Association between strong inflammatory response and low risk of developing visual loss and other cranial ischemic complications in giant cell (temporal) arteritis
- PMID: 9433866
- DOI: 10.1002/1529-0131(199801)41:1<26::AID-ART4>3.0.CO;2-0
Association between strong inflammatory response and low risk of developing visual loss and other cranial ischemic complications in giant cell (temporal) arteritis
Abstract
Objective: To identify clinical and biochemical parameters that have good predictive value for identifying giant cell (temporal) arteritis (GCA) patients who are at high or low risk of developing cranial ischemic events.
Methods: In this multicenter study, records of patients at 3 university hospitals in Barcelona were reviewed retrospectively. Two hundred consecutive patients with biopsy-proven GCA were studied.
Results: Thirty-two patients developed irreversible cranial ischemic complications. The duration of clinical symptoms before diagnosis was similar in patients with and those without ischemic events. Patients with ischemic complications less frequently had fever (18.8% versus 56.9%) and weight loss (21.9% versus 62%) and more frequently had amaurosis fugax (32.3% versus 6%) and transient diplopia (15.6% versus 3.6%). Patients with ischemic events had lower erythrocyte sedimentation rates (ESR) (82.7 mm/hour versus 104.4 mm/hour) and higher concentrations of hemoglobin (12.2 gm/dl versus 10.9 gm/dl) and albumin (37.4 gm/liter versus 32.7 gm/liter). Clinical inflammatory status and biologic inflammatory status were defined empirically (clinical: fever and weight loss; biologic: ESR > or =85 mm/hour and hemoglobin < 11.0 gm/dl). Patients not showing a clinical and biologic inflammatory response were at high risk of developing ischemic events (odds ratio [OR] 5, 95% confidence interval [95% CI] 2.05-12.2). The risk was greatly reduced among patients with either a clinical (OR 0.177, 95% CI 0.052-0.605) or a biologic (OR 0.226, 95% CI 0.076-0.675) inflammatory reaction. No patient with both a clinical and a biologic response developed ischemic events.
Conclusion: The presence of a strong acute-phase response defines a subgroup of patients at very low risk of developing cranial ischemic complications. Our findings provide a rationale for testing less aggressive treatment schedules in these individuals. Conversely, a low inflammatory response and the presence of transient cranial ischemic events provide a high risk of developing irreversible ischemic complications and require a prompt therapeutic intervention.
Comment in
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No association between the inflammatory response and the risk of developing irreversible cranial ischemic complications: comment on the article by Cid et al.Arthritis Rheum. 1998 Nov;41(11):2088-9. doi: 10.1002/1529-0131(199811)41:11<2088::AID-ART34>3.0.CO;2-B. Arthritis Rheum. 1998. PMID: 9811070 No abstract available.
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Acute-phase response and risk of developing ischemic complications in giant cell arteritis: comment on the article by Cid et al.Arthritis Rheum. 1999 Jan;42(1):190. doi: 10.1002/1529-0131(199901)42:1<190::aid-anr27>3.0.co;2-p. Arthritis Rheum. 1999. PMID: 9920033 No abstract available.
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Association between the inflammatory response and the risk of developing irreversible cranial ischemic complications: comment on the article by Cid et al and the letter by Nesher and Sonnenblick.Arthritis Rheum. 1999 Oct;42(10):2256-8. doi: 10.1002/1529-0131(199910)42:10<2256::AID-ANR36>3.0.CO;2-Q. Arthritis Rheum. 1999. PMID: 10524705 No abstract available.
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Acute-phase response and the risk of developing ischemic complications in giant cell arteritis: comment on the article by Cid et al.Arthritis Rheum. 2000 Jan;43(1):234-6. doi: 10.1002/1529-0131(200001)43:1<234::AID-ANR30>3.0.CO;2-8. Arthritis Rheum. 2000. PMID: 10643722 No abstract available.
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Trends in the inflammatory response in biopsy-proven giant cell arteritis: comment on the article by Cid et al, and the letters by Nesher and Sonnenblick and Liozon et al.Arthritis Rheum. 2000 Jun;43(6):1427-8. doi: 10.1002/1529-0131(200006)43:6<1427::AID-ANR35>3.0.CO;2-P. Arthritis Rheum. 2000. PMID: 10857809 No abstract available.
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