LAUSR

Sleep apnoea-hypopnoea syndrome (SAHS) is a disease that affects 2%--4% of the paediatric population.1,2 It consists in the recurrent collapse of the airway during sleep with cessation or reduction of airflow resulting in cycles of hypoxia followed by reoxygenation that in the long term can trigger an inflammatory cascade with systemic effects.2,3 One of the differences between SAHS in children and in adults is the type of repercussions it has on health. Thus, in the paediatric population the most frequent repercussions are growth delay and neurocognitive complications, while daytime somnolence and cardiovascular complications are more frequent in adults. One of the haematologic changes described in adults with SAHS is an increased haemoglobin concentration,4,5 in some cases in the range of polycythaemia,5 and such changes are believed to be secondary to an increased secretion of erythropoietin resulting from the recurrent hypoxia during sleep. Recently, some authors have started to analyse other factors,5 as not every patient with severe SAHS exhibits these changes. In addition, there is evidence of a directly proportional correlation between the severity of SAHS and the increase in the red blood cell distribution width (RDW).3 The RDW is currently being investigated as a proinflammatory marker (not only in the context of cardiovascular disease), and probably increases as a result of oxidative stress and chronic inflammation, which cause the release of cytokines that could act on the bone marrow and affect erythropoiesis.3 It has also been hypothesised that this association may be influenced by increased neurohormonal activity.3 Other factors that have been studied in the paediatric population include signs of metabolic disturbances, such as elevation of glycated haemoglobin in patients with SAHS,