Cases reported "Eosinophilia"

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1/172. Wells' syndrome (eosinophilic cellulitis): correlation between clinical activity, eosinophil levels, eosinophil cation protein and interleukin-5.

    Wells' syndrome (WS) (eosinophilic cellulitis) is characterized by the presence of oedematous skin lesions associated with eosinophilia of the tissues. It has recently been observed that in patients with this disease, increased eosinophil cation protein (ECP) and interleukin (IL) -5 can be detected in peripheral blood, with T lymphocytes that have mRNA for this lymphokine. We present a patient with WS in whom we found a close correlation between clinical activity, eosinophils in blood and bone marrow, and ECP and IL-5 levels in peripheral blood and tissues. We underline the major part played by IL-5 in this disease.
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2/172. Successful unrelated umbilical cord blood transplantation in a child with Omenn's syndrome.

    Omenn's syndrome is a variant of combined immunodeficiency disease (CID). Like other CID forms, it causes death unless the patient receives a bone marrow transplant (BMT). Previous reports have shown that BMTs from unrelated donors in Omenn's syndrome have very poor results, with a high rate of infections during transplantation and graft rejection, when compared with transplants from related donors or patients with other CID. This study discusses the case of a 19-month-old child with Omenn's syndrome, who received an unrelated cord blood stem cell transplant (CBT). Donor and recipient had 1 HLA-Ag mismatched on HLA-B. Symptomatology improved early after CBT. The child achieved leukocytes and platelet engraftment and was discharged on day 34. His follow-up has been uneventful and at this time, 27 months after CBT, immune functions have been recovered.
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3/172. Myelodysplastic syndrome that progressed to acute myelomonocytic leukemia with eosinophilia showing peculiar chromosomal abnormality: a case report.

    Myelodysplastic syndrome is a closely related group of acquired bone marrow disorders characterized by ineffective and dysplastic hematopoiesis. These clonal disorders frequently progress to acute leukemia. Acute myelomonocytic leukemia with eosinophilia is characterized by an increase in abnormal eosinophils in the bone marrow, relatively good clinical course and inv (16) chromosomal abnormality. We experienced one case of refractory anemia with excess blasts which progressed to refractory anemia with excess blasts in transformation and finally to acute myelomonocytic leukemia with eosinophilia showing peculiar chromosomal abnormalities of der (1;7).
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4/172. Pulmonary infiltrates after cytokine therapy for stem cell transplantation. Massive deposition of eosinophil major basic protein detected by immunohistochemistry.

    interleukin-2 (IL-2), a product of activated T-cells, is now being used in a number of protocols for cancer immunotherapy. In one stem cell transplantation protocol for breast cancer, IL-2 is used together with interferon-gamma (IFN-gamma) and cyclosporine to stimulate a graft-versus-tumor response and improve the likelihood of a prolonged remission. We present the case of a patient who developed peripheral eosinophilia, perihilar infiltrates, and hypoxemia after autologous stem cell transplantation and the use of recombinant IL-2 and IFN-gamma. Histologic analysis of transbronchial lung biopsies demonstrated a few eosinophils within the bronchial submucosa. Immunostaining using antibodies directed against eosinophil major basic protein (MBP), however, revealed massive extracellular deposition of this toxic granule protein throughout the lung parenchyma. IL-2 therapy is well known to induce a peripheral eosinophilia and to be associated with the capillary leak syndrome characterized by weight gain, edema, and oliguria. The findings noted in this case report suggest that the eosinophil activation that accompanies immunologic therapy with IL-2 can result in direct toxicity to the lung and a localized vascular leak syndrome. This syndrome should be considered in the differential diagnosis of pulmonary infiltrates that occur acutely after bone marrow transplantation with cytokine augmentation.
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5/172. eosinophilia during fludarabine treatment of chronic lymphocytic leukemia.

    Although eosinophilia has been reported as a side effect of purine analogues, there is no report on fludarabine-induced eosinophilia in chronic lymphocytic leukemia (CLL). During chemotherapy with fludarabine and cyclophosphamide, we observed two cases of significant eosinophilia. A 67-year-old patient with CLL developed bone marrow and peripheral blood eosinophilia up to 7.9x10(9)/l, the highest eosinophil count ever reported during treatment with a purine analogue. The eosinophilia persisted for 33 days. Another patient developed bone marrow eosinophilia without eosinophilia in the peripheral blood. These are the first documented cases of fludarabine-induced eosinophilia in CLL, and this side effect may conceivably be more common than previously recognized.
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6/172. Eosinophilic myelodysplasia transforming to acute lymphoblastic leukaemia.

    A 43 year old male presented with a marked eosinophilia and associated systemic symptoms. A diagnosis of myelodysplasia was made on the basis of bone marrow morphology and karyotype. Over a 12 month period the disease transformed into acute lymphoblastic leukaemia, confirmed by flow cytometry, cytochemistry, and immunohistochemistry. karyotyping was abnormal with 5q- and -7 which persisted from diagnosis through to blastic transformation. He died following initial induction chemotherapy. Eosinophilic myelodysplasia is an uncommon condition in haematological practice and no previous report of lymphoblastic transformation has been found.
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7/172. Myelodysplastic syndrome with atypical eosinophilia in association with ring chromosome 7. A case report.

    The presence of morphologically abnormal eosinophils in the bone marrow and/or peripheral blood has been rarely reported as a prominent feature in myelodysplastic syndromes (MDS). Specific chromosomal aberrations have been observed in such cases. We report a case of a 76-year-old man who presented with chronic, transfusion-dependent anemia. Peripheral blood smear analysis revealed anisocytes, mild leukopenia, and occasional hypersegmented eosinophils. A subsequent bone marrow biopsy and aspiration disclosed hypercellularity, and morphologic abnormalities within the megakaryocyte, erythroid, and myeloid series. The myeloid population was predominantly comprised of eosinophils with varying degrees of dyspoiesis. The constellation of hematologic findings were without a precise categorization according to the FAB classification of myelodysplastic syndromes. Subsequent cytogenetic techniques demonstrated a ring chromosome 7 in all 20 metaphases analyzed in cultured bone marrow cells. Eighty-five-percent of the analyzed cells showed a ring chromosome composed of both the long and short arms: r(7)(p22q36). In the remaining metaphases, the ring was composed of only the short arm: r(7)(p22q10). To our knowledge, these uncommon cytogenetic abnormalities have not been previously reported in association with MDS with morphologically atypical bone marrow or peripheral eosinophilia.
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8/172. Identification of new Fas mutations in a patient with autoimmune lymphoproliferative syndrome (ALPS) and eosinophilia.

    autoimmune lymphoproliferative syndrome (ALPS) is a rare, newly recognized, chronic lymphoproliferative disorder in children and is characterized by lymphadenopathy, splenomegaly, pancytopenia, autoimmune phenomena and expansion of double-negative (DN) T lymphocytes (TCR alpha beta , CD4-, CD8-). Defective lymphocyte apoptosis caused by mutations of the Fas (CD95) gene has been linked in the pathogenesis of ALPS, as binding of Fas-ligand to Fas can trigger apoptosis. Of the ALPS cases reported to date, point mutations, frameshifts and silent mutations in Fas all have been identified. We report two new point mutations in Fas in a child with ALPS and eosinophilia; studies on other family members established the pattern of inheritance for these mutations. Flow cytometric analysis of blood and tissues (spleen, lymph node, bone marrow) revealed abnormally expanded populations of DN T lymphocytes. Furthermore, activated lymphocytes and IFN gamma-activated eosinophils were resistant to Fas-mediated apoptosis. Eosinophil resistance to Fas-mediated apoptosis has not been previously described in ALPS. Sequencing of Fas revealed two separate mutations not previously reported. One mutation, a C to T change at base 836, was a silent mutation inherited from the mother, while the second mutation, a C to A change at base 916, caused a non-conservative amino acid substitution in the death domain of Fas, changing a threonine to a lysine. This mutation is associated with a predicted change in the structure of a part of the death domain from a beta-pleated sheet to an alpha-helix. We speculate that the mutation in the death domain prevents the interaction of Fas with intracellular mediators of apoptosis and is responsible for the autoimmune manifestations of ALPS and the abnormal lymphocytosis and eosinophilia in this patient.
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9/172. Complete haematological and cytogenetic response to interferon alpha-2a of a myeloproliferative disorder with eosinophilia associated with a unique t(4;7) aberration.

    A female patient with eosinophilia and cardiac symptoms was found to have a unique chromosomal aberration [t(4;7)(q11;p13)] of bone-marrow precursors. The disorder was classified as a chronic myeloproliferative syndrome with eosinophilia. Due to a significant increase in the white blood cell and eosinophil count during initial treatment with prednisone and hydroxyurea, Interferon alpha-2a was administered at a dose of 3-5 x 10(6) I.U. s.c., five times per week, and induced a long-term complete haematological and cytogenetic response. The clinical features of this case are presented and discussed in the context of the current literature.
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10/172. fluconazole-induced agranulocytosis with eosinophilia.

    fluconazole is a commonly prescribed antifungal agent with a favorable safety profile. A patient experienced agranulocytosis and eosinophilia associated with the drug. Similar bone marrow-suppressive effect due to the azoles is rarely described in the English-language literature.
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