Objective
Asthma is one of the most common diseases amongst children. Blood eosinophil count and neutrophil–lymphocyte ratio (NLR) are known as markers for phenotyping asthma. This study was performed to investigate blood eosinophil count and NLR as predictors of hospitalization in pediatric asthma exacerbations.
Data sources and study selections
In this cross-sectional study, children admitted to hospital ward for more severe asthma exacerbation were compared with non-hospitalized children with moderate to severe asthma exacerbation whose asthma exacerbation was managed in emergency department or outpatient clinic. We investigated patients’ characteristic and factors associated with hospitalization.
Results
A total of 211 children with moderate to severe asthma exacerbation (mean age $$5.76 \pm 3.28$$
5.76
±
3.28
years old) were enrolled in the study including 91 hospitalized patients and 120 non-hospitalized patients. For the prediction of hospitalization, an ROC Curve analysis was performed and revealed a cut-off of 298 cells/µL and 2.52 of blood eosinophil count and NLR, respectively. In multivariate analysis, not using an asthma action plan (OR 2.22, 95% CI 1.09–4.49; P = 0.027), a blood eosinophil count $$\ge$$
≥
298 (OR 8.79, 95% CI 4.44–17.4; P < 0.001) and an NLR $$\ge$$
≥
2.52 (OR 2.13, 95% CI 1.09–4.14; P = 0.027) were associated with hospitalization.
Conclusion
Blood eosinophil count and NLR were found to be higher in hospitalized children with more severe asthma exacerbation compared to non-hospitalized patients. These markers can be indicators for asthma exacerbation severity.
ADAM33 is a zinc-dependent metalloprotease of the ADAM family, which plays a vital biological role as an activator of Th2 cytokines and growth factors. Moreover, this protein is crucial for the normal development of the lung in the fetus two months after gestation leading to determining lung functions all over life. In this regard, mutations in ADAM33 have been linked with asthma risk factors. Consequently, identifying ADAM33 pathogenic nonsynonymous single-nucleotide polymorphisms (nsSNPs) can be very important in asthma treatment. In the present study, 1055 nsSNPs of human ADAM33 were analyzed using biocomputational software, 31 of which were found to be detrimental mutations. Precise structural and stability analysis revealed D219V, C669G, and C606S as the most destabilizing SNPs. Furthermore, MD simulations disclosed higher overall fluctuation and alteration in intramolecular interactions compared with the wild-type structure. Overall, the results suggest D219V, C669G, and C606S detrimental mutations as a starting point for further case-control studies on the ADAM33 protein as well as an essential source for future targeted mechanisms.
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