RESUMO
RATIONALE: Severe acute asthma (SAA) can be fatal, but is often preventable. We previously observed in a retrospective cohort study, a three-fold increase in SAA paediatric intensive care (PICU) admissions between 2003 and 2013 in the Netherlands, with a significant increase during those years of numbers of children without treatment of inhaled corticosteroids (ICS). OBJECTIVES: To determine whether steroid-naïve children are at higher risk of PICU admission among those hospitalised for SAA. Furthermore, we included the secondary risk factors tobacco smoke exposure, allergic sensitisation, previous admissions and viral infections. METHODS: A prospective, nationwide multicentre study of children with SAA (2-18â years) admitted to all Dutch PICUs and four general wards between 2016 and 2018. Potential risk factors for PICU admission were assessed using logistic regression analyses. MEASUREMENTS AND MAIN RESULTS: 110 PICU and 111 general ward patients were included. The proportion of steroid-naïve children did not differ significantly between PICU and ward patients. PICU children were significantly older and more exposed to tobacco smoke, with symptoms >1â week prior to admission. Viral susceptibility was not a significant risk factor for PICU admission. CONCLUSIONS: Children with SAA admitted to a PICU were comparable to those admitted to a general ward with respect to ICS treatment prior to admission. Preventable risk factors for PICU admission were >7â days of symptoms without adjustment of therapy and exposure to tobacco smoke. Physicians who treat children with asthma must be aware of these risk factors.
RESUMO
Decreased serum cortisol levels have been proposed to contribute to nocturnal airway obstruction. We investigated whether endogenous cortisol levels are lower, and also whether the 24-h cortisol variation is greater, in children with asthma than in control subjects and assessed the relationship between serum cortisol and nocturnal airflow limitation in children with asthma. Cortisol and FEV(1) were measured every 4 h over 24 h; blood eosinophils, airway responsiveness to methacholine and adenosine 5'-monophosphate (AMP) were measured at 0400 and 1600. Children with asthma had lower cortisol levels than did control subjects; at midnight the difference was significant. Subjects with nocturnal asthma (24-h FEV(1) variation > or =15%) had significantly lower cortisol levels than did control subjects at 0000, 0800, and 1200. A higher mean 24-h cortisol level in subjects with asthma was associated with a significantly higher FEV(1) as a percentage of the predicted value (FEV(1) %pred) at 0400, 0800, and 2000, yet not in control subjects. Higher 24-h cortisol variation was associated with lower FEV(1) %pred at all time points in both control subjects and subjects with nonnocturnal asthma. There was no significant association between the level or variation of cortisol and PD(20) methacholine (provocative dose of methacholine causing a 20% fall in FEV(1)), PD(20) AMP, or eosinophils. Our data suggest that lower cortisol levels contribute to both overall lower levels of FEV(1) especially at night. This may be due to a lack of suppression of airway inflammation.