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A 21‐year‐old white man presented with marked peripheral blood eosinophilia that later evolved into acute lymphocytic leukemia (FAB2 ALL). He died precipitously from refractory congestive heart failure immediately after antileukemic therapy was started. Autopsy revealed multiorgan infiltration with eosinophils and the typical cardiac findings of Löfflers endocarditis. Clinical and pathologic features of this and the 14 other cases of ALL and the hypereosinophilic syndrome (HES) reported in the English‐language literature are described. The eosinophilia in these cases is reactive and resolves with successful leukemia remission induction. Hydroxyurea is effective in rapidly lowering eosinophil counts. Early use of hydroxyurea in this disease may improve patient survival and decrease the risk of sudden cardiac death.
A 21‐year‐old white man presented with marked peripheral blood eosinophilia that later evolved into acute lymphocytic leukemia (FAB2 ALL). He died precipitously from refractory congestive heart failure immediately after antileukemic therapy was started. Autopsy revealed multiorgan infiltration with eosinophils and the typical cardiac findings of Löfflers endocarditis. Clinical and pathologic features of this and the 14 other cases of ALL and the hypereosinophilic syndrome (HES) reported in the English‐language literature are described. The eosinophilia in these cases is reactive and resolves with successful leukemia remission induction. Hydroxyurea is effective in rapidly lowering eosinophil counts. Early use of hydroxyurea in this disease may improve patient survival and decrease the risk of sudden cardiac death.
This case represents an example of an unusual T-cell lymphoblastic leukemia/lymphoma syndrome associated with eosinophilia and myeloid malignancy in a young boy. This case is one of only five reported ''leukemic'' variants of the disease and demonstrates the importance of considering this poor prognostic diagnosis in pediatric acute lymphoblastic leukemia. This case also illustrates the importance of an interactive multidisciplinary approach to the laboratory evaluation of a leukemia patient. ' 2005 Wiley-Liss, Inc.Key terms: acute lymphoblastic leukemia; acute myeloid leukemia; hypereosinophilic syndrome; g/d cells CASE REPORT A 9-year-old African-American male presented with a 3-week history of persistent low-grade fever, pneumonia, and massive cervical adenopathy despite oral and intravenous antibiotic therapies. He also reported a history of malaise; occasional shortness of breath with exertion; intermittent, spontaneously resolving chest wall pain; and a fleeting erythematous, macular rash. He denied a history of weight loss and night sweats. His initial examination was significant for grossly visible, 3-to 4-cm, matted bilateral cervical lymph nodes, bilateral shotty inguinal nodes, and no hepatosplenomegaly or testicular masses. A hemogram performed at that time demonstrated a normal total white count with 21% eosinophils, 6% blasts, and several vacuolated neutrophils with toxic granulations. Metabolic panel including liver function tests was normal except for high levels of lactate dehydrogenase (1,179 U/L) and alkaline phosphatase (132 U/L). Chest radiograph confirmed bibasilar interstitial pneumonia with no significant adenopathy and no mediastinal mass. The patient was diagnosed with an atypical pneumonia and admitted to the hospital for intravenous antibiotics, close observation, and further evaluation. Inpatient workup showed an acute mycoplasma infection (positive for immunoglobulin M and cold agglutinins and negative for immunoglobulin G) with negative serologic results for Epstein-Barr virus, cytomegalovirus, and human immunodeficiency virus. Purified protein derivative and control panel showed no evidence of tuberculosis or mumps. The patient remained clinically stable on room air with stable blood counts during his 48-h hospital stay before being discharged on oral clarithromycin therapy.One week later, the patient was readmitted due to progressively enlarging cervical adenopathy and respiratory distress. Hemogram showed worsening anemia, persistent blasts (4%), and increased eosinophilia (43%). Sedimentation rate was increased at 97. Repeat chest radiograph showed persistent pneumonia with bilateral perihilar adenopathy. Computed tomograms of the chest, abdomen, and pelvis demonstrated extensive bilateral submental, cervical, supraclavicular, mediastinal, perihilar, axillary, retroperitoneal, mesenteric, and inguinal lymphadenopathies. Multiple, heterogeneous, low-attenuation lesions consistent with lymphoma were noted in the spleen.
We report a case of hypereosinophilic syndrome associated with acute lymphoblastic leukemia (L1 type, FAB classification) which showed an abnormal karyotype. An 8-year-old boy was admitted to our hospital with complaints of fever and cough that had persisted for 2 weeks. Peripheral blood examination revealed remarkable eosinophilia (120,000/mm3) and a few lymphoblasts. Bone marrow examination also revealed many mature eosinophils and 20% lymphoblasts that were PAS and peroxidase negative. A direct chromosome analysis of the bone marrow cells demonstrated that 12.5% of the spontaneously dividing cells had an abnormal karyotype of 46XY, t(5;14) (q31;q32). The chest radiogram showed interstitial pneumonia-like densities, and the ECG had the pattern of a right bundle branch block. The therapy consisted of prednisolone, high dose of methylprednisolone, cyclophosphamide, and vincristine. This treatment failed to reduce the eosinophil count. On the 4th day after admission, the patient developed severe dyspnea, complete A-V block, and died. At postmortem, dense infiltrations of eosinophils in various stages of maturation were noted in lungs and liver.
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