Cases reported "Leukopenia"

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1/5. Cold-induced granulocyte agglutination. A cause of pseudoleukopenia.

    Transient cold agglutination of her granulocytes developed in a 60-year-old woman with a left upper lobe pneumonia during the acute phase of her illness. This phenomenon was manifested by pseudogranulocytopenia, multiple clumps of granulocytes on her peripheral blood smear, and abnormal distribution of granulocytes and monocytes on the white blood cell histogram when measured on an automated hematology analyzer (Coulter S-Plus IV, Coulter electronics Inc, Hialeah, Fla). The cause is postulated to be an IgM autoantibody directed against components of the granulocyte membranes. Spurious leukopenia is encountered infrequently with automated hematology analyzers. Cold-induced granulocyte agglutination should be recognized as a potential cause of pseudogranulocytopenia so that white blood cell counts can be accurately reported and unnecessary evaluation of patients for leukopenia can be avoided.
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2/5. quinidine-induced thrombocytopenia and leukopenia: demonstration and characterization of distinct antiplatelet and antileukocyte antibodies.

    A patient with the rare syndrome of simultaneous quinidine-induced thrombocytopenia and leukopenia was studied. A quinidine-dependent antiplatelet antibody was detected in her serum by platelet aggregometry and by indirect platelet-suspension immunofluorescence. A drug-dependent antileukocyte antibody was demonstrated by leukoagglutination and by granulocyte immunofluorescence. Both antibodies were found to belong to the IgG class by immunofluorescence using monospecific antisera. There appeared to be two distinct antibodies, since the antibody eluted off sensitized platelets reacted only with platelets and that eluted off sensitized granulocytes reacted only with granulocytes. In addition, the patient's serum and quinidine gave a negative reaction on immunofluorescence with platelets from a patient with bernard-soulier syndrome (BSS), which lack glycoprotein lb (GPlb) complex, but gave a positive reaction with BSS granulocytes. The quinidine-dependent antiplatelet antibody immunoprecipitated GPlb and a glycoprotein of molecular weight 22,000 (GPlb complex) from Triton-solubilized, periodate-labeled platelets. Similar attempts to identify the granulocyte surface receptor/antigen were unsuccessful. factor viii/von willebrand factor was not required for binding of the drug-dependent antibody to platelets.
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3/5. Acute and latent leukopenic reaction to antipyrine.

    During the past 10 yr over 100 subjects received test doses of antipyrine in our laboratory for drug metabolism studies without any noticeable untoward effects. The present case describes an immediate allergic reaction to antipyrine and a latent leukopenic reaction 8 wk later without any drug exposure. Leukoagglutination was demonstrated in vitro following the addition of antipyrine, aminopyrine, phenylbutazone, or sulfinpyrazone to blood taken from the subject.
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4/5. Four cases of spuriously low WBC count due to in vitro leukocyte agglutination: contribution of the hematology analyzer Coulter STKS in detecting this clinically misleading artefact.

    Four spuriously lowered WBC counts due to in vitro leukoagglutination were reported from an automated cell counter (Coulter STKS). Leukocyte aggregates (3 to 50 cells), detected in the peripheral blood smears, included different cell types, normal (neutrophils, eosinophils, monocytes, lymphocytes) or abnormal (lymphoma cells). The phenomenon was associated with either a spurious leukoneutropenia or an underestimation of hyperleucocytosis. Leukoagglutination was extensively investigated in 3 cases : as shown in several reports, leukoagglutination may occur with various features, especially due to temperature and anticoagulant dependence. Our four cases reflected this variability. Furthermore, one case was found both temperature-dependent and anticoagulant-independent, a pattern not yet described in the literature. A common STKS graphic pattern was found in our 4 cases, suggesting that hematology analyzers such as Coulter STKS may be useful to detect leukoagglutination. In conclusion, each leukoneutropenia and/or each suggestive graphic pattern must be controlled by means of a blood smear examination in order to rule out the possibility of in vitro leukoagglutination.
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5/5. association of pseudothrombocytopenia and pseudoleukopenia: evidence for different pathogenic mechanisms.

    A case of spurious automated leukocyte and platelet counts due to EDTA-dependent platelet-neutrophil agglutination is described. Whole blood anticoagulated with K3EDTA, sodium citrate and lithium heparin was analysed at short time intervals up to 6 h from sampling at 37 degrees C and at room temperature (RT = 27 degrees C). A phenomenon of platelet clumping occurred at both temperatures with all the anticoagulants (pseudothrombocytopenia), while platelet-granulocyte agglutination was present only with EDTA at RT. Aggregates consisting of up to 80 neutrophils were seen on the blood smear. The contemporary presence of platelet clumping caused a reduction of WBC count of only 25% the initial, while leukocyte differential was markedly altered (pseudolymphocytosis). Further experiments were performed mixing plasma and serum of the patient with packed cells (PC) from a normal donor in the presence of different anticoagulants and at various dilutions and temperatures. Platelet-neutrophil agglutination occurred only in the presence of EDTA at temperatures lower than 37 degrees C, and was abolished by plasma dilutions from 1:8 onwards. Similarly, it was inhibited by incubation with dithiothreitol (DTT), in contrast with platelet clumping. The latter phenomenon was triggered by an EDTA concentration lower than that necessary to cause platelet-neutrophil agglutination (0.5 mg ml-1 vs. 0.77 mg ml-1). Obtained results suggest the causal association of 2 different phenomena, both transferable to normal cells by means of patient plasma and serum. In the article the pathogenetic implications of the case are discussed.
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