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1/234. Chronic eosinophilic leukemia: successful treatment with an unrelated bone marrow transplantation.

    The optimal treatment of eosinophilic leukemia is still uncertain. We report the successful treatment of a 21-year-old patient with eosinophilic leukemia, without cytogenetic abnormalities, by bone marrow transplantation from an unrelated donor. The conditioning regimen for the transplantation consisted of fractionated total body irradiation and cyclophosphamide. Acute GVHD, grade I, post-transplantation was successfully treated. No other severe complications occured. The patient is alive in complete remission 21 months after unrelated bone marrow transplantation. ( info)

2/234. MRI findings of muscle involvement in idiopathic hypereosinophilic syndrome.

    A 40-year-old white man presented with fever, muscle pain, skin nodules and persistent hypereosinophilia over a period of 1 year. In addition, he had ventricular arrhythmias with episodes of tachycardia. Besides a lack of response to antiparasitic therapy, laboratory and pathological data excluded the diagnosis of trichinosis or any other parasitic infection. The patient's course of the disease over the previous 1(1)/2 years was compatible with hypereosinophilic syndrome. In a muscle biopsy several eosinophilic perivascular and leucocytic intravascular infiltrates were found, indicative of muscle involvement by the disease. This is a report on the MRI findings of muscle involvement in idiopathic hypereosinophilic syndrome. ( info)

3/234. Systemic lupus erythematosus, eosinophilia and Loffler's endocarditis. An unusual association.

    A 24-yr-old male, known since the age of 11 to have a nonerosive arthritis and later diagnosed as having systemic lupus erythematosus (SLE), developed subacute heart failure with diffuse lung infiltrates and died suddenly after having presented a moderate hypereosinophilia for 6 months for which no other causes besides the SLE were found. A post mortem examination revealed Loffler's endocarditis (endocarditis parietalis fibroplastica) with acute pulmonary capillaritis. This represents Loffler's endocarditis in the setting of SLE. To the best of the authors' knowledge, this association has not been reported before. ( info)

4/234. Allogeneic peripheral blood stem cell transplantation for hypereosinophilic syndrome with severe cardiac dysfunction.

    A 42-year-old male underwent an HLA-matched sibling PBSC transplant for hypereosinophilic syndrome (HES) diagnosed in August 1995. Prior to transplant he experienced progressive cardiac and pulmonary dysfunction with red cell and platelet transfusion dependence despite therapy with hydroxyurea, steroids and interferon. He received busulfan (16 mg/kg) and cyclophosphamide (120 mg/kg) as conditioning and standard GVHD prophylaxis with cyclosporin A and methotrexate. At day 336 he was transfusion independent without GVHD. Prompt reduction of the eosinophil count (<500/microl) and rapid improvement of cardiac function were documented, demonstrating the reversibility of organ dysfunction. Allogeneic PBSCT is an effective therapeutic option for patients with HES who fail conventional therapy. ( info)

5/234. AlphaIFN-induced hematologic and cytogenetic remission in chronic eosinophilic leukemia with t(1;5).

    Chronic eosinophilic leukemia (CEL) is a myeloproliferative disease characterized by excessive eosinophilic proliferation with clonal cytogenetic abnormalities. The most frequent cytogenetic abnormality is a break in the q 31-35 region of chromosome 5, where genes encoding for IL-3, IL-5 and GM-CSF (all cytokines involved in eosinophilopoiesis) are located. We report the case of a patient with CEL with t(1;5) (q23;q31), who obtained complete hematologic and major cytogenetic response after two years of alpha-interferon (alpha-IFN) therapy. Two other cases of complete response to alpha-IFN are reported in the literature. A trial with alpha-IFN could be considered as front line treatment in this rare disease. ( info)

6/234. The role of trisomy 8 in the pathogenesis of chronic eosinophilic leukemia.

    A case of chronic eosinophilic leukemia (CEL) manifesting as spinal cord compression by an extradural eosinophilic chloroma in a 32-year-old Chinese man was presented, who subsequently developed extramedullary transformation at the skin and then peritoneal cavity. Cytogenetic study of bone marrow cells at diagnosis showed a clonal karyotypic abnormality of trisomy 8 ( 8), which on fluorescence in situ hybridization (FISH) was shown to be present in a clone of abnormal eosinophils, hence showing the neoplastic nature of the eosinophilic proliferation. There was another population of abnormal eosinophils that did not show 8. At blastic transformation, all blast cells in ascitic fluid were shown by FISH to harbor 8. These findings suggest that 8 in this case may have arisen from clonal evolution and is not the primary genetic event in leukemogenesis, but 8 most probably imparts a further survival advantage to the clone responsible for subsequent blastic transformation. ( info)

7/234. Cerebral sinovenous thrombosis in the idiopathic hypereosinophilic syndrome in childhood.

    The idiopathic hypereosinophilic syndrome (HES) is a leukoproliferative disorder marked by a sustained overproduction of eosinophils and a distinct predilection to damage specific organs, especially the cardiovascular system. It is primarily a disease of middle-aged people. Occasional cases have been encountered in children. We report a case of an 11-year-old boy affected by idiopathic HES with an unusual rapidly fatal course. In addition to eosinophilic cellulitis, cerebral straight and superior sagittal sinus vein thrombosis (CVT) was evident on cranial CT. In our review of the English literature we were unable to find an association between idiopathic HES and CVT. ( info)

8/234. hypereosinophilic syndrome: progression of peripheral neuropathy despite controlled eosinophil levels.

    Idiopathic hypereosinophilic syndrome (HES) is a disorder of the hematopoietic system, characterized by persistent elevation in the total eosinophil count (> 1500/microliter) for over 6 months, associated with organ damage and no detectable underlying cause. Treatment is centered on the reduction of total circulating eosinophils, which generally leads to remission of symptoms. We report a 68-year-old female patient with HES and peripheral neuropathy, presenting with cutaneous lesions, mental changes, cardiac and pulmonary symptoms, followed by right foot drop and eventually paraparesis, which caused an inability to ambulate. Weakness progressed to include the upper extremities despite adequate control of eosinophilia by steroids. Worsening of the peripheral neuropathy can occur despite lowering of the eosinophil levels. ( info)

9/234. Loffler's endomyocarditis in the idiopathic hypereosinophilic syndrome.

    The idiopathic hypereosinophilic syndrome (HES) is a leukoproliferative disorder characterized by sustained eosinophilia (> 1.5 x 10(9)/l) and (multi-)organ dysfunction caused by infiltration of eosinophils. Especially the heart is frequently affected. In this report, we describe 2 patients with HES and Loffler's endomyocarditis. prednisone is the drug of choice for treatment. Both our patients responded very well to prednisone and came into remission. If prednisone fails, there are other therapeutic options like myelosuppressive drugs (hydroxyurea and vincristine) or interferon-alpha. We review the literature with regard to clinical presentation, diagnosis and treatment. ( info)

10/234. Surgical treatment of tricuspid regurgitation caused by Loffler's endocarditis.

    A 25-year-old man with a history of bone-marrow-transplantation for the treatment of Loffler's endocarditis underwent surgery for massive tricuspid regurgitation with paroxysmal atrial flutter. Dense fibrosis in the right ventricular endocardium with complete obliteration of the apex was seen intraoperatively, and the right ventricular cavity was diminished. Annular dilatation of the tricuspid valve and entrapment of the posterior leaflet to the endocardial fibrosis were also seen. Annuloplication at the posterior leaflet was performed. In addition, the right atrial free wall was widely resected and the septal and inferior vena cava-tricuspid valve isthmi were cryoablated for the treatment of atrial flutter. Postoperative catheterization revealed rather high right ventricular end-diastolic pressure. However, tricuspid regurgitation disappeared with the increased cardiac output. atrial flutter could not be induced by repetitive stimulation in the postoperative electrophysiological examination. ( info)
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