Cases reported "Neutropenia"

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1/10. Alteration of colony-stimulating factor output, endotoxemia, and granulopoiesis in cyclic neutropenia.

    Cellular and humoral factors involved in the regulation of granulopoiesis were evaluated in two patients with cyclic neutropenia by utilizing the agar-gel marrow culture technique to serially study marrow granulocytic colony-forming capacity (CFC) and the urinary output of colony-stimulating factor (CSF). CSF output varied inversely with peripheral neutrophil counts and directly with monocyte counts and evidence for infection (endotoxemia and/or staphylococcal abscesses). Following autologous infusion of one patient's plasma obtained during a period of neutropenia, increased urinary excretion of CSF occurred concomitant with increments in both marrow CFC and the proportion of granulocytic progenitor cells in dna synthesis. Neutrophil periodicity was not altered by the administration of the neutropenic plasma. These findings are consistent with the hypothesis that cyclic neutropenia is caused by a quantitatively decreased entry of stem cells or granulocytic progenitor cells into granulopoiesis.
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2/10. A case report of familial cyclic neutropenia.

    A 34-year-old female with cyclic neutropenia is reported. family studies showed that her three sons and her mother were also involved. Oscillations in the blood neutrophil counts were almost regular, with a periodicity of 21 days. Numbers of colony-forming unit--granulocyte macrophage (CFU-GM) formed from the bone marrow cells of normal volunteers co-cultured with the patient's serum or mononuclear cell-conditioned medium (MNC-CM) were examined. Her serum prepared during the neutropenic phase inhibited the growth of CFU-GM, while her MNC-CM stimulated it. Human granulocyte colony-stimulating factor (hG-CSF) level in her serum was persistently high, with the peak occurring during the neutropenic phase. These results suggest that some inhibitory factors in the serum may be pathophysiologically important for cyclic neutropenia. To control infections, a pharmacological dose of hG-CSF was administered for 7 days around the early neutropenic phase. Her peripheral neutrophil counts oscillated from 1,200/mm3 to 17,000/mm3 with G-CSF, and from 150/mm3 to 1,800/mm3 without G-CSF.
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3/10. Cyclic neutropenia: a cause of recurrent aphthous stomatitis not to be missed.

    Cyclic neutropenia is a rare hematological disorder consisting of recurrent episodes of aphthous stomatitis and skin infections caused by a periodic decrease in blood neutrophil counts. We present the case of such a patient successfully treated with steroids. Recurrent aphthous stomatitis with a periodicity of around 3 weeks should alert the dermatologist to the possibility of cyclic neutropenia.
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4/10. Some immunological and haematological aspects of human cyclic neutropenia.

    In addition to standard peripheral blood cell counts, sequential studies have been made of changes in the T-lymphocyte population and in the serum titres of the presumptive humoral regulators of haematopoiesis, Colony Stimulating Activity (CSA) and Erythroid Stimulating Activity (ESA), in a young woman with cyclic neutropenia (CN). In addition, serum immunoglobulins, C3 and total complement levels and serum protein concentrations were determined on several occasions during the study. Similar tests were done concomitantly on a haematologically normal, age and sex-matched control. Cell counts on peripheral blood from the subject with CN demonstrated a clearly defined periodicity in neutrophil and monocyte concentrations and equivocal fluctuations in reticulocyte numbers. There was no evidence of periodicity in the lymphocyte concentrations and the T-lymphocyte population appeared functionally normal. Spontaneous incorporation of tritiated thymidine into peripheral blood cells showed a highly significant correlation with the monocyte count, suggesting that these cells were responsible for the radioisotope uptake. CSA titres were elevated on all occasions tested and showed no evidence of periodicity. ESA showed some evidence of cycling with elevated levels being observed during the periods of neutropenia. serum complement levels were within the normal range but all classes of immunoglobulins were elevated and albumin levels were depressed.
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5/10. Cyclic neutropenia as a premalignant manifestation of acute lymphoblastic leukemia.

    A 20-year-old female from the philippines developed anemia and granulocytopenia. With androgen therapy, her anemia improved but she continued to show a pattern of fluctuating neutropenia consistent with human cyclic neutropenia: Blood neutrophil oscillation was regular with a periodicity of 21 days. She developed recurrent pharyngitis and apthous stomatitis but there was no cycling of other blood elements. bone marrow aspiration and biopsy showed normal developing myeloid cells, a clonal chromosomal abnormality, and myelofibrosis. During the fourth documented cycle, blasts appeared and complete lymphoblastic transformation ensued. Blast cells were CALLA positive, Ia positive, and contained intranuclear TdT; they were negative for E, EAC, and EA rosettes. She was treated for non-T, non-B CALLA-positive ALL and within 6 weeks was in a remission without evidence of cycling neutrophil counts. This young woman's case suggests that cyclic neutropenia may represent a previously unrecognized premalignant state associated with acute lymphoblastic leukemia.
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6/10. Cycling of peripheral blood and marrow lymphocytes in cyclic neutropenia.

    A 16-month-old male patient with cyclic neutropenia was found to have cyclic fluctuations of monocytes, lymphocytes, platelets, and eosinophils in the peripheral blood. Changes in lymphocyte counts were not obviously related to B, T, or natural killer cells. All classes of immunoglobulins were elevated throughout the cycle. Studies of the marrow morphology revealed remarkable cyclic oscillations of lymphoid as well as myeloid lineage cells. Granulocyte-macrophage progenitors (CFU-c) cycled and were virtually absent 1 wk prior to the neutropenic nadir. The cyclic changes in marrow lymphoid cell numbers were primarily due to changes in numbers of surface immunoglobulin negative (sIg-), cytoplasmic Ig (cIg ) pre-B cells. Pre-B cell numbers cycled from normal to extraordinarily elevated values with the same periodicity but reciprocal to the neutrophil cycle. We propose that the primary defect in cyclic neutropenia may either be a periodic failure of an early myeloid differentiation factor or a blunted response of early myeloid precursors to a common hemopoietic growth factor. This may lead to periodic fluctuations in the production or delivery of growth factors (or factor) that influence early stages of differentiation of other hemopoietic cells, including pre-B cells. The essential periodic deficiency is consequently reflected in deficient production of CFU-c accompanied by excessive production or accumulation of pre-B cells (and probably other hemopoietic precursors) in the marrow.
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7/10. lithium carbonate treatment in familial cyclic neutropenia.

    A patient with previously documented cyclic neutropenia was followed for 48 days on no treatment. Blood counts obtained at 3-day intervals confirmed the presence of cyclic neutropenia with virtually complete disappearance of neutrophils at the nadir of cycles with a periodicity of 21 days. lithium carbonate treatment was begun on day 49. serum lithium levels remained in the therapeutic range throughout the study interval of 58 days. periodicity and depth of neutropenia were not diminished during the study period.
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8/10. Cyclic oscillation of blood neutrophils in a patient with multiple myeloma.

    A patient with multiple myeloma developed periodic blood neutropenia (periodicity of 15-25 days) after 3 yr of intermittent treatment with cytotoxic agents. Peaks of serum colony-stimulating activity (CSA) level coincided with valleys of blood neutrophils. Fraction of marrow neutrophils in the multiplicative pool was high during blood neutrophil valleys and low during neutrophil peaks. In contrast, the maturation storage pool exhibited the reverse pattern. An increased fraction of marrow neutrophilic cells in the multiplicative pool was in active proliferation during a blood neutrophil valley and a decreased fraction during a blood neutrophil peak. These findings suggest that the marrow granulopoiesis was regulated through CSA. The defect causing the periodicity was probably related to the reduced number of neutrophils in the marrow maturation storage pool, which in turn may be related to a reduced and/or defective granulocytic stem cell pool size consequent to the long-term administration of cytotoxic drugs and/or infiltration of the marrow by myeloma cells.
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9/10. Recurrent impetiginized eczema as a presenting manifestation of cyclic neutropenia.

    A patient is described with a persistent, impetiginized dermatitis that worsened periodically, which was preceded by neutropenic episodes during which her circulating neutrophil count fell to 500-600/ml. Each episode lasted 24 h and had a 7-11 day periodicity. The importance of this case depends on the frequency and brevity of the neutrophil trough levels that made the dermatitis appear to be continuous. Similar cases may be more common than expected as isolated abnormal leukocyte counts may be disregarded as laboratory artefacts. Dermatologists should be cautious in managing patients with persistent atypical impetigo.
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10/10. Cyclic neutropenia in Crohn's ileocolitis: efficacy of granulocyte colony-stimulating factor.

    A 40-year-old patient with long-standing Crohn's ileocolitis in remission experienced cyclic neutropenia with a periodicity of 14 days. He was not receiving immunosuppressive or myelosuppressive therapy. The patient had staphylococcus aureus bacteremia resulting from central catheter infection, which was refractory to antibiotic therapy during the period of severe neutropenia. When granulocyte colony-stimulating factor (G-CSF) was administered, the cyclic neutropenia rapidly disappeared, the neutrophil and leukocyte counts normalized, and the sepsis resolved. When G-CSF therapy was discontinued, the leukocyte and absolute neutrophil counts again declined. With reinstitution of therapy, the leukocyte and absolute neutrophil counts recovered and normalized. Crohn's ileocolitis remained in remission during G-CSF therapy. This report confirms and extends one previous report of cyclic neutropenia associated with Crohn's disease and demonstrates in one patient the efficacy and safety of G-CSF on the hematologic, bacteriologic, and clinical manifestations of cyclic neutropenia associated with Crohn's disease.
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