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CASE REPORTS
JOURNAL ARTICLE
Correlation between infection and the onset of the giant cell (temporal) arteritis syndrome. A trigger mechanism?
Arthritis and Rheumatism 1995 March
OBJECTIVE: To assess for a correlation between infection and the onset of the giant cell (temporal) arteritis (GCA) syndrome.
METHODS: A matched case-control study design was used. Records of 100 patients with biopsy-proven GCA and 100 patients undergoing corrective surgery for hip fracture who did not have GCA were retrospectively reviewed. Non-GCA patients were sex-matched with GCA patients and were as old or older in age. The review period for GCA patients was up to 4 months before and during the occurrence of symptoms (median 2 months), and for non-GCA patients, it was up to 7 months before hip fracture. The prevalence of infection was compared using matched-pairs odds ratios and their 95% confidence intervals.
RESULTS: Infections were 3 times more likely to occur in GCA patients than in non-GCA patients (P < 0.05).
CONCLUSION: A correlation between the occurrence of infection and the onset of GCA is strongly suggested. We speculate that infection may act as a trigger mechanism in the pathogenesis of this syndrome.
METHODS: A matched case-control study design was used. Records of 100 patients with biopsy-proven GCA and 100 patients undergoing corrective surgery for hip fracture who did not have GCA were retrospectively reviewed. Non-GCA patients were sex-matched with GCA patients and were as old or older in age. The review period for GCA patients was up to 4 months before and during the occurrence of symptoms (median 2 months), and for non-GCA patients, it was up to 7 months before hip fracture. The prevalence of infection was compared using matched-pairs odds ratios and their 95% confidence intervals.
RESULTS: Infections were 3 times more likely to occur in GCA patients than in non-GCA patients (P < 0.05).
CONCLUSION: A correlation between the occurrence of infection and the onset of GCA is strongly suggested. We speculate that infection may act as a trigger mechanism in the pathogenesis of this syndrome.
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