RESUMEN
Background: Neonatal lung disease has a multifaceted etiopathology, including an explosive inflammatory sequence in the immature lung. Complement component 1 Esterase INHibitor (C1INH) is implicated in controlling inflammation in response to infection/injury. Aim: To explore for the first time the association of the C1INH rs4926 (Val480Met) variant and circulatory transcript expression levels in the neonates that had evidence of lung disease and the clinic-laboratory data. Methods: A total of 139 unrelated neonates were enrolled in this case-control study. C1INH genotyping and expression analyses were done using TaqMan Genotyping and Real-Time qPCR, respectively. Results: A/A genotype carriers were two times more likely to develop in newborns with lung disease under homozygote (A/A vs. G/G: OR = 2.66, 95%CI = 1.03-6.87, p = 0.039) and recessive (A/A vs. G/G-A/G: OR = 2.42, 95%CI = 1.07-6.06, p = 0.047) models. Also, a higher frequency of A/A genotype was observed in the patient's cohort complicated with sepsis (44.2 vs. 14.3%, p = 0.002). Neonates with lung disease with A variant had more risk for developing sepsis under homozygote (A/A vs. G/G: OR = 5.19, 95%CI = 1.73-15.6, p = 0.002), dominant (A/G-A/A vs. G/G: OR = 2.39, 95%CI = 1.02-5.58, p = 0.041), and recessive (A/A vs. G/G-A/G: OR = 5.38, 95%CI = 1.86-15.5, p < 0.001) models. Regression analysis revealed rs4926*A/A genotype as an independent predictor risk factor for sepsis development in cohorts with lung disease (adjusted OR = 4.26, 95%CI = 1.38-13.1, p = 0.012). The circulatory transcript was significantly downregulated in neonates with lung disease in whom rs4926*A/A carriers had the least expression levels (median: -2.86, IQR: -3.55 to -1.71; p < 0.001). ROC curve analysis revealed C1INH expression could differentiate between cohorts with/without subsequent development of sepsis, and the discrimination ability was enhanced when combined with circulatory IL-6 and CRP levels (AUC = 0.926, 95%CI = 0.87-0.97). Conclusion: The C1INH rs4926 variant might play an essential role in the susceptibility to neonatal lung disease and could predict sepsis development in this cohort. Furthermore, the circulatory expression levels of this gene were downregulated in the neonatal lung disease cohort, supporting its potential role in the pathophysiology of this disorder, and highlighting its promising role in future targeted therapy.
RESUMEN
BACKGROUND: In the context of a new but busy Pediatric Emergency Department, the risk of missing patients who need more emergent care can be reduced by timely and accurate triaging. In the emergency department of King Fahad Armed Forces Hospital, the Canadian Triage and Acuity Scale had already been implemented, including the pediatric version (PaedCTAS). However, a common observation remained that critical patients did not always receive priority with subsequent delays in management. To improve this accuracy, a training course was administered to health care professionals responsible for triaging of pediatric patients. AIM: To determine the effectiveness of a training course on accuracy of triaging of Pediatric Patients. METHODS: A triage training course was conducted over two months, with patient encounter sheets reviewed before the course for 6 months and after the course for 12 months. Accuracy was calculated by comparing it to level as determined by two pediatric emergency physicians. Also, admission rates were used as a surrogate marker to also determine accuracy. RESULTS: A total of 31 053 patient sheets were reviewed. There was a considerable improvement in the correct determination of all triage levels, with accuracy ranging from 56.5% to 78.3% before the course, and reaching from 79.1% to 90.8% after the course with a statistically significant difference. Triaging errors still present were mainly in the form of down-triage. CONCLUSION: Our training course in triage has a significant impact on the accuracy of triaging of ill pediatric patients. Further improvement can be obtained by repeated courses and direct feedback with debriefing sessions on challenges to triage level determination.
