Chest pain in children and adolescents is a common reason for emergency department visits and referrals to pediatric cardiologists, often driven by parental concern about potential cardiac causes. However, the vast majority of pediatric chest pain cases are benign and non-cardiac in origin. This narrative review examines the etiology, evaluation, and management of pediatric chest pain, emphasizing the importance of a thorough clinical history and physical examination in distinguishing between benign and serious conditions. This review also explores the role of diagnostic tests such as electrocardiograms, chest radiography, and echocardiography, highlighting the need to balance the avoidance of unnecessary tests with the imperative to rule out life-threatening cardiac conditions. Despite the low prevalence of cardiac causes, the variability in diagnostic approaches underscores the need for standardized evaluation algorithms. These could streamline care, reduce unnecessary resource utilization, and minimize anxiety for both patients and their families. Future studies should focus on assessing the effectiveness of such algorithms in improving clinical outcomes and resource management. The findings underscore the importance of a careful, evidence-based approach to the management of pediatric chest pain.

The COVID-19 pandemic has catalyzed the rapid expansion of telemedicine for managing chronic conditions such as type 1 diabetes (T1D) in children and adolescents. This narrative review aims to explore the role of telemedicine in pediatric T1D management by comparing its use before and after the pandemic. We conducted a comprehensive literature review covering studies published between 2000 and 2024, focusing on telemedicine applications in pediatric T1D care. The review includes clinical trials, systematic reviews, and observational studies examining telemedicine’s impact on glycemic control, patient satisfaction, and healthcare delivery. Results reveal that telemedicine has enhanced access to care, improved glycated hemoglobin (HbA1c) levels, and reduced diabetic ketoacidosis and hypoglycemic events. Patients and caregivers expressed high satisfaction, especially when using continuous glucose monitoring and insulin pump technologies integrated with telemedicine platforms. However, challenges such as digital literacy gaps, variability in healthcare provider training, and logistical issues like reimbursement policies persist. The pandemic highlighted the potential of telemedicine to supplement traditional in-person care, showing promise in enhancing patient outcomes and reducing healthcare burdens. Further research is needed to optimize telemedicine models for T1D, addressing barriers to implementation and exploring its long-term cost-effectiveness. This review underscores telemedicine’s evolving role as a complementary approach in managing pediatric T1D, advocating for the development of standardized care protocols to fully integrate digital health solutions into routine clinical practice.

Background: β-haemoglobinopathies, including sickle cell disease and transfusion-dependent β-thalassaemia, are among the most common monogenic disorders worldwide and represent a major global health burden. Conventional treatments, such as blood transfusions, iron chelation, fetal haemoglobin induction, and allogeneic haematopoietic stem cell transplantation, have im-proved outcomes but remain limited by treatment-related toxicity, donor availability, and incom-plete curative potential. Methods: A narrative literature review was conducted using PubMed up to 2025. Search terms included “sickle cell disease,” “sickle cell anemia,” “β-thalassemia,” “transfu-sion-dependent beta-thalassemia,” “gene therapy,” “gene addition,” “gene editing,” “CRISPR-Cas9,” “lentiviral vector,” “children,” “paediatric,” and “pediatric.” Relevant clinical tri-als, reviews, consensus statements, and guidelines were selected and qualitatively analysed. Results: Gene therapy for β-haemoglobinopathies is based mainly on two strategies: gene addition and gene editing. Gene addition uses lentiviral vectors to introduce functional or modified β-globin genes into autologous haematopoietic stem cells, whereas gene editing targets regulatory pathways, particu-larly BCL11A, to reactivate fetal haemoglobin synthesis or correct disease-causing mutations. Clin-ical studies have shown encouraging outcomes, including transfusion independence in many pa-tients with β-thalassaemia and marked reduction or elimination of vaso-occlusive crises in sickle cell disease. Paediatric and adolescent data are increasingly promising, although still limited. Conclu-sion: Gene therapy is reshaping the treatment landscape of β-haemoglobinopathies by offering a personalised and potentially curative approach. However, long-term safety, conditioning toxicity, fertility preservation, accessibility, costs, and implementation in high-prevalence regions remain critical challenges. Further studies are needed to optimise patient selection and expand equitable access.

Background: β-haemoglobinopathies, including sickle cell disease and transfusion-dependent β-thalassaemia, are among the most common monogenic disorders worldwide and represent a major global health burden. Conventional treatments, such as blood transfusions, iron chelation, fetal haemoglobin induction, and allogeneic haematopoietic stem cell transplantation, have improved outcomes but remain limited by treatment-related toxicity, donor availability, and incomplete curative potential. Methods: A narrative literature review was conducted using PubMed up to 2025. Search terms included “sickle cell disease,” “sickle cell anemia,” “β-thalassemia,” “transfusion-dependent beta-thalassemia,” “gene therapy,” “gene addition,” “gene editing,” “CRISPR-Cas9,” “lentiviral vector,” “children,” “paediatric,” and “pediatric.” Relevant clinical trials, reviews, consensus statements, and guidelines were selected and qualitatively analysed. Results: Gene therapy for β-haemoglobinopathies is based mainly on two strategies: gene addition and gene editing. Gene addition uses lentiviral vectors to introduce functional or modified β-globin genes into autologous haematopoietic stem cells, whereas gene editing targets regulatory pathways, particularly BCL11A, to reactivate fetal haemoglobin synthesis or correct disease-causing mutations. Clinical studies have shown encouraging outcomes, including transfusion independence in many patients with β-thalassaemia and marked reduction or elimination of vaso-occlusive crises in sickle cell disease. Paediatric and adolescent data are increasingly promising, although still limited. Conclusions: Gene therapy is reshaping the treatment landscape of β-haemoglobinopathies by offering a personalised and potentially curative approach. However, long-term safety, conditioning toxicity, fertility preservation, accessibility, costs, and implementation in high-prevalence regions remain critical challenges. Further studies are needed to optimise patient selection and expand equitable access.