Introduction Symptomatic venous thromboembolism (VTE) is diagnosed in 3%–14% of patients during pediatric acute lymphoblastic leukemia (ALL) therapy. There are well‐known risk factors, but the role of others as inherited thrombophilia is still controversial. Prophylaxis with low molecular weight heparin (LMWH) has been described, but its use is not globally accepted. Methods A retrospective multicentric study in ALL patients 1–18 years old following SEHOP‐PETHEMA‐2013 treatment guideline was performed to evaluate VTE rate, anticoagulant treatment, outcome, risk factors, and safety and usefulness of LMWH administration as primary thromboprophylaxis in children with inherited thrombophilia. Results A total of 652 patients were included in the study. VTE incidence was 8.7%. Most of the cases occurred during induction therapy associated with central venous catheter. Univariant analysis showed that family history of thrombosis, presence of mediastinal mass, high‐risk treatment group, and inherited thrombophilia were statistically significant risk factors. LMWH administration seemed to decrease VTE rate in patients with inherited thrombophilia and those with T‐cell ALL phenotype. Conclusion Most of the VTE cases occurred in patients without inherited thrombophilia, but when it is present, the VTE risk is higher. LMWH administration was useful to decrease VTE in these patients.

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Introduction: Children and adolescents treated with anthracyclines are at increased risk of developing cardiomyopathy. Although several guidelines are available, no consensus exists on an optimal strategy scheme for predict or avoid anthracycline-induced cardiotoxicity. Methods: Cardiotoxicity was defined as a reduction in left ventricle ejection fraction >10% from baseline and <53%, and/or global longitudinal strain drop of >15%.The incidence of cardiotoxicity, its relation with cumulative anthracycline doses, clinical significance and reversibility were retrospectively evaluated in a paediatric population (0-18 years) treated with anthracycline at a tertiary hospital (2010-2020). Analysis of 3 genetic polymorphisms related to cardiotoxicity (RARG (rs2229774), SLC28A3(rs7853758) and UGT1A6(rs17863783)) was performed. Results: A total of 84 patients (45 males) were included. The mean age at diagnosis was 10.7± 3.8 years with average cumulative anthracycline dose 195 mg/m2 (60-460mg/m2). Median follow-up was 5 years. Anthracycline-induced cardiotoxicity occurred in 12 (14,2%) of treated patients, 75% were asymptomatic. 5 patients experimented acute cardiotoxicity during treatment. 8 patients were treated with ACE-inhibitors and/or beta-blockers. 11 patients had full function recovery. Cumulative doxorubicin dose was a risk factor of cardiotoxicity, being affected 9/20 treated with >250 mg/m2; 3/51 treated with 100-250m2; while no patient out of 13 receiving <100 mg/m2 had an abnormal echocardiogram (P <0.01). A higher percentage of patients treated with mediastinum radiation and chemotherapy (3/7:42%) presented cardiotoxicity compared to those with chemotherapy only (9/77:9%) (p0.09). Younger age, female sex or the presence of genetic polymorphisms studied were not statistically significant risk factors. Conclusions: Dose-dependent anthracycline risk for developing cardiomyopathy was confirmed. However, previously identified risk factors including female sex, early age at diagnosis and genetic polymorphism were not replicated in this population, possibly due to the small sample size and the relatively short follow-up period. A tailored monitoring strategy based on cardiac risk stratification is needed.