Severe asthma in children: An official statement from Saudi Pediatric Pulmonology Association.

In Saudi Arabia, the prevalence of pediatric asthma ranges between 8% and 25%. However, there are no sufficient data regarding severe asthma in childhood in Saudi Arabia. Therefore, a task force has been formed by the Saudi Pediatric Pulmonology Association which is a subsidiary group of the Saudi Thoracic Society and consists of Saudi experts with well-respected academic and clinical backgrounds in the fields of pediatric asthma as well as other respiratory diseases to write a consensus on definitions, phenotypes, and pathophysiology, evaluation, and management. To achieve this, the subject was divided into various sections, each of which was assigned to at least 2 experts. Without a central literature review, the authors searched the literature using their own strategies. To reach an agreement, the entire panel reviewed and voted on proposed findings and recommendations.

Endothelial dysfunction in children without hypertension: potential contributions of obesity and obstructive sleep apnea.

BACKGROUND: Endothelial dysfunction can develop in the context of both obesity and obstructive sleep apnea (OSA) in children. However, the potential interactions between OSA and obesity have not been defined. METHODS: Children who were prepubertal and nonhypertensive were recruited. Endothelial function was assessed in a morning fasted state, using a modified hyperemic test involving cuff-induced occlusion of the radial and ulnar arteries, and blood was drawn for assessment of myeloid-related protein 8/14 (MRP8/14) levels using a commercial enzyme-linked immunosorbent assay. Overnight polysomnography defined the presence of OSA or absence of OSA (NOSA) in subjects investigated for sleep-disordered breathing. Anthropometric measurements were performed to assign subjects to obese (OB) and nonobese (NOB) categories. RESULTS: Fifty-four children with OSA who were obese and nonobese (mean age, 7.90 ± 0.26 years; mean BMI z-score, 1.70 ± 0.3; obstructive apnea-hypopnea index [OAHI], 7.36 ± 1.09) were compared with 54 children without OSA who were obese and nonobese (mean age, 8.26 ± 0.24 years; mean BMI z-score, 1.41 ± 0.18; OAHI, 0.86 ± 0.07). Of those subjects, 62.5% of the OB-OSA category, 38.7% of the OB-NOSA category, and 20.0% of the NOB-OSA category had evidence of endothelial dysfunction, compared with 0.0% of the NOB-NOSA category (P < .01). The degree of endothelial dysfunction in all groups was associated with circulating MRP8/14 levels (r = 0.343, P < .001). CONCLUSIONS: Both obesity and OSA can independently increase the risk for endothelial dysfunction, and the concurrent presence of both markedly increases such risk. Although the mechanisms underlying endothelial dysfunction remain unclear, a potential role for MRP8/14 as an inflammatory biomarker of endothelial dysfunction is suggested.

Endothelial dysfunction in obese non-hypertensive children without evidence of sleep disordered breathing.

BACKGROUND: Endothelial dysfunction is a complication of both obesity and obstructive sleep apnea syndrome (OSAS), the latter being highly prevalent among obese children. It is unknown whether obesity causes endothelial dysfunction in children in the absence of OSAS. This study examines endothelial function in obese and non-obese children without OSAS. METHODS: Pre-pubertal non-hypertensive children were recruited. Endothelial function was assessed in a morning fasted state, using a modified hyperemic test involving cuff-induced occlusion of the radial and ulnar arteries. The absence of OSAS was confirmed by overnight polysomnography. Anthropometry was also performed. RESULTS: 55 obese children (mean age 8.6 +/- 1.4 years, mean BMI z-score: 2.3 +/- 0.3) were compared to 50 non-obese children (mean age 8.0 +/- 1.6 years, mean BMI z-score 0.3 +/- 0.9). Significant delays to peak capillary reperfusion after occlusion release occurred in obese compared to non-obese children (45.3 +/- 21.9 sec vs. 31.5 +/- 14.1 sec, p < 0.01), but no differences in the magnitude of hyperemia emerged. Time to peak reperfusion and percentage of body fat were positively correlated (r = 0.365, p < 0.01). CONCLUSIONS: Our findings confirm that endothelial dysfunction occurs early in life in obese children, even in the absence of OSAS. Thus, mechanisms underlying endothelial dysfunction in pediatric obesity are operational in the absence of sleep-disordered breathing.