ABSTRACT
In adults, asthma treatment with high doses of inhaled corticosteroids has resulted in dermal thinning. The aim of this study was to investigate the skin thickness in children with asthma during budesonide treatment. In a double-blind study, 113 children, 5-10 y old, with persistent asthma received budesonide 400 microg twice daily for 1 mo and thereafter 200 microg twice daily for 5 mo. Thereafter, 56 children received 100 microg twice daily for 1 y, whereas 57 other children used budesonide periodically for exacerbations. An additional 54 children were treated with disodium cromoglycate (DSCG) for 18 mo. Skin thickness was measured on each forearm before and after treatment for 6, 12, and 18 mo using a 20-MHz high-resolution ultrasonic device. The initial 6-mo budesonide treatment resulted in a greater reduction in mean skin thickness in the forearms compared with DSCG (right: -35.9 versus -5.9 microm; p = 0.004; left: -30.6 versus -7.3 microm; p = 0.03). At month 18, the inter-group differences were no longer significant. Budesonide inhalations in daily doses of 400-800 microg in prepubertal children with newly detected asthma may cause minor dermal thinning. The changes were reversible during low dose or periodic treatment with budesonide.
Subject(s)
Anti-Asthmatic Agents/administration & dosage , Asthma/drug therapy , Bronchodilator Agents/administration & dosage , Budesonide/administration & dosage , Skin/drug effects , Skinfold Thickness , Administration, Inhalation , Anti-Asthmatic Agents/adverse effects , Atrophy , Bronchodilator Agents/adverse effects , Budesonide/adverse effects , Child , Child, Preschool , Cromolyn Sodium/administration & dosage , Double-Blind Method , Drug Administration Schedule , Drug Therapy, Combination , Female , Finland , Forearm , Humans , Male , Severity of Illness Index , Skin/diagnostic imaging , Skin/pathology , Time Factors , Treatment Outcome , UltrasonographyABSTRACT
BACKGROUND: Respiratory and other symptoms are often associated with exposure to microbes present in water-damaged buildings. MATERIAL AND METHODS: We examined 82 consecutive patients referred to the Indoor Air Clinic, Helsinki University Hospital, due to symptoms suspected of having been caused by long-term exposure to water damage in the home or workplace. Exposure to water damage was assessed by building inspections and microbial analyses as needed. Bronchoalveolar lavage, lung function measurements, skin prick tests to inhalant allergens and radiological examinations were performed in all patients. Leucocyte subsets in peripheral blood were analysed in 35 patients. RESULTS: Marked water damage was detected in the homes or workplaces of 47 (59%) patients; the remaining 34 patients formed the control group. The exposed group expressed more symptoms in total than the control group: fatigue, conjunctival symptoms, rhinitis with sinusitis, recurrent bronchitis and asthma were more common in the exposed group, but a significant difference was seen only for headache. In BAL (bronchoalveolar lavage) samples, lymphocytes represented 25% of the total cell population in non-smoking-exposed patients compared with 12% in control patients (p=0.004). In peripheral blood, CD19 leucocytes were significantly decreased in the exposed group (7.5% versus 12.3%; p<0.01). CONCLUSIONS: Confirmed exposure to water damage was associated with an increase in symptoms. Exposure to water damage caused a significant change in the cellular composition in BAL fluid (lymphocytosis) and blood (decrease of CD19 cells). The depletion of CD19 leucocytes in peripheral blood may indicate an active immune response in the lungs.
