Persistent airflow limitation in adult-onset nonatopic asthma is associated with serologic evidence of Chlamydia pneumoniae infection

Citation
A. Ten Brinke et al., Persistent airflow limitation in adult-onset nonatopic asthma is associated with serologic evidence of Chlamydia pneumoniae infection, J ALLERG CL, 107(3), 2001, pp. 449-454
Citations number
33
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
00916749 → ACNP
Volume
107
Issue
3
Year of publication
2001
Pages
449 - 454
Database
ISI
SICI code
0091-6749(200103)107:3<449:PALIAN>2.0.ZU;2-M
Abstract
Background: Persistent airflow limitation may develop in patients with asth ma, particularly in adults with nonatopic (intrinsic) disease. Although the underlying mechanisms are still unknown, respiratory infections might be i nvolved. Objective: We investigated the annual loss of lung function in relation to seropositivity to Chlamydia pneumoniae in different subgroups of patients w ith severe asthma according to age at onset of asthma and atopic status. Methods: One hundred one nonsmoking outpatients with a pulmonologist's diag nosis of severe asthma (32 men and 69 women; mean age, 46.0 years; range, 1 8-75 years) were included in a cross-sectional study. C pneumoniae-specific serum IgG and IgA were measured by means of ELISA. The estimated decline i n lung function was calculated from the relationship between postbronchodil ator FEV1/vital capacity (percent predicted) and the duration of asthma and expressed as the slope of the regression line. Results: Patients with adult-onset nonatopic asthma and positive IgG antibo dies to C pneumoniae had a significantly steeper slope of the regression li ne compared with the other subgroups of asthmatic patients (P = .001), bein g indicative of a 4-fold greater estimated decline in postbronchodilator FE V1/vital capacity (2.3% vs 0.5% predicted per year of asthma duration). Conclusion: These results suggest that C pneumoniae infection might promote the development of persistent airflow limitation in patients with nonatopi c adult-onset asthma. It remains to be established whether viable pathogens that are accessible for therapeutic intervention are still present in the lower airways.