Clostridium difficile infection (CDI) is one of the most common causes of nosocomial infectious diarrhea in children during anticancer therapy or undergoing hematopoietic stem cell transplantation (HSCT) in Europe. Immunosuppression in these patients is a risk factor for CDI. Malignant diseases, age, acute graft-versus-host disease (aGVHD), HLA mismatch, or use of total body irradiation may play an important role in CDI course. The aim of this study was to evaluate the incidence, course, and outcome of CDI in children treated for malignancy or undergoing HSCT. Between 2012 and 2015, a total number of 1846 patients were treated for malignancy in Polish pediatric oncological centers (PHO group) and 342 underwent transplantation (HSCT group). In PHO group, episodes of CDI occurred in 210 patients (14%). The incidence of CDI was higher in patients with hematological malignancies in comparison to that with solid tumors. Patients with acute myeloblastic leukemia had shorter time to episode of CDI than those with acute lymphoblastic leukemia. Patients over 5 years and treated for acute leukemia had more severe clinical course of disease in PHO group. In HSCT group, CDI occurred in 29 (8%) patients. The incidence of CDI was higher in patients transplanted for acute leukemia. The recurrence rate was 14.7% in PHO and 20.7% in HSCT patients. CDI incidence was highest in patients with hematological malignancies. Most of patients experienced mild CDI. Age < 5 years and diagnosis other than acute leukemia were the positive prognostic factors influencing clinical CDI course.

Background: Childhood acute lymphoblastic leukemia (ALL) survivors are at an increased risk of cardiovascular disease including arterial hypertension (AH). The objectives of this study were to assess the prevalence of AH using 24-hour ambulatory blood pressure monitoring, explore characteristics of AH, and define risk factors for the development of AH in childhood ALL survivors. Patients and Methods: The study comprised 81 childhood ALL survivors (5 to 25 y of age) after a median follow-up time of 5 years. The control group consisted of 52 healthy children (5 to 17 y of age) without any known severe or chronic medical condition. Ambulatory blood pressure monitoring was performed in all patients and controls. Serum lipids were measured in all patients and controls. Results: ALL survivors were more likely to have AH than controls (odds ratio, 2.47; 95% confidence interval, 1.08-5.63; P=0.0315). The mean time from ALL diagnosis until diagnosis of AH was 5.1±2.97 years. Day-time diastolic SDS and day-time mean arterial pressure SDS were significantly higher in ALL cohort compared with the controls (−0.3±1.43 vs. −0.76±0.95; P=0.04 and 1.44±1.64 vs. 0.92±1.03; P=0.047). Childhood ALL survivors with AH were more likely to be systolic extreme dippers and reverse systolic/diastolic dippers compared with those with normal blood pressure (P<0.05). There was no association of AH with leukemia subtype, leukemia risk group, sex, central nervous system irradiation, and obesity. Conclusions: The prevalence of AH in childhood ALL survivors may be as high as 37%. We recommend regular monitoring of blood pressure in childhood ALL survivors early in the follow-up.

Conclusions:The study confirms that the reduced intensity protocols are very effective in ML-DS patients. The only cause of deaths was toxicities; however, systematic decrease of the treatment-related mortality was noticed.

Background: The aim of the study was to analyze the treatment outcome and genetic characteristics of acute promyelocytic leukemia (APL) in children in Poland from 2005 to 2018. Methods: All 41 patients diagnosed with APL in Poland during the analysis period were eligible for the study. In period I (2005-2015), 33 patients were treated with chemotherapy and all-trans retinoic acid (ATRA), and in period II (2015-2018), 3 patients (high risk) received induction chemotherapy with ATRA and arsenic trioxide (ATO), and 5 patients (standard risk) received ATRA and ATO without chemotherapy. Results: Probability of 5-years overall survival (OS), event-free survival (EFS), and relapse-free survival (RFS) was 0.819 ± 0.069, 0.831 ± 0.063, and 0.961 ± 0.037, respectively, in the whole cohort. Four (11%) early deaths were observed. One patient died of severe infection in the course of disease progression. Relapse occurred in one patient, who died finally because of disease progression. All events occurred in the patients from period I. Variant APL was identified in one patient (successfully treated with chemotherapy with ATRA) and complex translocation in one patient (the only patient with relapse). Additional chromosomal aberrations were found in 26% of patients and Czogała et al. Pediatric APL-Outcome and Genetics FLT3-ITD mutation was detected in 44% of patients; none of those changes influenced clinical outcome. Conclusion: Treatment outcome in the analyzed group is similar to the results reported by other study groups. The main cause of death was coagulation disorders in the early stage of disease. Early, accurate diagnosis followed by specific treatment enables the reduction in the number of early deaths.

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It is well known that the rate of arterial hypertension (AH) in childhood acute lymphoblastic leukemia (ALL) survivors is significantly higher than that in the healthy pediatric population; however, the mechanism of this phenomenon is not fully understood. The developing cardiovascular system in children is thought to be highly susceptible to the toxic effects of chemotherapy, which causes damage to the blood vessel wall, including the endothelium. Endothelin-1 (ET-1) is a marker of endothelial damage, and it contributes to AH. Endothelial progenitor cells (EPCs) are derived from the bone marrow and participate in the process of blood vessel repair. The aim of this study was to determine the relationship between the rate of circulating EPCs and plasma levels of ET-1 with respect to hypertension in childhood ALL survivors. The study included 88 childhood ALL survivors and 44 healthy children as controls. All patients and controls had 24-h blood pressure monitoring with a HolCARD CR-07 device. The number of EPCs and the ET-1 serum concentration were measured in the peripheral blood of patients and controls using flow cytometry and enzyme-linked immunosorbent assay, respectively. A correlation was found between the number of EPCs and the ET-1 concentration in the peripheral blood of healthy children and normotensive ALL survivors. However, such a correlation was not found in hypertensive childhood ALL survivors. We conclude that dysregulation of the 'ET-1 and EPC axis' may contribute to the development of AH in some childhood ALL survivors.

Background: From 1983, standardized therapeutic protocols for pediatric acute myeloid leukemia (AML) based on the BFM group experience were introduced in Poland. We retrospectively analyzed the results of pediatric AML treatment in Poland from 1983 to 2019 (excluding promyelocytic, therapy-related, biphenotypic, and Down syndrome AML). Methods: The study included 899 children suffering from AML treated with the following: AML-PPPLBC 83 (1983–1993, n = 187), AML-PPGLBC 94 (1994–1997, n = 74), AML-PPGLBC 98 (1998–2004, n = 151), AML-BFM 2004 Interim (2004–2015, n = 356), and AML-BFM 2012 (2015–2019, n = 131). Results: The probability of three-year overall survival was 0.34 ± 0.03, 0.37 ± 0.05, 0.54 ± 0.04, 0.67 ± 0.03, and 0.75 ± 0.05; event-free survival was 0.31 ± 0.03, 0.34 ± 0.05, 0.44 ± 0.04, 0.53 ± 0.03, and 0.67 ± 0.05; and relapse-free survival was 0.52 ± 0.03, 0.65 ± 0.05, 0.58 ± 0.04, 0.66 ± 0.03, and 0.78 ± 0.05, respectively, in the subsequent periods. A systematic reduction of early deaths and deaths in remission was achieved, while the percentage of relapses decreased only in the last therapeutic period. Surprisingly good results were obtained in the group of patients treated with AML-BFM 2012 with unfavorable genetic abnormalities like KMT2A-MLLT10/t(10;11)(p12;q23) and DEK-NUP214/t(6;9)(p23;q24), while unsatisfactory outcomes were found in the patients with FLT3-ITD. Conclusions: The use of standardized, systematically modified therapeutic protocols, with the successive consideration of genetic prognostic factors, and advances in supportive care led to a significant improvement in AML treatment outcomes over the last 40 years.

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