Exhaled nitric oxide fractions are well correlated with clinical control in recurrent infantile wheeze treated with inhaled corticosteroids.

Fractional exhaled nitric oxide (FeNO) is a non-invasive marker of bronchial inflammation in asthma. However, the interest of FeNO measurement remained limited in infantile wheeze. The aim of this prospective study was to evaluate the feasibility and reproducibility of FeNO off-line measurement in very young children with recurrent wheeze and to assess whether clinical control of infantile wheeze correlates with FeNO levels. Two exhalation samples were collected in mylar balloon during quite tidal breathing. FeNO measurements were performed off-line by a NO analyzer. The participating patients were aged ≤36 months, wheezes had started before the age of 24 months, and they were receiving maintenance treatment with inhaled corticosteroids for at least 3 months duration. The studied population comprised of 40 uncontrolled infants with persistent wheezy respiratory symptoms, median age 14.5 months, and 40 with optimal controlled infantile wheeze, median age 14 months. The reproducibility was excellent (r = 0.95; p < 0.0001). There was a significant difference in FeNO levels between the groups of persistent wheeze and well-controlled infants: 19.8 (2.5-99.3) ppb vs. 7.7 (0.6-29.5) ppb, p < 0.0001. At a FeNO level >15 ppb, the predictive values for uncontrolled disease were as follows: positive predictive value = 65%, negative predictive value = 90%. FeN0 levels were not increased by atopy or passive tobacco. Off-line assessment of FeNO is feasible, reproducible, and well accepted in wheezy very young children. Optimal clinical control of infantile wheeze appeared to be associated with the control of bronchial inflammation when evaluated by FeNO measurements.

Bolus methylprednisolone efficacy for uncontrolled exacerbation of cystic fibrosis in children.

We present here the clinical course of 4 children with cystic fibrosis, deltaF508/deltaF508, who were admitted with severe respiratory distress and in whom no improvement was obtained by intensive antibiotic therapy and systemic corticosteroids. Chest computed-tomography scans showed hyperinflation and atelectasis. The severity of these exacerbations was explained neither by visible mucus plugging nor by allergic bronchopulmonary aspergillosis. We hypothesized that these clinical features were related to a severe inflammatory process in small airways. Therefore, a high-dose short course of methylprednisolone (1 g/1.73 m(2) per day for 3 days) was given; all the patients' conditions were dramatically improved, and the therapy was safe. To our knowledge, this is the first reported use of bolus methylprednisolone in the treatment of uncontrolled pulmonary exacerbation in children with cystic fibrosis.