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ARTICLE

Association of Chronic Nasal Carriage of Staphylococcus aureus and Higher Relapse Rates in Wegener Granulomatosis

right arrow Coen A. Stegeman, MD; Jan W. Cohen Tervaert, MD; Willem J. Sluiter, PhD; Willem L. Manson, MD; Paul E. de Jong, MD; and Cees G. M. Kallenberg, MD

1 January 1994 | Volume 120 Issue 1 | Pages 12-17

Objective: To examine possible risk factors for relapse, including chronic nasal carriage of Staphylococcus aureus and serial antineutrophil cytoplasmic antibody (ANCA) determinations in patients with Wegener granulomatosis.

Design: Observational cohort study.

Setting: Outpatient clinic at a university-affiliated hospital.

Patients: Consecutive patients (n = 71) with biopsy-proven Wegener granulomatosis who were seen during follow-up at the outpatient clinic from January 1988 to July 1991. Fourteen patients were ineligible or dropped out; 57 patients were analyzed.

Measurements: Serial ANCA determinations and swab cultures of both anterior nares for S. aureus taken at each visit every 4 to 6 weeks. Occurrence of infections and relapses of Wegener granulomatosis were identified according to strict, predefined criteria.

Results: Thirty-six of the 57 patients (63%; 95% CI, 49% to 76%) were found to be chronic nasal carriers of S. aureus (≥ 75% of nasal cultures positive for S. aureus). Proportional-hazards regression analysis identified chronic nasal carriage of S. aureus (adjusted relative risk, 7.16; CI, 1.63 to 31.50), creatinine clearance above 60 mL x min–1 (adjusted relative risk, 2.94; CI, 1.27 to 6.67), and a history of previous relapses of Wegener granulomatosis (adjusted relative risk, 1.33; CI, 0.98 to 1.78) as independent risk factors for relapse. Twenty-two of 33 patients persistently or intermittently positive for ANCA had a relapse as opposed to only 1 of 21 persistently negative patients. Relapses of Wegener granulomatosis were not related to diagnosed infections.

Conclusion: Chronic nasal carriage of S. aureus identifies a subgroup of patients with Wegener granulomatosis who are more prone to relapses of the disease, suggesting a role for S. aureus in its pathophysiology and a possible clue for treatment.

Author and Article Information
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From University Hospital Groningen, the Netherlands.
Requests for Reprints: Coen A. Stegeman, MD, Department of Internal Medicine, Division of Nephrology, State University Hospital, Ooster-singel 59, 9713 EZ, Groningen, the Netherlands.
Acknowledgment: The authors thank Dr. J. Hermans, PhD, for statistical advice.
Grant Support: By grant 89.0872 from the Dutch Kidney Foundation.




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