期刊
JOURNAL OF RHEUMATOLOGY
卷 39, 期 4, 页码 787-794出版社
J RHEUMATOL PUBL CO
DOI: 10.3899/rheum.111133
关键词
SYSTEMIC SCLEROSIS; AUTOANTIBODIES; ANTICENTROMERE ANTIBODIES; CENP-A ANTIBODIES; CENP-B ANTIBODIES
类别
资金
- Canadian Institutes of Health Research
- Scleroderma Society of Canada
- Actelion Pharmaceuticals
- Pfizer Inc.
- Fonds de la recherche en Sante du Quebec
Objective. To study the clinical phenotypes of centromeric proteins (CENP)-A- and CENP-B-positive patients with systemic sclerosis (SSc) and to compare them to anticentromere antibody (ACA)-positive and negative SSc patients. Methods. Sera samples were collected from 802 patients with SSc enrolled in a multicenter cohort study. Antibodies to CENP-A and B were detected by ELISA, and ACA by indirect immunofluorescence. Associations with clinical and other serological manifestations of SSc were investigated. Results. CENP-A antibodies were detected in 276 (34%), CENP-B in 286 (36%), and ACA in 279 (35%) patients. Patients having ACA. CENP-A, and/or CENP-B resembled each other and differed from the remainder of the cohort in the following respects: older chronologically and at disease onset; more commonly women; more likely to have limited disease and lower skin scores; less likely to have finger ulcers, digital tuft resorption, or finger contractures; more likely to have pulmonary hypertension; less likely to have interstitial lung disease, scleroderma renal crisis, inflammatory arthritis, and inflammatory rnyositis; and having lower overall disease severity. CENP-A and/or B status was predictive of the extent of skin involvement over time. Patients with limited disease who were CENP-A-negative at baseline were more likely to progress to diffuse disease compared to CENP-A-positive patients (OR 2.55, 95% CI 1.37, 4.85, p = 0.004). Conclusion. Clinical immunology laboratories are increasingly using high-throughput ELISA tests for CENP antibodies, with or without ACA detected by indirect immunofluorescence. The phenotype of CENP-A and/or B-positive patients is generally similar to that associated with ACA. (First Release March 1 2012; J Rheumatol 2012:39:787-94; doi:10.3899/rheum.111133)
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