RESUMEN
This narrative review study investigates the correlations between obesity, allergies, and sleep-disordered breathing in pediatric populations. Searches for pertinent articles were conducted on the Medline PubMed Advanced Search Builder, Scopus, and Web of Science databases from unlimited to April 2024. Sleep-disordered breathing causes repeated upper airway obstructions, leading to apneas and restless sleep. Childhood obesity, which affects around 20% of children, is often associated with sleep-disordered breathing and allergies such as asthma and allergic rhinitis. It is distinguished between diet-induced obesity (resulting from excess of diet and physical inactivity) and genetic obesity (such as is seen in Down syndrome and Prader-Willi syndrome). In children with diet-induced obesity, chronic inflammation linked to weight can worsen allergies and increase the risk and severity of asthma and rhinitis. Furthermore, the nasal congestion typical of rhinitis can contribute to upper respiratory tract obstruction and obstructive sleep apnea. A vicious circle is created between asthma and sleep-disordered breathing: uncontrolled asthma and sleep-disordered breathing can worsen each other. In children with genetic obesity, despite alterations in the immune system, fewer allergies are observed compared to the broader population. The causes of this reduced allergenicity are unclear but probably involve genetic, immunological, and environmental factors. Additional research is necessary to elucidate the underlying mechanisms. The present narrative review study emphasizes the importance of jointly evaluating and managing allergies, obesity, and obstructive sleep apnea in children considering their close interconnection.
RESUMEN
BACKGROUND: The role of vertebral artery hypoplasia (VAH) in stroke pathophysiology is still debated. In this study, we correlated extra- and intra-cranial vertebral artery ultrasound findings with brain CT/MRI and clinical outcome. MATERIALS AND METHODS: We recruited all consecutive first-ever stroke patients with a documented acute ischemic brain lesion and a complete extra-intracranial ultrasound evaluation. Those with previous stroke, or with anterior and posterior strokes were excluded. The prevalence of VAH diagnosed by ultrasound was recorded both in anterior circulation and posterior circulation infarctions. In the latter group, we compared the risk profile, topographic and neuroradiological lesion features, etiology and clinical outcome based on the presence of VAH. RESULTS: The study included 750 patients [436 males (58%); mean age 65 years; age range 18-90] with first-ever acute ischemic stroke: 193 (25.7%) with a posterior circulation infarction, 557 (74.3%) with an anterior circulation infarction. VAH was more often detected in the former group (33.7 vs. 14.1%; p < 0.0001). Patients with posterior circulation stroke and VAH had a significantly higher frequency of basilar artery stenosis [OR 2.07 (1.00-4.26); p < 0.05], stenosis of the contralateral vertebral artery [64 vs. 36%; OR 3.22 (1.24-8.37); p < 0.05], and fetal-type variant of the posterior cerebral artery [25 vs. 13%; OR 2.17 (1.00-4.68); p < 0.05]. CONCLUSIONS: According to our study, VAH identifies patients at higher risk of posterior circulation stroke, and higher frequency of contralateral vertebral artery stenosis and basilar artery stenosis.