No abstract

Although after oesophageal atresia (OA) repair in infancy, respiratory problems are common, their natural history remains unclear. We assessed morbidity, pulmonary function (PF), and bronchial hyperresponsiveness (BHR) in adults with repaired OA respiratory.588 patients who underwent surgery for OA during 1947-1985 were identified and those 262 who were alive and had their native oesophagus were included. Respiratory symptoms and respiratory symptom-related quality of life (RSRQoL) were assessed by questionnaire and interview, and the patients underwent spirometry, a histamine challenge test, and an exhaled nitric oxide test. For the questionnaires, we added 287 carefully matched general populationderived controls.Among the 101 (58 male) patients, median age 36 yrs (range 22-56 yrs), respiratory morbidity was significantly increased compared to controls. Patients had more respiratory symptoms and infections, as well as asthma and allergies, and more often impaired RSRQoL (p,0.001 for all). PF tests revealed restrictive ventilatory defect in 21 (21%) patients, obstructive ventilatroy defect in 21 (21%) patients, and both in 36 (36%) patients. A total of 41 (41%) had BHR, and in 15 (15%), it was consistent with asthma. The most significant risk factors for restrictive ventilatory defect were thoracotomy-induced rib fusions (OR 3.4, 95% CI 1.3-8.7; p50.01) and oesophageal epithelial metaplasia (OR 3.0, 95% CI 1.0-8.9; p50.05).After repair of OA, respiratory-related morbidity, restrictive ventilatory defect and BHR extended into adulthood. Nearly half the patients had BHR and over half had a restrictive ventilatory defect. Thoracotomy-induced rib fusions and gastro-oesophageal reflux-associated oesophageal epithelial metaplasia were the strongest risk factors for restrictive ventilatory defect.

Objective:To compare the effect of inhaled budesonide given daily or as-needed on mild persistent childhood asthma.Patients, design and interventions:176 children aged 5–10 years with newly detected asthma were randomly assigned to three treatment groups: (1) continuous budesonide (400 μg twice daily for 1 month, 200 μg twice daily for months 2–6, 100 μg twice daily for months 7–18); (2) budesonide, identical treatment to group 1 during months 1–6, then budesonide for exacerbations as needed for months 7–18; and (3) disodium cromoglycate (DSCG) 10 mg three times daily for months 1–18. Exacerbations were treated with budesonide 400 μg twice daily for 2 weeks.Main outcome measures:Lung function, the number of exacerbations and growth.Results:Compared with DSCG the initial regular budesonide treatment resulted in a significantly improved lung function, fewer exacerbations and a small but significant decline in growth velocity. After 18 months, however, the lung function improvements did not differ between the groups. During months 7–18, patients receiving continuous budesonide treatment had significantly fewer exacerbations (mean 0.97), compared with 1.69 in group 2 and 1.58 in group 3. The number of asthma-free days did not differ between regular and intermittent budesonide treatment. Growth velocity was normalised during continuous low-dose budesonide and budesonide therapy given as needed. The latter was associated with catch-up growth.Conclusions:Regular use of budesonide afforded better asthma control but had a more systemic effect than did use of budesonide as needed. The dose of ICS could be reduced as soon as asthma is controlled. Some children do not seem to need continuous ICS treatment.

Athletes’ symptoms may only occur in extreme conditions, which are far from normal. Exercise may increase ventilation up to 200 l/min for short periods in speed and power athletes, and for longer periods in endurance athletes such as swimmers and cross‐country skiers. Increasing proportions of young athletes are atopic, i.e. they show signs of IgE‐mediated allergy which is, along with the sport event (endurance sport), a major risk factor for asthma and respiratory symptoms. Mechanisms in the etiology and clinical phenotypes vary between disciplines and individuals, and it may be an oversimplification to discuss athlete’s asthma as a distinct and unambiguous disease. Nevertheless, the experience on Finnish Olympic athletes suggests at least two different clinical phenotypes, which may reflect different underlying mechanisms. The pattern of ‘classical asthma’ is characterized by early onset childhood asthma, methacholine responsiveness, atopy and signs of eosinophilic airway inflammation, reflected by increased exhaled nitric oxide levels. Another distinct phenotype includes late onset symptoms (during sports career), bronchial responsiveness to eucapnic hyperventilation test, but not necessarily to inhaled methacholine, and a variable association with atopic markers and nitric oxide. A mixed type of eosinophilic and neutrophilic airway inflammation seems to affect especially swimmers, ice‐hockey players, and cross‐country skiers. The inflammation may represent a multifactorial trauma, in which both allergic and irritant mechanisms play a role. There is a significant problem of both under‐ and overdiagnosing asthma in athletes and the need for objective testing is emphasized. Follow‐up studies are needed to assess the temporal relationship between asthma and competitive sporting, taking better into account individual disposition, environmental factors (exposure), intensity of training and potential confounders.

Data on the efficacy of corticosteroids on respiratory picornavirus-induced wheezing are limited. To determine whether prednisolone is effective in rhinovirus- or enterovirus-induced recurrent wheezing, we conducted a controlled trial comparing oral prednisolone (2 mg/kg/day in three divided doses for 3 days) with placebo in hospitalized wheezing children and studied post hoc virus-specific efficacy in early wheezing (<3 episodes, reported elsewhere) and in recurrent wheezing (>or=3 episodes). Virus-negative children where excluded. Our primary endpoint was the time until children were ready for discharge. Secondary endpoints included oxygen saturation and exhaled nitric oxide during hospitalization, duration of symptoms, blood eosinophil count, and impulse oscillometry 2 wk after discharge, and occurrence of relapses during the following 2 months. Virus-specific effects were analyzed with interaction analysis in a multivariate regression model. During the study period, 661 patients were hospitalized, 293 randomized, and 59 were accepted in this analysis (mean age 2.6 yr, s.d. 1.3). Prednisolone did not significantly decrease the time until ready for discharge in all patients (prednisolone vs. placebo, medians, 18 vs. 24 h, p = 0.11). However, prednisolone decreased the time until ready for discharge in children with picornavirus infection (respectively, 12 vs. 24 h, p = 0.0022) and more specifically, in children with enterovirus infection (6 vs. 35 h, p = 0.0007). In the secondary endpoints, prednisolone decreased the duration of cough and dyspnea in rhinovirus-affected children (p = 0.033 for both). Prospectively designed clinical trial is needed to test the hypothesis that prednisolone reduces symptoms in picornavirus-affected wheezing children.

Early treatment of new-born high-risk children with certain probiotic strains has reduced the risk of atopic eczema. Whether probiotics reduce risk for airway inflammation in long term is not known. We aimed at studying the effect of probiotic treatment during the six first months of life on airway inflammation at age 5 yr. In a randomized double-blind allergy prevention trial between 2000 and 2007 in Helsinki, Finland, we gave a probiotic combination, plus pre-biotics, or placebo, to 1018 children during 6 months from birth. At age 5, we measured exhaled nitric oxide (FE(NO) ) in a randomized sub-population of 160 children. Allergic diseases and IgE-sensitization were assessed in all infants. FE(NO) did not differ between probiotic and placebo groups, median (interquartile range, IQR) 5.45 (4.3-7.3) vs. 5.70 (3.9-6.8) ppb, p = 0.22. FE(NO) was elevated among those suffering from asthma during the first 5 yr than in healthy non-sensitized children (p = 0.009). FE(NO) correlated positively with serum total and allergen-specific IgE concentrations. Early intervention with probiotics and pre-biotics does not affect airway inflammation later in childhood.

ObjectiveManagement of asthma could be improved by measuring exhaled nitric oxide (FENO). Portable hand‐held FENO analyzer (NIOX MINO) is practical and small and could be used also in the primary care office. It has demonstrated good repeatability and correlation with stationary device (NIOX) in adults and school aged children, but so far there have been no reports on young children. The aim of this study was to compare conventional chemiluminescence device (NIOX) with a hand‐held electrochemical device (NIOX MINO) in young children.DesignPaired measurements of FENO were performed with the stationary chemiluminescence‐based analyzer (NIOX) and with portable electrochemical device (NIOX MINO) in children with asthmatic symptoms and age‐matched controls.ResultsFifty‐five children with mean (range) age of 5.7 (3.9–8.5) years were evaluated with both devices. Measurements were successful with both devices in 40 out of 57 children. NIOX MINO was more difficult to use than NIOX in this age group, success rates being 73% and 93%, respectively (P = 0.004). The reproducibility was similar and there was a close correlation between FENO measured by the two devices (r = 0.97, P < 0.001). However, Bland–Altman plot demonstrated limits of agreement that were relatively wide compared to low levels of FENO in the sample. Both devices were sensitive enough to distinguish higher FENO levels in children with asthmatic symptoms, compared to healthy controls.ConclusionsWe conclude that NIOX MINO can be used as a screening tool for the assessment of airway inflammation in children from the age of 4 years, but its applicability is limited by lower measurement success rate and relatively poor accuracy and detection limit at low levels of FENO. Pediatr Pulmonol. 2011; 46:627–631. © 2011 Wiley‐Liss, Inc.

Background: Preschool wheeze is highly prevalent; 30%-50% of children have wheezed at least once before age six. Wheezing is not a disorder; it is a symptom of obstruction in the airways, and it is essential to identify the correct diagnosis behind this symptom. An increasing number of studies provide evidence for novel diagnostic tools for monitoring and predicting asthma in the pediatric population. Several techniques are available to measure airway obstruction and airway inflammation, including spirometry, impulse oscillometry, whole-body plethysmography, bronchial hyperresponsiveness test, multiple breath washout test, measurements of exhaled NO, and analyses of various other biomarkers. Methods: We systematically reviewed all the existing techniques available for measuring lung function and airway inflammation in preschool children to assess their potential and clinical value in the routine diagnostics and monitoring of airway obstruction. Results: If applicable, measuring FEV1 using spirometry is considered useful. For those unable to perform spirometry, whole-body plethysmography and IOS may be useful. Bronchial reversibility to beta2-agonist and hyperresponsiveness test with running exercise challenge may improve the sensitivity of these tests. Conclusions: The difficulty of measuring lung function and the lack of large randomized controlled trials makes it difficult to establish guidelines for monitoring asthma in preschool children.