WEGENERS-GRANULOMATOSIS - ROLE OF ENVIRONMENTAL EXPOSURES

Citation
Ge. Duna et al., WEGENERS-GRANULOMATOSIS - ROLE OF ENVIRONMENTAL EXPOSURES, Clinical and experimental rheumatology, 16(6), 1998, pp. 669-674
Citations number
15
Categorie Soggetti
Rheumatology
ISSN journal
0392856X
Volume
16
Issue
6
Year of publication
1998
Pages
669 - 674
Database
ISI
SICI code
0392-856X(1998)16:6<669:W-ROEE>2.0.ZU;2-1
Abstract
Objective The etiology of Wegener's granulomatosis (WG) remains unknow n. The predominant involvement of the airways and the presence of neut rophilic alveolitis at disease onset have led us to postulate that an inhaled agent may trigger the onset of WG. This study is designed to a nalyze differences in self-reported environmental exposures between pa tients with WG and various control populations. Methods We conducted a standard interviewer-administered questionnaire case controlled surve y of 101 patients with WG, 54 healthy controls, 24 patients with sarco idosis or idiopathic pulmonary fibrosis, and 45 patients with various inflammatory rheumatologic diseases. We assessed environmental exposur es for one year prior to the onset of symptoms or prior to the intervi ew date for healthy controls. Results Seasonal differences in the onse t of WG were not apparent. More than 75% of the patients in all groups noted remarkable environmental exposure to inhaled substances (fumes or particulate matter), within one year prior to disease onset for WG and other diseases or prior to the interview date for healthy controls . Differences between WG and control groups were apparent in several c ategories of exposure. Statistically significant differences occurred in regard to avocational exposure to fumes or particulate materials (W G > healthy controls and rheumatic disease controls), residential expo sure to particulate materials from construction (WC > pulmonary diseas e controls) and occupational exposure to pesticides (WG > healthy, pul monary and rheumatic disease controls). Conclusion This study confirms the absence of seasonal differences in the onset of WG. It also demon strates high rates of self-reported environmental exposures to inhaled substances in WG and all control populations. It is possible that mor e significant differences in the quality, quantity and intensity of ex posure to inhaled potential precipitants of WG had occurred between gr oups, but were not detected by our survey Alternatively, the absence o f substantial differences in patients with WG and controls may reflect the more important role of host susceptibility factors.