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Remission Induction (remission + induction)

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Medical Sciences100%

Terms modified by Remission Induction

  • remission induction therapy
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    Selected Abstracts

    Remission induction, consolidation and novel agents in development for adults with acute myeloid leukaemia

    HEMATOLOGICAL ONCOLOGY, Issue 1 2010
    Mehdi Hamadani
    Abstract Chemotherapy regimens used for remission induction in AML have not changed significantly over the last several decades. However the recognition of the prognostic value of cytogenetics and genomics has been a major advance which is helping clarify the most optimal post-remission consolidation strategy among various risk groups. We are not only beginning to realize the pitfalls of a ,one-fits-all' approach with intensive, cytarabine-based chemotherapy as the mainstay, but we are finally beginning to reap the rewards of decades of basic, translational, and clinical research. Developing individualized, ,targeted' therapy for each AML patient based on unique molecular features of disease remains a daunting goal yet one that we can now begin to envision. Hypothesis-based study designs,from pre-clinical/laboratory experiments to phase-I and subsequent efficacy trials,provide the foundation for advances in the diagnosis, risk stratification, and treatment for patients with AML. Here we critically review the literature for the management of AML, try to give recommendations regarding the appropriate induction and remission strategy, clarify the role of stem cell transplantation and discuss novel agents on the horizon. Copyright © 2009 John Wiley & Sons, Ltd. [source]

    Advances in paediatric rheumatology: Beyond NSAIDs and joint replacement

    JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2004
    JE Munro
    Over the previous three decades there have been a number of dramatic changes in our understanding of both the pathogenesis and epidemiology of the rheumatic diseases of childhood. Improvements in the classification of paediatric-onset arthritides and international collaboration in terms of multicentre research have led to the development of new therapeutic agents and better methods of outcome assessment for these chronic and often disabling conditions. Fortunately for children with paediatric rheumatic diseases treatment regimes are now available that provide excellent disease control for many and remission induction for some. Challenges include clearer definition of the genetics and pathogenesis of the diseases, delineation of reliable biological markers for diagnosis and monitoring of disease activity. The future should also herald early identification of those with a poorer prognosis, together with the design of more powerful, safer and cheaper remission-inducing agents, given to the right patients at the right time. [source]

    Prospective study of hemostatic alterations in children with acute lymphoblastic leukemia,

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2010
    Paola Giordano
    In a group of newly diagnosed acute lymphocytic leukemia (ALL) children we evaluated a number of hemostatic and inflammatory markers at diagnosis and at different time points during chemotherapy for the remission induction to identify alterations in the plasma levels of prothrombotic markers before and during the course of chemotherapy. The following plasma markers were evaluated: thrombin-antithrombin complex (TAT), D-Dimer, plasminogen activator inhibitor 1 (PAI-1), antithrombin, fibrinogen, von Willebrand factor (VWF) antigen and high molecular weight VWF (HMW-VWF) multimers, P-selectin, tumor necrosis factor alpha (TNF-,), and interleukin 6 (IL-6). Plasma samples were collected at the following time points: at T0 (baseline) and T1 (+24 days of therapy), T2 (+36 days therapy), and T3 (+64 days therapy). The results show that, at diagnosis, ALL children presented with laboratory signs of increased thrombin generation and fibrin formation (i.e. high TAT and D-dimer levels), fibrinolysis inhibition (i.e. high PAI-1 level), endothelial activation (i.e., high HMW-VWF and soluble P-selectin levels) and inflammation (i.e. high TNF-alpha and IL-6 levels). After starting induction therapy, the thrombin generation markers and inflammatory cytokines significantly decreased. To the opposite, PAI-1 and P-selectin significantly increased, suggesting an insult by chemotherapy on the vascular endothelium. These effects were more evident during steroid administration. Symptomatic venous thromboembolism (VTE) episodes developed in two cases during induction therapy, which did not allow the evaluation of the predictive value for VTE of laboratory markers. Am. J. Hematol., 2010. © 2010 Wiley-Liss, Inc. [source]

    Urinary CD4+ effector memory T cells reflect renal disease activity in antineutrophil cytoplasmic antibody,associated vasculitis

    ARTHRITIS & RHEUMATISM, Issue 9 2009
    Wayel H. Abdulahad
    Objective Numbers of circulating CD4+ effector memory T cells are proportionally increased in patients with proteinase 3 antineutrophil cytoplasmic antibody,associated vasculitis (AAV) whose disease is in remission and are decreased during active disease, which presumably reflects their migration toward sites of inflammation. Since renal infiltrating cells may appear in urine, we investigated the presence of CD4+ effector memory T cells in urinary sediment as a reflection of renal disease activity in AAV. Methods CD4+ effector memory (CD45RO+CCR7,CD3+CD4+) T cells were quantitated in the urine and peripheral blood of patients with AAV with renal involvement (n = 33), patients with AAV without renal involvement (n = 18), patients with AAV whose disease was in remission (n = 29), and patients with active disease (n = 22), using 4-color flow cytometric analysis. Numbers and percentages of urine CD4+ effector memory T cells in 12 patients with AAV with active renal disease were obtained over several weeks of followup during remission induction. Results A notable increase in urine CD4+ effector memory T cell numbers was observed in patients with active renal AAV compared with patients whose disease was in remission and patients with active disease without renal involvement. The increase in these cells in the urine of patients with active renal AAV was accompanied by a reciprocal decrease in these cells in peripheral blood. Results from followup analysis showed a clear reduction in urine CD4+ effector memory T cells following treatment. Moreover, a negative correlation was observed between percentages of circulating and urine CD4+ effector memory T cells, consistent with their migration toward sites of inflammation. Conclusion Our findings indicate that the presence of CD4+ effector memory T cells in urine reflects renal involvement in AAV. Flow cytometric analysis of these cells in urine may contribute to assessing renal disease activity in patients with AAV. [source]

    Acute pulmonary failure during remission induction chemotherapy in adults with acute myeloid leukemia or high-risk myelodysplastic syndrome

    CANCER, Issue 1 2010
    Ali Al Ameri MD
    Abstract BACKGROUND: Acute pulmonary failure during remission induction therapy is a serious complication in patients with acute myeloid leukemia (AML). To the authors' knowledge, the course and prognosis of such patients is not well known. METHODS: A total of 1541 patients referred for remission induction chemotherapy of AML or high-risk myelodysplastic syndrome were retrospectively reviewed. RESULTS: A total of 120 (8%) patients developed acute pulmonary failure within 2 weeks of the initiation of chemotherapy; 87 of these patients (73%) died during remission induction, whereas 17 (14%) achieved a complete response. The median survival among the 120 patients with early acute pulmonary failure was 3 weeks. Predictive factors for the development of early acute pulmonary failure by multivariate analysis were: male sex (P = .00038), acute promyelocytic leukemia (P = .00003), poor performance status (P = .001), lung infiltrates at diagnosis (P = .000001), and increased creatinine (P = .000005). Patients who had 0 to 1, 2, 3, or 4 to 5 adverse factors were found to have estimated predictive incidences of acute pulmonary failure of 3%, 13%, 23%, and 34%, respectively. CONCLUSIONS: Preventive approaches at the start of induction therapy in patients at high risk of pulmonary failure may improve the outcome of these patients. Cancer 2010. © 2010 American Cancer Society. [source]

    Haematopoietic stem cell transplantation in the treatment of severe autoimmune disease: results from phase I/II studies, prospective randomized trials and future directions

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2005
    A. Tyndall
    Summary Around 700 patients have received an autologous haematopoietic stem cell transplant (HSCT) as treatment for a severe autoimmune disease (AD). The majority of these have been within the context of phase I/II clinical trials and following international guidelines proposed 7 years ago. In general, a positive benefit/risk ratio has led to phase III prospective randomized controlled trials in multiple sclerosis (MS), systemic sclerosis (SSc) and rheumatoid arthritis (RA) in Europe. In the US, similar trials are being planned for SSc, MS and systemic lupus erythematosus (SLE). Transplant related mortality (TRM) has fallen in all disease subgroups since the inception due to more appropriate patient selection, and so far a clear advantage of the more intense myeloablative regimens in terms of remission induction and relapse rate has not emerged. Although each AD has a different profile, over a third of patients have sustained a durable remission, often with no further need for immunosuppressive drugs. In those who relapsed, many responded to agents which pre transplant had been ineffective. The study of immune reconstitution and gene expression pre and post HSCT is being undertaken to further understand the mechanism of autoimmunity. [source]