2008/02/01 by Óscar Sans Capdevila, Ehab Dayyat, David Gozal · 1 citation
Medicine · Neuroscience · #Bioinformatics #Biology #Clinical phenotype #Diabetes mellitus #Disease #Endocrine system #Endocrinology #Gastroesophageal reflux and treatments #Genetics #Hormone #Intensive care medicine #Internal medicine #Medicine #Neuroscience of respiration and sleep #Obstructive Sleep Apnea Research #Obstructive sleep apnea #Pathology #Pediatrics #Phenotype #Sleep apnea #Type 2 diabetes
paper · doi:10.1513/pats.200708-138mg
openalex publication_date 2008/02/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/04
Obstructive sleep apnea (OSA) in children has emerged not only as a relatively prevalent condition but also as a disease that imposes a large array of morbidities, some of which may have long-term implications, well into adulthood. The major consequences of pediatric OSA involve neurobehavioral, cardiovascular, and endocrine and metabolic systems. The underlying pathophysiological mechanisms of OSA-induced end-organ injury are now being unraveled, and clearly involve oxidative and inflammatory pathways. However, the roles of individual susceptibility (as dictated by single-nucleotide polymorphisms), and of environmental and lifestyle conditions (such as diet, physical, and intellectual activity), may account for a substantial component of the variance in phenotype. Moreover, the clinical prototypic pediatric patient of the early 1990s has been insidiously replaced by a different phenotypic presentation that strikingly resembles that of adults afflicted by the disease. As such, analogous to diabetes, the terms type I and type II pediatric OSA have been proposed. The different manifestations of these two entities and their clinical course and approaches to management are reviewed.