No abstract

Invasive pulmonary aspergillosis is a frequent complication in immunocompromised patients. The role of the prolonged use of steroids in predisposing to invasive aspergillosis has been recognized, but exceptionally described in asthmatic patients. We report the case of a 59-year-old woman with bronchial asthma treated with steroid therapy for a long time, who developed an invasive pulmonary aspergillosis with an unusual combination of invasive and allergic disease. It seems reasonable to think that allergic disease due to allergic bronchopulmonary aspergillosis (ABPA) preceded the terminal invasive process. Adjunctive therapy with antifungal agents in patients with ABPA is considered, since there is the risk of an invasive pulmonary aspergillosis.

Pulmonary hyperinflation is a major medical problem in patients with advanced chronic obstructive pulmonary disease (COPD) or acute asthma. The apparent beneficial effects of pulmonary hyperinflation on lung mechanics, such as an increased airway patency and lung elastic recoil, are by far overwhelmed by the deleterious effects on the pressure generating capacity of the respiratory muscles. Moreover, the ventilatory workload can be remarkably increased: 1) by the displacement of the respiratory system toward the upper, flat portion of the pressure-volume curve; 2) by the need to expand the chest wall and not only the lungs; and 3) by the intrinsic positive end-expiratory pressure (PEEPi) systematically associated with dynamic hyperinflation.In mechanically ventilated patients, the mechanisms underlying pulmonary hyperinflation as well as its pathophysiological consequences do not differ from those described in spontaneously breathing patients. However, there are some specific issues that should be taken into account, namely the effect of the endotracheal tube and the mode and setting of the ventilator. In mechanically ventilated patients, pulmonary hyperinflation increases the risk of barotrauma and may hamper weaning due to the excessive burden of PEEPi, which can even lead to ineffective inspiratory efforts.Because of its harmful consequences, pulmonary hyperinflation must be treated aggressively by pharmacological therapy and, when needed, by ventilatory treatment. The setting of the ventilator must be predetermined to ensure the longest possible time for expiration, and positive end-expiratory pressure can be applied to prevent an excessive workload for the patient and ineffective inspiratory efforts.

Respiratory muscle strength, assessed by maximal inspiratory mouth pressure (Pi,max), and endurance, assessed as the length of time a subject could breathe against inspiratory resistance with a target mouth pressure ≥70% of Pi,max (Tlim), were measured in 20 symptomless asthmatic children, in order to assess the reproducibility of such measurements and their relationship to traditional pulmonary function tests or tests of bronchial hyperresponsiveness. After recording lung volumes and bronchial response to methacholine, Pi,max and Tlim were measured twice in the same morning, with a 30‐minute interval between each experimental trial. Mean (±SD) values of Pi,max were 72.2 ± 20.6 cmH2O in the first and 75.8 ± 22.9 cmH2O in the second trial. Tlim was 154 ± 65 and 164 ± 66 seconds in the first and in the second trial respectively. A lack of agreement between different measurements was seen for both Pi,max and Tlim. The coefficient of repeatability was 24.8 for Pi,max and 92.3 for Tlim. A significant correlation between age and Pi,max as well as between body mass index and Pi,max were shown; no similar correlation was found for Tlim. No correlation was found between Pi,max and Tlim in either of the two successive runs or between either Pi,max or Tlim and lung volumes or bronchial response to methacholine. Our study shows that at this time the reproducibility of Pi,max or Tlim in children with asthma in remission seems to be poor, although Pi,max has a better reproducibility than Tlim. A standardized procedure to measure Pi,max, should be obtainable in the near future. This would improve its clinical usefulness since Pi,max is the only noninvasive test to assess respiratory muscle strength that can identify subjects at risk to develop respiratory muscle fatigue during an acute asthmatic attack. Pediatr. Pulmonol. 1997; 24:385–390. © 1997 Wiley‐Liss, Inc.

Regular treatment with beta 2-adrenergic agonists is controversial in bronchial asthma. To investigate whether beta 2-adrenergic agonists can be used safely if associated with low doses of inhaled steroids, for a short period, without a deterioration of asthma control, we have examined 24 mild asthmatics. In a parallel, double-blind, placebo-controlled study, 1 week of run-in and run-out period framed 3 weeks of treatment. All patients received inhaled beclomethasone dipropionate (BDP 250 micrograms t.i.d.); after 1 week, 12 patients inhaled 400 micrograms of broxaterol and 12 patients received placebo t.i.d. FVC, FEV1, PD20-FEV1 methacholine, morning and evening PEF, and PEF amplitude % mean were measured before, during, and after treatment. No significant changes were noted in patients receiving inhaled broxaterol. There were no differences in symptoms and the use of rescue medication (salbutamol spray). We conclude that short-term regular treatment with beta 2-adrenergic agonists is not associated with a deterioration in asthma control in mild asthmatics inhaling low doses of steroids.