Cancer is a growing public health problem; it is responsible annually for millions of deaths worldwide. Fluoropyrimidines are highly effective and commonly prescribed anti-neoplastic drugs used in a wide range of chemotherapy regimens against several types of malignancies. 5-fluorouracil and its prodrugs affect neoplastic cells in multiple ways by impairing their proliferation, principally through the inhibition of thymidylate synthase. Fluoropyrimidine-induced cardiotoxicity was described more than 50 years ago, but many details such as incidence, mechanisms, and treatment are unclear and remain disputed. Severe cardiotoxicity is not only life-threatening, but also leads to withdrawal from an optimal chemotherapy regimen and decreases survival rate. Differences in the frequency of cardiotoxicity are explained by different chemotherapy schedules, doses, criteria, and populations. Proposed pathophysiological mechanisms include coronary vasospasm, endothelial damage, oxidative stress, Krebs cycle disturbances, and toxic metabolites. Such varied pathophysiology of the cardiotoxicity phenomenon makes prevention and treatment more difficult. Cardiovascular disturbances, including chest pain, arrhythmias, and myocardial infarction, are among the most common side effects of this class of anti-neoplastic medication. This study aims to summarize the available data on fluoropyrimidine cardiotoxicity with respect to symptoms, incidence, metabolism, pathophysiological mechanism, diagnosis, management, and resistance.

Since the establishment of a clear link between maternal alcohol consumption during pregnancy and certain birth defects, the research into the treatment of FASD has become increasingly sophisticated. The field has begun to explore the possibility of intervening at different levels, and animal studies have provided valuable insights into the pathophysiology of the disease, forming the basis for implementing potential therapies with increasingly precise mechanisms. The recent reports suggest that compounds that reduce the severity of neurodevelopmental deficits, including glial cell function and myelination, and/or target oxidative stress and inflammation may be effective in treating FASD. Our goal in writing this article was to analyze and synthesize current experimental therapeutic interventions for FASD, elucidating their potential mechanisms of action, translational relevance, and implications for clinical application. This review exclusively focuses on animal models and the interventions used in these models to outline the current direction of research. We conclude that given the complexity of the underlying mechanisms, a multifactorial approach combining nutritional supplementation, pharmacotherapy, and behavioral techniques tailored to the stage and severity of the disease may be a promising avenue for further research in humans.

Background: Fetal Alcohol Spectrum Disorder (FASD) is a consequence of prenatal alcohol exposure (PAE) associated with a range of effects, including dysmorphic features, prenatal and/or postnatal growth problems, and neurodevelopmental difficulties. Despite advances in treatment methods, there are still gaps in knowledge that highlight the need for further research. The study investigates the effect of PAE on the autonomic system, including sex differences that may aid in early FASD diagnosis, which is essential for effective interventions. Methods: During gestational days 5 to 20, five pregnant female Wistar rats were orally administered either glucose or ethanol. After 22 days, 26 offspring were born and kept with their mothers for 21 days before being isolated. Electrocardiographic recordings were taken on the 29th and 64th day. Heart rate variability (HRV) parameters were collected, including heart rate (HR), standard deviation (SD), standard deviation of normal-to-normal intervals (SDNN), and the root mean square of successive differences between normal heartbeats (RMSSD). Additionally, a biochemical analysis of basic serum parameters was performed on day 68 of the study. Results: The study found that PAE had a significant impact on HRV. While electrolyte homeostasis remained mostly unaffected, sex differences were observed across various parameters in both control and PAE groups, highlighting the sex-specific effects of PAE. Specifically, the PAE group had lower mean heart rates, particularly among females, and higher SDNN and RMSSD values. Additionally, there was a shift towards parasympathetic activity and a reduction in heart rate entropy in the PAE group. Biochemical changes induced by PAE were also observed, including elevated levels of alanine transaminase (ALT) and aspartate aminotransferase (AST), especially in males, increased creatinine concentration in females, and alterations in lipid metabolism. Conclusions: PAE negatively affects the development of the autonomic nervous system, resulting in decreased heart rate and altered sympathetic activity. PAE also induces cardiovascular abnormalities with sex-specific effects, highlighting a relationship between PAE consequences and sex. Elevated liver enzymes in the PAE group may indicate direct toxic effects, while increased creatinine levels, particularly in females, may suggest an influence on nephrogenesis and vascular function. The reduced potassium content may be linked to hypothalamus–pituitary–adrenal axis overactivity.

Introduction: Anorexia nervosa (AN) is a psychiatric disorder with a high mortality rate and significant prevalence in the paediatric population. Preliminary reports during the COVID-19 pandemic suggested an increased incidence of AN among children and adolescents. The objective of this study was to analyse new cases of AN before, during, and after the pandemic, with a particular focus on the physical manifestations of the disease. Methods: This single-centre, retrospective study included new AN cases from the hospital database of a regional paediatric hospital (a reference centre for AN) between 2013 and 2023. Data analysed included the duration of the disease, body mass index (BMI), weight loss, length of hospitalisation, laboratory markers (leukopenia, anaemia, hypoproteinaemia, hyperferritinaemia, hypophosphataemia, dyslipidaemia, and hypothyroxinaemia) and clinical features of malnutrition (such as amenorrhea bradycardia, pericardial effusion, and cortical/subcortical atrophy). Results: This study was conducted in a Polish regional hospital. We analysed 228 hospitalized female patients aged 10 to 18 years diagnosed with AN, focusing on clinical characteristics, biochemical markers, and the impact of the COVID-19 pandemic. The COVID-19 pandemic was shown to have a significant impact, with longer hospitalisations observed during and after the pandemic and a lower BMI on admission post-pandemic compared to pre-pandemic. In addition, nutritional treatment became more prevalent over time while biochemical markers such as anaemia, hypothyroidism, hypophosphataemia, and dyslipidaemia were statistically more common post-pandemic. Conclusions: This study demonstrates a significant impact of the COVID-19 pandemic on the clinical course and hospitalisation patterns of paediatric patients with AN. These findings suggest that the pandemic may have exacerbated disease severity and altered treatment approaches, emphasizing the need for enhanced clinical management and follow-up strategies for AN in the paediatric population during such health crises.

Background/Objectives: Fetal alcohol spectrum disorders comprise a range of neurodevelopmental disorders caused by prenatal alcohol exposure. Recent investigations have revealed that among patients with neurodevelopmental disorders, serum cobalamin (vitamin B12) levels are substantially higher than those of healthy controls. Patients with fetal alcohol spectrum disorders similarly present with higher levels of cobalamin, yet the significance of cobalamin in the pathogenesis of fetal alcohol spectrum disorders remains to be established. This study aimed to examine cobalamin and other cobalamin status markers in patients with fetal alcohol spectrum disorders in comparison with healthy controls. Methods: In total, 80 patients were enrolled in the study—41 diagnosed with fetal alcohol spectrum disorders and 39 healthy controls. The diet history method was used to assess vitamin B12 intake for three days preceding blood sampling. Total vitamin B12 (cobalamin), holotranscobalamin, methylmalonic acid and soluble transcobalamin receptor (CD320) were measured in serum samples. Results: The daily intake of vitamin B12 was higher in patients with fetal alcohol spectrum disorders compared to controls, both in the simple analysis and after adjusting for age (OR for patients with FASDs: 1.82; 95% CI: 1.16–2.87). An elevated serum cobalamin level was noted in some patients from the group with fetal alcohol spectrum disorders. No statistically significant differences were found between the groups in serum levels of cobalamin, holotranscobalamin, CD320 or methylmalonic acid. However, the correlations between cobalamin and its metabolites differed in fetal alcohol spectrum disorders as compared to those in the control group. Conclusions: Our study did not find any deficits of vitamin B12 and its metabolites in patients with fetal alcohol spectrum disorders. Further studies to investigate the role of vitamin B12 in the pathogenesis of fetal alcohol spectrum disorders should be established given the fact that both high and low levels of vitamin B12 may have negative health impacts.