Cases reported "Neutropenia"

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1/17. Demonstration of drug-dependent antibodies in two patients with neutrophenia and successful treatment with granulocyte-colony-stimulating factor.

    BACKGROUND: Many drugs have been reported as being capable of inducing immune neutropenia, but the causative drug-dependent antibodies were rarely demonstrated. STUDY DESIGN AND methods: This report describes the results of serologic testing and treatment in two children with immune neutropenia related to cefotaxime and metamizole, respectively. serum samples were tested in the presence and the absence of the drugs using the granulocyte agglutination test (GAT), the granulocyte immunofluorescence test (GIFT), and the monoclonal antibody-specific immobilization of granulocyte antigens (MAIGA) assay. RESULTS: The serum of one child contained cefotaxime-dependent antibodies that were detectable by the GAT and the MAIGA assay, but not by the GIFT. The serum of the other child gave positive reactions in the GAT and GIFT due to HLA antibodies and in the MAIGA assay only in the presence of metamizole. While cefotaxime-dependent antibody was directed against CD16, the metamizole antibody was directed against CD11b and CD35. The administration of granulocyte-colony-stimulating factor led to an abrupt increase in circulating neutrophils in both cases. CONCLUSION: The use of more than one technique is necessary for detection of drug-dependent antibodies against neutrophils, and early administration of granulocyte-colony-stimulating factor may result in fewer complications in these patients.
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2/17. A possible role for maternal HLA antibody in a case of alloimmune neonatal neutropenia.

    BACKGROUND: Alloimmune neonatal neutropenia (ANN) is caused by a reaction of maternal alloantibodies with paternally inherited antigens on the fetal neutrophils. While human neutrophil antigens (HNA) antibodies are found in half of ANN cases, specific antibodies have not been defined in the remaining cases. STUDY DESIGN AND methods: Reported here is a neonate with omphalitis due to neutropenia. To elucidate the cause of ANN, flow cytometric and PCR analyses were used. Reactions of the patient's and mother's sera with neutrophils, lymphocytes, and platelets were examined by lymphocytotoxicity test (LCT), anti-human immunoglobulin-LCT, and mixed passive hemagglutination test. RESULTS: The maternal sera reacted with neutrophils, lymphocytes, and platelets of the patient and father. The platelet adsorption eliminated the reaction of the maternal serum with the patient's neutrophils. The HLA typing of the family and an LCT using a panel of lymphocytes of 20 HLA-typed donors showed hla-a2 antigen as a target of antibodies in the maternal serum. According to anti-human immunoglobulin-LCT, the anti-HLA-A2 was present in the neonatal serum. On the other hand, HNA antibodies were not detectable in the patient's or the mother's serum. CONCLUSION: These results suggest that the transplacental passage of the maternal HLA antibody caused neutropenia in this patient.
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3/17. EDTA-induced pseudo-neutropenia resolved with kanamycin.

    This report describes a case of spurious neutropenia caused by EDTA-dependent in vitro agglutination of neutrophils. After raising the temperature of the sample to 37 degrees C the agglutination was irreversible, but it resolved completely after addition of kanamycin. Previously this method has been shown to be effective in EDTA-dependent pseudo-thrombocytopenia, but this is the first report demonstrating successful application in EDTA-dependent pseudo-neutropenia.
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4/17. vancomycin-induced neutropenia in a patient positive for an antineutrophil antibody.

    A 48-year-old man, hospitalized after experiencing subarachnoid hemorrhage secondary to a basilar aneurysm, received vancomycin for methicillin-resistant staphylococcus aureus sepsis. He developed neutropenia 16 days after the start of vancomycin therapy, and his white blood cell count decreased to a nadir of 1200 cells/mm3. vancomycin was discontinued, and granulocyte-colony stimulating factor (G-CSF) therapy was begun. The patient was rechallenged with a single dose of vancomycin 1 g in preparation for intraarterial aneurysm coiling. His white blood cell count dropped to 600 cells/mm3 but returned to normal with continued G-CSF therapy. A diagnosis of vancomycin-induced neutropenia was considered. Subsequent testing by granulocyte agglutination and granulocyte immunofluorescence assays revealed that his serum was positive for an antigranulocyte antibody. A test for HLA antibody reactivity was negative. Monoclonal antibody immobilization of granulocyte antigens assay failed to determine the antigen specificity of his granulocyte antibody.
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5/17. Granulocyte serology findings in juvenile symptomatic idiopathic autoimmune neutropenia using a multiassay procedure. Report on 21 cases.

    The serological findings on 21 children with idiopathic autoimmune neutropenia are reported. A multiassay procedure was adopted including agglutination, immunofluorescence and cytotoxicity tests. Beside a cause-effect correlation between granulocyte antibodies and clinical course, a serologic polymorphism was found. As the sensitivity of each assay seemed to be related to the characteristics of the involved antigens and antibodies, as well as to the intrinsic sensitivity of the tests, the performance of a multiassay procedure appears to be advisable for the diagnosis and the follow-up of autoimmune neutropenia.
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6/17. Altered glycosylation leads to Tr polyagglutination.

    BACKGROUND: Polyagglutination refers to red blood cells (RBCs) that are agglutinated by a high proportion of ABO-matched adult sera but not by cord sera. Polyagglutinable RBCs have been associated with microbial infection, myeloproliferative disorders, and myelodysplasia. lectins aid in the identification of polyagglutination. CASE STUDY: A Hispanic male infant with mild hemolytic anemia, a "Bernard-Soulier-like" syndrome, intermittent neutropenia, mitral valve regurgitation, ligament hyperlaxity, and mild mental retardation was studied. The patient's Group O RBCs were polyagglutinable; they were agglutinated by normal human sera, several lectins [including Arachis hypogea, salvia sclarea, salvia horminum, glycine max, ulex europaeus, griffonia simplicifolia I, and Gr. simplicifolia II], and some monoclonal antibodies. His RBCs were not agglutinated by cord sera, dolichos biflorus, or phaseolus lunatus. sodium dodecyl sulfate-polyacrylamide gel electrophoresis on the RBC membranes followed by staining with periodic acid-Schiff stain showed markedly reduced staining of glycophorins A and B. Staining with Coomassie brilliant blue revealed that Band 3 has a faster mobility than normal. CONCLUSIONS: Collectively, the results suggest that the patient's RBCs have a reduction in n-acetylneuraminic acid on both N- and O-glycans, exposing, respectively, beta1,4-galactosidase and beta1,3-galactosidase. The patient likely has an altered glycosyltransferase that results in defective glycosylation in RBCs and other cell lineages. This type of polyagglutination was named Tr.
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7/17. Alloimmune neonatal neutropenia and thrombocytopenia associated with maternal anti HNA-1a, HPA-3b and HLA antibodies.

    The incidence of alloimmune neonatal neutropenia combined with neonatal alloimmune thrombocytopenia is very low. We report a case of a neonate who suffered severe neutropenia and thombocytopenia with widespread petechial spots. The presence of alloantibodies in mother's and patient's sera was analyzed by lymphocytotoxicity test, agglutination test, granulocyte indirect immunofluorescence test, platelet immunofluorescence test (PIFT) and solid phase enzyme-linked immunosorbent assay. Human neutrophil antigens (HNA) and human platelet antigen (HPA) genotypes were tested by polymerase chain reaction analyses. The mother's and patient's sera reacted with neutrophils and lymphocytes of the father. PIFT revealed the presence of IgG anti-platelet antibodies in the patient's serum but the test was negative in the maternal serum. Analyses of HNA-1 and HPA genotypes of the family revealed maternal-neonatal HNA-1a and HPA-3b mismatch. The study of the mother's and patient's sera showed the presence of anti HNA1a, HPA-3b and HLA antibodies specific for HLA-A3 and HLA-B38 antigens. These results suggest that the transplacental passage of maternal HNA-1a, HPA-3b and HLA alloantibodies caused neutropenia and thrombocytopenia in this patient.
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8/17. A case of neonatal alloimmune neutropenia associated with anti-human neutrophil antigen-1a (HNA-1a) antibody.

    Neonatal alloimmune neutropenia (NAN) is an uncommon disease of the newborn provoked by the maternal production of neutrophil-specific alloantibodies, whereby neutrophil IgG antibodies cross the placenta and induce the destruction of fetal neutrophils. Affected newborns are usually identified by the occurrence of bacterial infections. The most frequent antigens involved in NAN are the human neutrophil antigen-1a (HNA-1a), HNA-1b, and HNA-2a. We report a neonate who was delivered at 36 weeks and had a severe neutropenia but who responded well to recombinant human granulocyte colony-stimulating factor (rhG-CSF). Anti-HNA-1a antibody was identified by mixed passive hemagglutination assay in both the sera of the baby and the mother. The baby had HNA-1a and HNA-1b but the mother had only HNA-1b on granulocytes. This is the first Korean report of NAN in which the specificity of the causative antibody was identified.
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9/17. Autoimmune neutropenia in infancy due to anti-NA1 antibody: detection of antibody with immunofluorescence and agglutination test.

    The sera from two patients with chronic neutropenia in infancy were examined for the presence of antineutrophil antibodies and their specificity against neutrophil antigen by using granulocyte indirect immunofluorescence test and microleukocyte agglutination test. In the microleukocyte agglutination test, the patients' sera reacted with neutrophils from their parents and normal unrelated donors having the neutrophil antigen NA1, but not with neutrophils from NA1- donors. After the absorption of patients' sera with NA1 neutrophils, the antibody activity was completely abolished, resulting in the confirmation of the anti-NA1 antibody. In contrast, the granulocyte indirect immunofluorescence test showed positive reactions against both NA1 and NA1- neutrophils, and the specificity for anti-NA1 was found in the results of the sera absorbed with NA1 neutrophils. This suggested that the absorption experiment might be necessary to determine the specificity of the antibody for neutrophil antigen. Thus, we confirmed two cases with autoimmune neutropenia caused by anti-NA1 antibody. A combination of agglutination and immunofluorescence techniques would be recommended for investigation of neutrophil antibodies against the neutrophil-specific antigen.
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ranking = 7
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10/17. Microcapillary agglutination assay for detection of specific antileukocyte reactivity in neutropenic patients.

    serum leukoagglutinating activity against the leukocytes of four patients with neutropenia was demonstrated using a modified microcapillary agglutination test. Cells from a panel of donors proved useful in attempting to define the identity of the antigens involved. In one instance anti-HLA-A9 activity could be demonstrated in a patient possessing HLA-A9. In the other three individuals no definite antigen assessment to HLA Series A and B antigens or the Lalezari series of neutrophil antigens could be made. Two of the patients' sera showed cross-reactivity and may be reactive with the same antigen or antigenic group. The microcapillary agglutination test appears to be useful in the evaluation of possible cases of autoimmune neutropenia.
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