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)

Antibodies directed against antigens on the granulocyte (neutrophil) membrane can cause a variety of disorders including neonatal immune neutropenia, immune neutropenia after bone marrow transplantation, autoimmune neutropenia, and drug-induced immune neutropenia. Since granulocyte alloantibodies can lead to severe pulmonary transfusion reactions (TRALI), febrile transfusion reactions and refractoriness to granulocyte transfusions, they also play an important part in blood transfusion. The implicated human neutrophil alloantigens (HNA) have been renamed in the recently introduced HNA nomenclature which is based on the antigen's glycoprotein location. The Fc gamma Receptor IIIb (CD16, HNA-1) and the NB1 glycoprotein (CD177, HNA-2) represent the major immunogenic molecules of the neutrophil membrane. They bear the clinically most important antigens HNA-1a,-1b,-1c (NA1, NA2, SH) and HNA-2a (NB1), respectively. For the detection of granulocyte antibodies, a combination of immunofluorescence and agglutination tests together with a panel of freshly isolated, typed test neutrophils has been shown to represent the best means of detection. The introduction of the glycoprotein-specific assay "MAIGA" has improved alloantibody identification considerably. To facilitate and improve neutrophil typing, PCR-SSP techniques have been established for HNA-1a,-1b, and -1c genotyping.
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PMID:Granulocyte immunology. 1173 15

Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion-related mortality. To explore the pathogenesis of TRALI, we developed an in vivo mouse model based on the passive transfusion of an MHC class I (MHC I) mAb (H2Kd) to mice with the cognate antigen. Transfusion of the MHC I mAb to BALB/c mice produced acute lung injury with increased excess lung water, increased lung vascular and lung epithelial permeability to protein, and decreased alveolar fluid clearance. There was 50% mortality at a 2-hour time point after Ab administration. Pulmonary histology and immunohistochemistry revealed prominent neutrophil sequestration in the lung microvasculature that occurred concomitantly with acute peripheral blood neutropenia, all within 2 hours of administration of the mAb. Depletion of neutrophils by injection of anti-granulocyte mAb Gr-1 protected mice from lung injury following MHC I mAb challenge. FcRgamma-/- mice were resistant to MHC I mAb-induced lung injury, while adoptive transfer of wild-type neutrophils into the FcRgamma-/- animals restored lung injury following MHC I mAb challenge. In conclusion, in a clinically relevant in vivo mouse model of TRALI using an MHC I mAb, the mechanism of lung injury was dependent on neutrophils and their Fc gamma receptors.
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PMID:Neutrophils and their Fc gamma receptors are essential in a mouse model of transfusion-related acute lung injury. 1671 Apr 75

Bone marrow suppression after intensive chemotherapies in patients with myeloid leukemia is severe, resulting in the reduction of the number of white blood cells, red blood cells, and platelets. Supportive therapies are indispensable for the management of these leukemia patients. The improvement of blood cell transfusion can decrease side effects of chemotherapies and establish the safety. But we still have notable side effects of transfusion such as TRALI (transfusion-related acute lung injury), platelet immunologic refractory state, and so on. Cytokine therapy especially with G-CSF (granulocyte colony-stimulating factor) administration, changed the treatment of myeloid leukemia. G-CSF can shorten the duration of neutropenia and decrease the risk of infection. Recently the effects of Epo (erythropoietin) on chemotherapy-induced anemia have been demonstrated. We discuss here the indications of blood cell transfusion and cytokine therapies in the treatment for myeloid leukemia.
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PMID:[Supportive therapies for myeloid leukemia including blood transfusion and growth factors]. 1986 Jan 96

Transfusion-related acute lung injury (TRALI) is a leading cause of transfusion related morbidity and mortality. Current concepts regarding the pathogenesis of this disorder imply a "two-hit" model in which neutrophils are sequestered in the pulmonary capillary bed, and subsequently activated by substances in the transfused blood product. We report a case of TRALI in a patient with neutropenia and discuss the possible factors contributing to the respiratory symptoms in this patient. We also emphasise the importance of recognising mild cases of TRALI in order to investigate the implicated donor/s appropriately, and to minimise the risk for more severe episodes in other patients.
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PMID:Transfusion-related acute lung injury in a neutropenic patient. 2183 Nov 20

Fetal and neonatal alloimmune thrombocytopenia (FNAIT) and neonatal alloimmune neutropenia (NAN) are two rare complications of newborns caused by antibodies against paternal inherited antigens. Human platelet (HPA) and neutrophil antigens (HNA) are the common targets. Human leukocyte antigen (HLA) class I proteins are also expressed on platelets and neutrophils and anti-HLA antibodies have occasionally been implicated in these complications. We report a premature twin infant who presented with severe thrombocytopenia and neutropenia clinically compatible with FNAIT and NAN, from a mother with no identifiable HPA or HNA antibodies, but with very high levels of complement-fixing antibodies against paternal inherited HLA. These antibodies were also detected in the infant. HLA antibodies are commonly present in multiparous women who deliver healthy infants. They can, however, be cytotoxic and cause clinical complications after blood products transfusion (TRALI and becoming refractory to platelets transfusion) and after organ transplantation (allogeneic organ rejection).
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PMID:Implication of antibodies against human leukocyte antigen in simultaneous presentation of fetal and neonatal alloimmune thrombocytopenia and neutropenia. 3031 77