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Basophils possess membrane bound IgE molecules, and immunological activation leads to a secretory process with cell degranulation and histamine release. Heterologous anti IgE, concanavaline A, and phytohaemagglutinin are potent non-cytotoxic releasing agents. They operate by a mechanism similar to that of immunological activation. Heavy water is not a histamine releasing inducer but it increases histamine release of the cells. We studied the histamine release reaction of leukaemic basophils in 10 patients and found a physiological response such as that previously reported with normal human basophils. [ABSTRACT FROM PUBLISHER]

Seven patients with relapsed acute leukaemia were treated with high-dose melphalan (HDM) followed by the infusion of autologous cryopreserved remission marrow. Toxicity was minimal and all seven patients had a complete response. Four patients are still in unmaintained remission at 14, 13, 10, and 3 months, the first two having received a second course of HDM to consolidate the result. The role of HDM as a form of intensification therapy for patients with acute myeloid leukaemia in first remission should be investigated. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Hypereosinophilia can cause severe cardiac complications. The association between an acute lymphoblastic leukemia and hypereosinophilia was rare. We report a case of a 29-year-old man who presented a heart failure secondary to necrotic myocarditis related to an acute eosinophilic lymphoblastic leukaemia. Exegesis: The patient developed a heart failure and secondary a cardio-embolic stroke, due to a large mobile left ventricle thrombosis. His peripheral blood showed a total white count of 28,500 leucocytes/mm3 with 18,800 eosinophils/mm3. The myelogram cytology showed precursor B-cell acute lymphoblastic leukaemia with hypereosinophilia. Conclusion: The possibility of the rapid emergence of cardiac lesions in hypereosinophilic syndromes warrants very close physician vigilance. An Echocardiography and MRI performed at the early stage and in the follow-up allow to detect and to manage these cardiac disorders. [Copyright &y& Elsevier]

This article describes the first reported case of dramatic lymphocytosis flare after initiation of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy for an indolent lymphoma. The study patient exhibited a marginal zone lymphoma with mild nodal involvement but packed infiltration of the bone marrow. After initiation of RCHOP therapy, lymphocyte count increased from 329 to 707 × 10⁹/L at day 7. Patient exhibited grade III infusion-related side effect during rituximab therapy. Lymphocyte flare was not accompanied with other clinical manifestation such as lymph node enlargement. Because patient's bone marrow aspirate showed a packed infiltration, it was hypothesized that lymphocytosis flare was a link to lymphocyte release from bone marrow and lymphocyte demargination. This report highlights the necessity to be vigilant after initiation of RCHOP therapy for lymphoma when pathologist notified a pack infiltration of the bone marrow.

We report the case of a patient bearing a T315I-mutant chronic myeloid leukemia resistant to nilotinib, successfully treated with omacetaxine and then with dasatinib. After 9 months of nilotinib, the patient achieved a major molecular response but relapsed 3 months later due to the T315I mutation. Because third-generation tyrosine kinase inhibitor was not available and the patient refused bone marrow transplantation, he received two cycles of omacetaxine. This treatment had been stopped after two cycles because of clinical intolerance, but a major molecular response and total disappearance of the T315I clone was obtained. Treatment with dasatinib was then started and after 34-month follow-up the patient is still in major molecular response, thus suggesting that eradication of the T315I mutation could be achieved without third-generation tyrosine kinase inhibitors.

Romiplostim, a thrombopoietic agent with demonstrated efficacy against immune thrombocytopenia (ITP) in prospective controlled studies, was recently licensed for adults with chronic ITP. Only France has allowed romiplostim compassionate use since January 2008. ITP patients could receive romiplostim when they failed to respond to successive corticosteroids, intravenous immunoglobulins, rituximab, and splenectomy, or when splenectomy was not indicated. We included the first 80 patients enrolled in this program with at least 2 years of follow-up. Primary platelet response (platelet count ≥ 50 × 10(9)/L and double baseline) was observed in 74% of all patients. Long-term responses (2 years) were observed in 47 (65%) patients, 37 (79%) had sustained platelet responses with a median platelet count of 106 × 10(9)/L (interquartile range, 75-167 × 10(9)/L), and 10 (21%) were still taking romiplostim, despite a median platelet count of 38 × 10(9)/L (interquartile range, 35-44 × 10(9)/L), but with clinical benefit (lower dose and/or fewer concomitant treatment(s) and/or diminished bleeding signs). A high bleeding score and use of concomitant ITP therapy were baseline factors predicting romiplostim failure. The most frequently reported adverse events were: arthralgias (26%), fatigue (13%), and nausea (7%). Our results confirmed that romiplostim use in clinical practice is effective and safe for severe chronic ITP. This trial was registered at www.clinicaltrials.gov as #NCT01013181.

Introduction: Hypereosinophilia can cause severe cardiac complications. The association between an acute lymphoblastic leukemia and hypereosinophilia was rare. We report a case of a 29-year-old man who presented a heart failure secondary to necrotic myocarditis related to an acute eosinophilic lymphoblastic leukaemia., Exegesis: The patient developed a heart failure and secondary a cardio-embolic stroke, due to a large mobile left ventricle thrombosis. His peripheral blood showed a total white count of 28,500 leucocytes/mm3 with 18,800 eosinophils/mm3. The myelogram cytology showed precursor B-cell acute lymphoblastic leukaemia with hypereosinophilia., Conclusion: The possibility of the rapid emergence of cardiac lesions in hypereosinophilic syndromes warrants very close physician vigilance. An Echocardiography and MRI performed at the early stage and in the follow-up allow to detect and to manage these cardiac disorders.

In view of the recent development of new tests of biochemistry and molecular biology the assessment of iron status should be reconsidered and updated. The French Society of Clinical Biology (SFBC) and the French Society of Hematology (Cellular Hematology Group) recommend algorithms in the diagnosis of iron deficiency and iron overload bearing in mind the best efficiency and health economy. These recommendations are based on the known sensibility and specificity of each test. The analytical requirements for the determination of the tests as well as the clinical and biological signs evoking an iron deficiency or overload are recalled.

The authors report two cases of acute myeloid leukemia with prevalent cutaneous lesions. The positivity of granulo-monocytic antibodies and the exclusive cutaneous site of the lesions drove them previously to the diagnosis of histiocytic sarcoma. These cases stress the problem of the immunological identification of cutaneous lymphomas of "histiocytic" type.