In our study, we provided intriguing evidence for a worse cardiometabolic profile in a cohort of non-obese children with OSAS.
Sleep-Related Breathing Disorders (SRDB) are common in children and adolescents [39–41], with a different severity ranging from primary snoring to OSAS. OSAS is a complex disease in which several risk factors (e.g. inflammation, obesity, etc.) are interrelated[42,43]. To date, available scientific findings in this field are still conflicting and mainly focused on subjects with obesity. Given the well-recognized role of obesity as major cardiometabolic risk factor[36–38], studies examining OSAS subjects with obesity might suffer from some limitations due to the potential pathophysiological overlap between these diseases.
In this perspective, findings from our non-obese population allow to expand knowledge in this research area. In fact, it could be supposed that gas exchange abnormalities and sleep disturbance characterizing OSAS promote inflammatory responses, as supported by the increased CRP levels observed in our cohort.
The association between SRDB and cardiovascular disease in pediatric age has been well documented, particularly in children with endothelial function impairment[39–41]. More, these patients experienced recurrent episodes of hypoxiemia leading to an increase in sympathetic activity, oxidative stress, and inflammation (mainly expressed as elevated serum C-reactive protein levels) that enhanced endothelial dysfunction[39,40].
Evidence also supported a close relationship between the night-time breathing habits and non-specific biochemical markers of inflammation with particular reference to the findings of neutrophilia in OSAS children [44–47]. In this regard, results from our study not only confirmed these findings but provided further evidence in a non-obese pediatric cohort, by underscoring the pivotal pathogenic role of the inflammation also in a such selected population.
As previously reported, both metabolic (including metabolic syndrome, insulin-resistance (IR), and non-alcoholic fatty liver disease(NAFLD)) and cardiovascular derangements have been closely linked to OSAS patients with obesity[48,49].
Interestingly, our data seem to draw a worse cardiometabolic profile also in non-obese children with OSAS. According to previous findings [50,51], pediatric OSAS also showed a close relationship with fatty liver independently of the presence of a metabolic dysfunction as obesity status.
In addition to the pathogenic role of inflammation, dysregulation of other metabolic pathways involving insulin signaling and hepatic homeostasis might be supposed as further harmful players in the tangled puzzle of OSAS pathophysiology.
Considering the design of the study (including a selected population such as non-obese children with OSAS and a control group), our results might add to the existing knowledge on the pediatric OSAS development. Therefore, a careful management of these patients by taking into account also the impact of the hypoxemia correction on the metabolic impairments is highly recommended.
However, our study has some limitations that deserve mention. Firstly, our population, although well-characterized, is limited. The lack of a more comprehensive metabolic evaluation (e.g. lipid profile, glucose metabolism assessment) did not allow to provide evidence for a wider cardiometabolic risk in these patients. On the other hand, the presence of a control group enhances the strength of our findings.
In conclusion, a worse cardiometabolic profile has been found also in non-obese children with OSAS. In light of this, therapeutic strategies for hypoxiemia correction might also pay the way for a better cardiometabolic management, by improving the long-term quality of life of non-obese children with OSAS[42,53]. Further studies are needed to provide a better characterization of these selected patients.