Common variable immunodeficiency (CVID) is the most common symptomatic antibody deficiency, characterized by heterogeneous genetic, immunological, and clinical phenotypes. It is no longer conceived as a sole disease but as an umbrella diagnosis comprising a spectrum of clinical conditions, with defects in antibody biosynthesis as their common denominator and complex pathways determining B and T cell developmental impairments due to genetic defects of many receptors and ligands, activating and co-stimulatory molecules, and intracellular signaling molecules. Consequently, these genetic variants may affect crucial immunological processes of antigen presentation, antibody class switch recombination, antibody affinity maturation, and somatic hypermutation. While infections are the most common features of pediatric CVID, variants in genes linked to antibody production defects play a role in pathomechanisms of immune dysregulation with autoimmunity, allergy, and lymphoproliferation reflecting the diversity of the immunogenetic underpinnings of CVID. Herein, we have reviewed the aspects of genetics in CVID, including the monogenic, digenic, and polygenic models of inheritance exemplified by a spectrum of genes relevant to CVID pathophysiology. We have also briefly discussed the epigenetic mechanisms associated with micro RNA, DNA methylation, chromatin reorganization, and histone protein modification processes as background for CVID development.

Sleep problems are one of the key, but insufficiently addressed, health issues in children and adolescents. 40-50 % of youth are thought to be impacted by them. This review examines the connections between sleep disorders (SD) and mental health conditions such as anxiety disorders, bipolar disorder, depression, ADHD, and eating disorders, such as anorexia nervosa, bulimia nervosa, binge eating disorder, night eating disorder, and aversive-restrictive food intake disorder, revealing the interrelationships between these phenomena. Various SDs, such as insomnia, obstructive sleep apnea, circadian rhythm disorders, and chronotype, are investigated. SD can be correlated with and caused by the development of mental health disorders, as well as be a direct consequence or exacerbating factor. During adolescence, sleep disruption exacerbates heterogeneously the susceptibility to disordered mental health. It hinders its treatment, leading to chronic symptoms and a significant deterioration in quality of life, creating a vicious cycle. We explore and attempt to integrate the neurobiological pathophysiology of disorders and their connections to sociobehavioral concepts of psychopathology in this article. This comprehensive review provides an overview of the most recent findings on SD, with emphasis on how they affect mental health in childhood and adolescence. Additionally, it highlights the use of pharmacological and behavioral approaches to the treatment of insomnia, with and without comorbidities. The study aims to encourage clinicians to broaden their awareness of the interdisciplinary nature of sleep and mental health, which is essential to the care of young patients.

Common variable immunodeficiency (CVID) is the most common symptomatic antibody deficiency, characterized by heterogeneous genetic, immunological, and clinical phenotypes. It has no longer been conceived as a sole disease but as an umbrella diagnosis comprising a spectrum of clinical conditions with defects in antibody biosynthesis as their common denominator and complex pathways determining B and T cell developmental impairments due to genetic defects of many receptors and ligands, activating and co-stimulatory molecules, and intracellular signaling molecules. Consequently, these genetic variants may affect crucial immunological processes of antigen presentation, antibody class switch recombination, antibody affinity maturation, and somatic hypermutation. While infections are the most common features of pediatric CVID, variants in genes linked to antibody production defects play a role in pathomechanisms of immune dysregulation with autoimmunity, allergy, and lymphoproliferation reflecting the diversity of the immunogenetic underpinnings of CVID. Herein, we have reviewed the aspects of genetics in CVID, including the monogenic, digenic, and polygenic models of inheritance exemplified by a scope of genes relevant to CVID pathophysiology. We have also briefly discussed the epigenetic mechanisms associated with micro RNA, DNA methylation, chromatin reorganization, and histone protein modification processes as background for CVID development.