Autism spectrum disorders (ASD) are a heterogeneous group of neurodevelopmental disorders characterized by a number of dysfunctions in communication, social interactions and repetitive rigid patterns of behavior, interests, and activities. Despite much research, the causes of ASD remain elusive. In addition to genetic and epigenetic etiology, scientists have indicated inflammation, deregulation of cytokines, anti-brain autoantibodies, gut microbiota, and deregulated immunity as mechanisms possibly involved in the development of ASD phenotype. The aim of the study was to analyze the levels of IgA, IgE, and IgM immunoglobulins in the blood serum in patients with ASD to find out whether certain blood parameters are deregulated in that group of patients. The results suggest altered production of the immune cells in ASD patients which may be considered in the assessment of immune functions. Also, PCT% and LYMPH elevated values in patients with ASD might be of clinical relevance, possibly of predictive value for clinical preliminary diagnosis and therapy.

The growing number of patients after oncological treatment makes knowledge about potential cardiovascular complications of cancer therapy particularly important. Early recognition of symptoms enables the rapid initiation of appropriate therapy and improves outcomes. Education in this field increases awareness of the need for regular cardiology follow-up and adherence to health recommendations. It is advisable for patient education on the risk of cardiotoxicity to be included during visits with both the oncologist and the cardiologist. A self-developed questionnaire was used. It consisted of 40 questions (including 16 from the Health Behavior Scale) and 8 additional sociodemographic questions. An anonymous questionnaire was completed by 243 patients of the cardio-oncology outpatient clinic operating within the Department of Cardiology in Poland. In the survey conducted, patients were asked to define the concept of cardio-oncology; only 23.5% of respondents provided a correct answer. The highest level of awareness was observed among individuals under the age of 40 (p = 0.001) and of higher education levels (p < 0.001). Better knowledge was also noted among respondents who recalled being informed by their doctor about complications (p < 0.001) and among those who had undergone cardiological examinations (p = 0.005). The findings further revealed that respondents who recognized the importance of cardiac monitoring following therapy were significantly more likely to engage in health behaviors (p < 0.001). Particularly concerning was the limited communication regarding cardiovascular risks associated with cancer treatment. Only 24.3% of patients reported having been informed (or recalled being informed) by their oncologist about the potential cardiotoxic effects of anticancer drugs. Approximately one-third of respondents (32%) had not been referred for a cardiology consultation during their cancer treatment. Despite this, an overwhelming majority (95.5%) expressed the belief that a cardiologist should assess all oncology patients. These findings underscore critical deficiencies in patients’ education within the field of cardio-oncology. Health education interventions during oncological follow-up visits are needed

Cancer therapy-related cardiovascular toxicity (CTR-CVT) is an umbrella term for myocardial, vascular, electrical, and inflammatory complications of cytotoxic, targeted, immune, and radiation-based therapies. Cancer therapy-related cardiac dysfunction (CTRCD) is used here more narrowly for treatment-related myocardial dysfunction, typically identified by changes in left ventricular ejection fraction, global longitudinal strain, and/or cardiac biomarkers. The pathophysiology of CTR-CVT is multifactorial, but the implicated pathways should not be interpreted as equally causal. The dominant initiating mechanism is therapy-specific - anthracycline injury is best supported by topoisomerase IIβ (TOP2B)-mediated DNA damage with secondary mitochondrial and redox injury; HER2-directed toxicity by disruption of NRG1-ERBB2/ERBB4 survival signalling; fluoropyrimidine toxicity by coronary vasomotor dysfunction; VEGF-pathway inhibition by endothelial dysfunction and hypertension; immune checkpoint inhibitor toxicity by loss of immune tolerance; and radiotherapy injury by endothelial and microvascular damage with progressive fibrosis. Mitochondrial dysfunction, oxidative stress, inflammation, calcium dysregulation, apoptosis, and ferroptosis frequently act as downstream or amplifying pathways, although the clinical relevance of several regulated cell-death mechanisms remains incompletely established. Genetic susceptibility may further modify risk, but the strength of evidence differs among reported loci. Replicated pharmacogenetic associations, rare variants in established cardiomyopathy genes, and preliminary candidate-gene findings should therefore be considered separately. Most available studies remain limited by small cohorts, heterogeneous phenotyping, ancestry imbalance, and incomplete external replication. This review critically evaluates the hierarchy and strength of mechanistic and genetic evidence and discusses the extent to which these findings can currently inform risk stratification, surveillance, prevention, and treatment in precision cardio-oncology. Graphical Abstract