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- Title
Staphylococcal toxic-shock-syndrome-toxin-1 as a risk factor for disease relapse in Wegeners granulomatosis.
- Authors
E. R. Popa; C. A. Stegeman; W. H. Abdulahad; B. van der Meer; J. Arends; W. M. Manson; N. A. Bos; C. G. M. Kallenberg; J.-W. Cohen Tervaert
- Abstract
Objectives. Nasal carriage of Staphylococcus aureus constitutes a risk factor for disease exacerbation in Wegeners granulomatosis (WG). We hypothesized that staphylococcal superantigens (SAg) are a determinant of S. aureus-related risk for disease relapse in WG. Methods. In a retrospective longitudinal cohort study in 62 WG patients, we investigated the presence of the staphylococcal SAg genes sea, seb, sec, sed, see, tsst-1 and eta in S. aureus strains isolated from WG patients during an observation period of seven years. Subsequently, we assessed whether relapses of WG were associated with the presence of SAg-positive staphylococci. Results. Of 1718 swab cultures analysed, 709 (41.2%) were S. aureus-positive. Fifty-one patients carried S. aureus, of whom 37 (72.5%) patients carried at least one SAg-positive S. aureus strain. Of the 709 S. aureus-positive cultures, 326 (46%) contained at least one SAg gene. Except for see, all assessed SAg genes were detected. sea was found most frequently, followed by sec, tsst-1 and eta and finally, by sed and seb. Using a multivariate, time-dependent Cox regression analysis we found that the presence of S. aureus was associated with relapses of WG (RR 3.2; 95% CI 1.2â8.4). The risk for relapse was modulated by the presence and type of SAg, with tsst-1 being associated with an increased risk for relapse (RR 13.3, 95% CI 4.2â42.6). Conclusion. The risk for relapse of WG increases with the presence of tsst-1-positive S. aureus. Eradication of tsst-1-positive S. aureus in WG may show whether disease relapses can be prevented.
- Subjects
STAPHYLOCOCCAL diseases; POISONS; DISEASES; GRANULOMATOSIS with polyangiitis
- Publication
Rheumatology, 2007, Vol 46, Issue 6, p1029
- ISSN
1462-0324
- Publication type
Article
- DOI
10.1093/rheumatology/kem022