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

In this article two patients are reported with recurrent upper airways and ENT-infections. Laboratory investigation showed a persistent neutropenia. The bone marrow aspirations showed a normal cellularity of the erythroid series and the megakaryocytes. The myeloid series were normal with a decreased number of mature segmented neutrophils. In these patients the serum levels of immunoglobulins were within normal range and antibodies against the white cells could not be demonstrated. By the age of 2-3 years the recurrence of infections had decreased and infections of importance have not been reported since. By that age the peripheral white count was not abnormal. This combination of signs and symptoms is known as 'chronic benign neutropenia'. The etiology is obscure. Our investigation in one case (by that time recovered) showed a diminished growth of the myeloid series of donor bone marrow in the presence of patient's serum. This suggests a plasma-factor responsible for the maturation of the myeloid series. This finding has not yet been reported in the literature.
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PMID:[Chronic benign neutropenia possibly caused by a plasma factor]. 351 46

Between February 1983 and April 1986 we studied peripheral blood and bone marrow samples from 20 patients with human immunodeficiency virus (HIV) related disease. 14 patients had AIDS, three had ARC, two had PGL and one had ITP as a sole manifestation of HIV related disease. Peripheral blood abnormalities included marked anisocytosis and poikilocytosis, rouleaux formation, neutropenia, lymphopenia, monocytopenia, a left shift in the granulocyte series and, in the patients with AIDS, vacuolated monocytes. The most frequent bone marrow abnormalities were reticuloendothelial iron block, dyserythropoiesis, megaloblastic change and erythroid hypoplasia. Excess histiocytes were noted in four marrows, one exhibiting haemophagocytosis. None of the bone marrows showed lymphopenia. Eight of the 20 marrows were difficult or impossible to aspirate. None of the trephine biopsies showed increased reticulin. The causes of these abnormalities are probably multiple and include opportunistic infections, drug therapy, immune mechanisms and possibly direct insult by the HIV virus.
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PMID:Peripheral blood and bone marrow abnormalities in patients with HIV related disease. 356 82

Cephalosporin treatment in man has been associated with blood dyscrasias that include a time- and dose-related anemia, neutropenia, and thrombocytopenia, the hematopathology of which remains poorly characterized. A similar hematologic syndrome can be produced in dogs following daily intravenous injections of 540-840 mg/kg cefazedone or 400-500 mg/kg cefonicid for 1-3 months. Using this animal model, histologic and cytologic changes in blood, bone marrow, spleen, and liver were studied over the course of the cephalosporin-induced cytopenias. Peripheral blood cytologic observations included an absence, generally, of erythroid regenerative changes, increased numbers of macroplatelets, spherocytosis, erythroblastemia, and toxic neutrophil morphology. Interim and postmortem cytologic and histologic observations of bone marrow included hypoplastic and toxic changes, primarily in cytopenic dogs receiving high doses of cefonicid, and regenerative changes in hematopoietic tissue of affected cefazedone-treated animals. The latter included variable erythroid hyperplasia, increased megakaryocytes, and decreased marrow fat and was accompanied by evidence of extra-medullary hematopoiesis and increased hemosiderin and hemophagocytosis in liver and splenic tissue. The incidence and severity of these changes were dose-dependent, corresponded with the cytopenias observed peripherally, and, like the cytopenias, were fully reversible. These observations suggest that the hematologic syndrome associated with cephalosporin treatment in the dog has multiple toxicologic mechanisms, which include peripheral cytotoxic effects and bone marrow damage with depressed or ineffective hematopoiesis.
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PMID:The hematopathology of cefonicid- and cefazedone-induced blood dyscrasias in the dog. 362 87

Fifteen patients with chronic benign idiopathic neutropenia (CBIN) with neutrophil counts less than 1.0 X 10(9)/1 have been studied. The mean age was 33 years (range 23-50) comprising 11 females and 4 males. Bone marrow cellularity was normal except in two patients who showed slight reduction and one who had a slight increase. Bone marrow differential counts were normal apart from a small increase in the percentage of promyelocytes and reduction in the myeloid/erythroid ratio in some patients. Peripheral blood counts showed no 'compensatory' monocytosis. Epinephrine stimulation tests showed no evidence of excess neutrophil margination. After endotoxin administration there was a one- to two-fold increase in neutrophil counts in three patients, a three-fold increase in three patients and a greater than four-fold increase in the remaining nine patients. The findings suggest that the benign course of CBIN is not due to excess neutrophil margination nor to compensatory monocytosis, but that at least one mechanism includes a functionally adequate release of neutrophils to the peripheral blood under conditions of stress with subnormal delivery of neutrophils under basal conditions. The variability in responses to endotoxin suggests that CBIN is not entirely homogeneous with respect to mechanism. The findings of relatively normal bone marrow cellularity and differential counts and a normal or substantial neutrophil response to endotoxin appear characteristic. They may help predict a benign clinical course in neutropenic patients and assist diagnosis of the CBIN variant of idiopathic neutropenia.
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PMID:Bone marrow granulocyte reserve in chronic benign idiopathic neutropenia. 365 40

Neutropenia is a life-threatening sequel of hematological disorders and a dominant factor limiting the dosage of cytotoxic chemotherapy. The role of the neutrophil is of such importance in defence against microbial invasion that measures that modify the behaviour of residual hemopoietic tissue to promote a modest increase in neutrophils, can confer considerable benefit by reducing the frequency and severity of infection. Such a change can be mediated in bone marrow depression by diversion of more progeny of immature precursors into the neutrophil series, or by enhancement of the stimulatory drive operating on neutrophil production. The former effect can be achieved by hypertransfusion of red cells to reduce the demand on the limited precursor population for cells of the erythroid series. The latter effect can be achieved by administration of lithium carbonate. Neutropenia caused by autoimmune injury to the neutrophil series can also be successfully modified by measures which suppress the underlying immune dyscrasia or the function of the reticulo-endothelial system. Corticosteroid administration and splenectomy can be helpful in certain specific types of neutropenia. Administration of cyclophosphamide and azathioprine has both mutagenic and marrow suppressive potential, but can induce remissions in severe chronic isolated neutropenia and in systemic lupus erythematosis.
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PMID:New concepts in management of neutropenia. 385 79

Hematologic abnormalities were defined in 31 rhesus monkeys (Macaca mulatta) with simian acquired immune deficiency syndrome (SAIDS). Animals manifested anemia (hypochromic/microcytic), severe neutropenia and progressive lymphopenia, monocytosis and occasional thrombocytopenia. Bone marrow studies showed erythroid hyperplasia with a marked left shift and adequate megakaryocytes. Two animals showed profound hypoplasia of all hematopoietic elements. Most animals were iron deficient, but the course of the anemia suggested additional factors. There was no evidence of immune hemolysis. The pathogenesis of these abnormalities is not clear and will require further study. This reproducible disease will allow studies to elucidate the mechanisms of viral-induced hematologic abnormalities.
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PMID:Hematologic abnormalities in simian acquired immune deficiency syndrome. 395 29

Marrow hypoplasia is described in CBA/H mice that drank water containing 300 mg/liter cadmium chloride for 12 months. This was characterized by a significant reduction of the totipotent stem cells (CFU-s), granulocyte-monocyte progenitor cells (GM-CFUc), and erythroid progenitor cells (CFU-e). The bone marrow cellularity and the proliferative capacity of GM-CFUc in vitro were decreased. The animals reflected these marrow alterations by demonstrating an anemia with reticulocytopenia and neutropenia. They did not show increased mortality or increased susceptibility to infections; however, their body weight was significantly reduced. In addition, iron deficiency was demonstrated in the cadmium-treated mice. The animals had a hypochromia of the peripheral red cells and diminished marrow iron stores. Thus, the anemia of cadmium toxicity is probably the combined result of bone marrow hypoplasia and iron deficiency.
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PMID:Long-term oral cadmium produces bone marrow hypoplasia in mice. 397 72

Myelopoiesis and marrow adherent cells were evaluated in C57Bl/6J mice at two and four weeks after treatment with 0.1 mg 17 beta-estradiol cyclopentylpropionate. Estradiol-treated mice were lymphopenic and eosinopenic at two and four weeks; in addition, neutropenia occurred at four weeks. Numbers of lymphoid, granulocytic, and erythroid cells were decreased in the marrow at two and four weeks. The numbers of granulocyte-macrophage and fibroblast colony-forming units in the humeral marrow were also decreased at two and four weeks. However, the hematopoietic ability of marrow adherent cells was unchanged in estradiol-treated mice. Thymic cortical atrophy, metaphyseal osteosclerosis, and neutrophilic infiltration of the uterus occurred in estradiol-treated mice.
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PMID:Myelopoiesis and marrow adherent cells in estradiol-treated mice. 403 44

Bone marrow and peripheral blood cells of patients with non-leukemic neutropenia contain and elaborate a granulocyte-progenitor cell inhibitory activity. The inhibitory activity is common to the neutropenias of the various etiologies studied, which included congenital, idiopathic, autoimmune, cyclical, common variable immuno-deficiency with hypogammaglobulinemia and drug induced states. It derives from non-adherent, low density, slowly sedimenting and non-E-rosetting cells and appears to require RNA and protein synthesis, but not cell division, for its production. The material is not species specific, inhibits autologous and allogeneic normal CFUgm and leukemic CFUgm, is not cell-cycle specific in action and is most effective against granulocyte colony forming cells (CFUg), less effective against mixed granulocyte-macrophage colony forming cells (CFUgm) and least or non-effective against macrophage colony forming cells (CFUm). This inhibitory activity has no influence on cells which generate CFUc in suspension culture or on the erythroid colony forming (CFUe) and burst forming (BFUe) units. It is different from other known inhibitory activities such as lactoferrin, leukemia inhibitory activity, E type prostaglandins, interferon and immunoglobulins. This inhibitory activity, while at present an in vitro phenomenon, may be produced as a secondary response within a compromised host.
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PMID:Specific inhibitory activity against granulocyte-progenitor cells produced by non-T lymphocytes from patients with neutropenia. 616 31

A group of patients with neutropenia or erythroid aplasia associated with T cell proliferation were evaluated to assess the phenotype(s) and functions of T cells observed in these conditions. These patients have near normal numbers of helper/inducer cells but an excess of cells belonging to the suppressor/cytotoxic subset. The characteristic phenotype of these cells is E+, OKT3+, OKT1+1-, OKT8+, Fc gamma R+, and they frequently bear HLA-DR antigen. These cells respond poorly to T cell mitogens and will suppress the response of normal peripheral blood mononuclear cells to mitogens. They fail to suppress PWM-induced immunoglobulin synthesis. Although the natural killer activity in these patients is sometimes low, this subset of T cells possesses cytotoxic capability demonstrable in assays for antibody-dependent cell-mediated cytotoxicity. The evidence for a direct effect of the T cells on BFUE and CFUGM is poor.
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PMID:Cytopenia and T cell proliferation. 621 25


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