone marrow cells. Both granulocyte (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) increase neutrophil counts and ameliorate phagocytic and bactericidic function of neutrophils. We report eight cases of AIDS patients with serious infections and neutropenia (< 750 cells/microliters), who were treated concomitantly with recombinant human G-CSF (3-4 micrograms subcutaneously per kilogram body weight daily). G-CSF treatment was well tolerated in all patients and showed no side effects or disturbances of other lineages than neutrophils. Life-threatening bacterial infections were treated successfully by stimulating the neutrophil immune system. This therapy shortened the duration of subsequent treatment with antibiotics. Since human immunodeficiency virus infects CD4-positive monocytes and macrophages, which are stimulated by GM-CSF, G-CSF seems to be the cytokine of choice, if stimulation of the neutrophil lineage is warranted.
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PMID:Granulocyte colony-stimulating factor treatment in AIDS patients. 128 Apr 96

A total of 36 patients with advanced non-small-cell lung cancer (NSCLC) were treated with a combination of 5-day continuous i.v. infusion of cisplatin (25 mg/m2 daily), bolus infusion of vindesine (3 mg/m2) on days 1 and 8, and s.c. injection of recombinant human granulocyte-colony-stimulating factor (2 micrograms/kg daily) on days 6-21. Treatment was repeated every 3-4 weeks. Responding patients with stage IIIA or IIIB disease received chest radiation therapy (50-60 Gy) after this treatment. One complete response and 23 partial responses were observed, for an overall response rate of 66.7% (24/36; 95% confidence limits, 51.3%-82.1%). The median duration of response was 5.7 months and the median overall survival was 10.1 months. WHO grade 3 or 4 leukopenia and neutropenia occurred in 22 (61%) and 27 (75%) patients, respectively, but the mean duration of leukopenia (< 2,000/mm3) and neutropenia (< 1,000/mm3) was 3.4 and 3.5 days, respectively, and there was no instance of life-threatening infection. Thrombocytopenia and anemia of grade 3 or 4 occurred in 28% and 36% of our subjects, respectively. Grade 2 nausea and vomiting occurred in 47% of the patients. Elevated serum creatinine levels (> 1.5 mg/dl) were observed in 3 (8%) of the 36 patients. One patient died of acute renal failure induced by hemorrhage of a gastric ulcer. This regimen is effective in the treatment of NSCLC and further studies of this combination are warranted.
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PMID:Phase II study of cisplatin as a 5-day continuous infusion with vindesine plus recombinant human granulocyte-colony-stimulating factor in the treatment of advanced non-small-cell lung cancer. 128 May 37

A 72 year-old woman was admitted to our hospital for hematoemesis. After admission, endoscopic examination showed esophageal varices with a red color sign which indicated endoscopic injection sclerotherapy (EIS). Concurrently, however, laboratory findings revealed severe neutropenia in peripheral blood, while bone marrow examination showed marked reduction of mature granulocytes with mild myeloid hyperplasia. As a result of those hematological abnormalities, EIS was halted. Concerning the pathogenesis of this neutropenia, immunofluorescence technique using flow cytometry disclosed the presence of anti-neutrophil autoantibody in the serum, giving a clinical diagnosis of autoimmune neutropenia (AIN). Thereafter, a conventional regimen of corticosteroids as an initial therapy and steroid pulse therapy as a succeeding maneuver were instituted, but in vain. As a last resort, 125 micrograms/body of rhG-CSF was given daily subcutaneously. As a consequence, significant increase in granulocyte count, though transient, was attained, which made EIS possible without any episodes of infections. It seems most likely that a high dose of rhG-CSF exerts beneficial effects as a prophylactic and therapeutic regimen against infections in patients with AIN.
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PMID:[The successful treatment of G-CSF in autoimmune neutropenia with liver cirrhosis complicated by esophageal varices]. 128 93


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