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Cardiometabolic risk profile in non-obese children with obstructive sleep apnea syndrome

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Abstract

Obstructive sleep apnea syndrome (OSAS) in childhood is a complex disease primarily due both to adenotonsillar hypertrophy and pediatric obesity. Notably, inflammation has been recognized as one of the most important shared pathogenic factor between obesity and OSAS resulting in an increased cardiometabolic risk for these patients. To date, evidence is still limited in non-obese population with OSAS. We aimed to evaluate the cardiometabolic risk profile of a pediatric population of non-obese subjects affected by OSAS. A total of 128 school-aged children (mean age 9.70 ± 3.43) diagnosed with OSAS and 213 non-OSAS children (mean age 9.52 ± 3.35) as control group were enrolled. All subjects underwent a complete clinical and biochemical assessment (including white blood cell count (WBC), platelet count (PLT), mean platelet volume (MPV), % of neutrophils (NEU%), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), serum glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), uric acid, fasting insulin, iron, ferritin, and transferrin levels). A significant association between inflammation markers (including WBC, PLT, MPV, NEU%, ferritin, CPR, and ESR) and OSAS was found (all p < 0.001). Children with OSAS also showed increased transaminase, glucose, uric acid, and insulin levels (all p < 0.001) compared to healthy controls.

Conclusion: Taken together, these findings suggested a worse cardiometabolic profile in non-obese children with OSAS. Given the pivotal pathogenic role of inflammation both for hypoxiemia and metabolic derangements, therapeutic strategies for OSAS might also counteract the increased cardiometabolic risk of these patients, by improving their long-term quality of life.

What is Known:

• Pediatric OSAS has shown a close relationship with obesity and its cardiometabolic comorbidities.

• Inflammation represents the hallmark of both obesity and OSAS.

What is New:

• Non obese children with OSAS presented with a worse cardiometabolic risk profile.

• OSAS treatment might serve as an effective approach also for the increased cardiometabolic risk of these children.

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Availability of data and material

The datasets generated during and/or analyzed during the current study are available from the corresponding author on request.

Code availability

STATISTICA software (data analysis software system, version 6, StatSoft, Inc. (2001).

Abbreviations

AHI:

Apnea/hypopnea index

ALT:

Alanine aminotransferase

AST:

Aspartate aminotransferase

BASO%:

% Of Basophils

BMI-SDS:

Body Mass Index Standard Deviation Score

Ca:

Calcium

Cl:

Chlorine

CRP:

C reactive protein

EOS%:

% Of eosinophils

ESR:

Erythrocyte sedimentation rate

Fe:

Iron

GGT:

Gamma-glutamyl transpeptidase

HGB:

Hemoglobin

HCT:

Hematocrit

IR:

Insulin resistance

K:

Potassium

LDH:

Lactate dehydrogenase

LINF%:

% Of lymphocytes

MCV:

Mean corpuscular volume

MONO%:

% Of Monocytes

MPV:

Mean platelet volume

Na:

Sodium

NAFLD:

Non Alcoholic Fatty Liver Disease

NEU%:

% Of neutrophils

ODI:

Oxygen desaturation index

P:

Phosphorus

PLT:

Platelet count

RBC:

Red blood cell count

WBC:

White blood cell count

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Conceptualization, ADS, GM, MC; Data curation, IB, CF, MC; Formal analysis, ADS; Investigation, MC; Methodology, ADS, MC; Project administration, GF; Supervision, AV; Writing — original draft, ADS, MC.

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Correspondence to Anna Di Sessa.

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This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of University of Campania (Protocol code 13887, approval date 09/03/2015; EudraCT number 2015–001164-19).

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Written informed consent was obtained from the parents of all the enrolled children.

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The authors declare no competing interests.

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Communicated by Peter de Winter

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Di Sessa, A., Messina, G., Bitetti, I. et al. Cardiometabolic risk profile in non-obese children with obstructive sleep apnea syndrome. Eur J Pediatr 181, 1689–1697 (2022). https://doi.org/10.1007/s00431-021-04366-8

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