Chronic bronchitis is the most frequent late respiratory disease among Iranians exposed to mustard gas during the Iraq-Iran war. The aim of this study was to investigate efficacy of oral and intravenous corticosteroid therapy in improving lung function in mustard gas induced chronic bronchitis patients. 65 mustard gas-exposed chronic bronchitis patients, who were not responsive to standard treatments in exacerbation occasions, were randomly divided into two groups: an intravenous group (39 patients) receiving 500 mg intravenous methylprednisolone daily, and an oral group (26 patients) receiving 1 mg/kg oral prednisolone daily. Corticosteroid was tapered over the study period in both groups. Spirometery was performed on admission and on day 8 of therapy for assessment of effectiveness of therapy. There was significant improvement in spirometery indexes of both groups in approximately half of the patients over the study period. Furthermore, there was no difference between the pulse corticosteroid versus oral corticosteroid therapy in these patients. Since short-term corticosteroid therapy has a significant effect on lung function of almost fifty percent of patients with mustard gas-induced chronic bronchitis in exacerbation occasions, we suggest a short-term bolus steroid treatment to triage the patients into responders and non-responders for subsequent treatment.
A unique chronic obstructive pulmonary disease (COPD), provisionally called "mustard lung", which occurs as a late complication of sulfur mustard (SM) exposure among SM-exposed Iranians, is presently poorly characterized. This investigation evaluates p53 immunoreactivity in bronchial epithelium of individuals with histories of tobacco use and/or SM exposure, as a tool to help define mustard lung. In this study, 68 COPD patients were segregated into two groups, 35 mustard-exposed patients (including 8 smokers) and 33 unexposed patients (including 16 smokers). Disease severity was assessed with pulmonary function tests. p53 protein in bronchial tissue obtained as biopsies was quantitated by immunostaining. Among nonsmokers, 41.2% of unexposed subjects and 14.8% of exposed subjects expressed p53. Among smokers, 25% of the unexposed group and 50% of the exposed group expressed the protein. Initial data trends suggest an additive contribution of SM exposure and smoking to p53 immunoreactivity. These results illustrate the use of p53 immunoreactivity in the characterization of COPD, including mustard lung.
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