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Objective: Anthracyclines are widely used in the treatment of acute lymphoblastic leukemia (ALL). However, cardiotoxicity is the most critical side effect that requires dose limitation. It is thought to occur at first exposure, but the clinical presentation may occur years later. In this study, we aimed to determine the time of initial damage and cardiotoxicity that develops in children with ALL. Methods: In this prospective study, 13 patients with newly diagnosed intermediate-risk precursor B cell ALL treated with the ALL-IC BFM 2009 protocol were included. Conventional echocardiography, tissue Doppler imaging (TDI), and speckle-tracking echocardiography (STE) were performed in all the patients before chemotherapy, after completing the induction phase, and at the end of the reinduction phase. Results: The mean age of the patients was 7.8±4.6 (3.1–16.3) years. Myocardial velocity during systole (Sm) determined by TDI at the interventricular septum significantly decreased during the induction phase. Despite a decrease in STE parameters, a statistically significant reduction was determined in the global longitudinal strain rate at both left and right ventricles at the end of the induction. Nevertheless, a statistically significant increase was observed among the conventional echocardiographic findings in the left ventricular end-diastolic diameter at the end of the reinduction. Conclusion: During the treatment of ALL, subclinical anthracycline-associated cardiotoxicity develops in the early stages of treatment. The findings detected by TDI and STE could be missed by conventional echocardiography. We recommend evaluating patients with these newly developed techniques to detect subclinical cardiotoxicity at an early stage and starting appropriate therapy on time. [ABSTRACT FROM AUTHOR]

Background. Febrile neutropenia (FN) is a common and serious complication in patients with leukemia. Hemostasis and inflammation are two interrelated systems in response to infection. We aimed to investigate the course of thrombin formation in febrile neutropenia attack of children with acute lymphoblastic leukemia (ALL). Methods. Thrombin generation was monitored in children treated for ALL at diagnosis of febrile neutropenia (FN) (t0), at 48th hour of FN (t1) and after recovery from neutropenia (t2). Results. Twenty-nine patients and 50 healthy children as control were enrolled into the study. Mean endogenous thrombin potential (ETP) and mean peak value of thrombin results at t1 were significantly higher than at t0, t2 and control groups, respectively. A positive but statistically nonsignificant correlation between ETP values at t1 and duration of neutropenia was observed. Conclusion. Although thrombin generation is enhanced both due to chemotherapy or malignancy itself, our results revealed that thrombin formation also increased in neutropenic infection of children with leukemia. [ABSTRACT FROM AUTHOR]

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