Adenoid hypertrophy (AH) is a common disease in otorhinolaryngology. Children with chronic snoring and hypoxia are susceptible to long-term nasal obstruction, while long-term open-mouth breathing may cause craniofacial bone development disorders and dull facial expressions, the so-called adenoid face. The purpose of this work is to analyze the influence of AH-induced airway obstruction (AO) on the growth and development of craniomaxillofacial structure and respiratory function (RF) in children. The clinical data of 56 AH children (observation group) and 42 healthy children with physical examination (control group) who visited the Hebei Eye Hospital during the same period were retrospectively analyzed. All children received acoustic rhinometry and X-ray cephalometric measurements. The upper airway structure, sleep disorder score, and A / N value of nasopharyngeal lateral X-ray images were compared between cases and controls. For AH children, sleep tests were also performed to assess their RF. X-ray cephalometric measurements of facial morphology showed obvious vertical growth, mandibular retrognathia, and enlarged mandibular angle in AH children. AH mainly affects the size of the nasopharyngeal and oropharyngeal airway. AH children presented with higher nasal airway resistance ( 5.11 ± 1.95 cmH2O/L min) and lower nasopharyngeal volume (NPV) ( 16.86 ± 3.93 cm3) than controls. Of the AH children, 45 had abnormal RF, including 4 with obstructive sleep apnea syndrome. The A / N value of nasopharyngeal lateral X-ray images was significantly higher in AH children than in controls. Besides, worse sleep quality was found in AH children. The above differences were all of statistical significance. The above indicates that AH can affect the size of the nasopharyngeal and oropharyngeal airway, change children’s respiratory mode and RF, increase nasal resistance, and decrease NPV, resulting in upper respiratory tract stenosis, as well as craniomaxillofacial and oral malformations, which affects children’s normal growth and development.
Background: Long noncoding RNA (lncRNA) THRIL targets microRNA (miR)-34a and miR-125b to modify immunity, inflammation, and respiratory injury. The current study aimed to determine the inter-correlation of lncRNA THRIL with miR-34a and miR-125b and their relationship with childhood asthma risk, severity, and inflammation. Methods: Exacerbated asthma children (N=65), remissive asthma children (N=65), and healthy controls (N=65) were enrolled in this case-control study. LncRNA THRIL, miR-34a, and miR-125b in peripheral blood mononuclear cells, as well as inflammatory cytokines in serum, were detected by reverse transcription-quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Results: LncRNA THRIL was highest in exacerbated asthma children, then in remissive asthma children, and lowest in healthy controls (P<0.001); reversely, miR-34a (P<0.001) and miR-125b (P=0.004) exhibited the opposite treads. LncRNA THRIL (area under curve (AUC)=0.686) and miR-34a (AUC=0.614) could predict exacerbation risk of asthma, while miR-125b failed. Interestingly, lncRNA THRIL was negatively related to miR-34a and miR-125b in exacerbated asthma children and remissive asthma children (all P<0.05) but not in healthy controls (both P>0.05). Specifically, in exacerbated asthma children: lncRNA THRIL is related to increased eosinophil count (P=0.013), immunoglobulin E (P=0.020), tumor necrosis factor-α (P=0.002), interleukin-1β (P=0.004), interleukin-6 (P=0.012), interleukin-17 (P=0.004) and exacerbated severity (P=0.030); Meanwhile, miR-34a and miR-125b linked with decreased levels of most of the above indexes (most P<0.05). Conclusion: LncRNA THRIL negatively relates to miR-34a and miR-125b, correlate with inflammatory cytokines, and exacerbated the risk and severity of childhood asthma, indicating their potential as biomarkers for childhood asthma management.
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