OBJECTIVE: To evaluate whether scleroderma patients who are double-positive for anti-interferon-inducible protein 16 (anti-IFI-16) antibodies and anticentromere (anti-CENP) antibodies are at increased risk for significant digital vascular events relative to patients positive for anti-CENP antibodies alone. METHODS: Sera from 165 scleroderma patients who tested positive for anti-CENP antibodies upon clinical evaluation were reassayed for both anti-CENP and anti-IFI-16 antibodies using enzyme-linked immunosorbent assay testing. Patients who were positive for anti-CENP antibodies alone were then compared to patients who were double-positive for both anti-IFI-16 and anti-CENP antibodies. The association between a history of significant digital vascular events (digital pits, ischemic digital ulcers, and/or gangrene) and double-positive antibody status was examined using chi-square tests. After completion of univariate analysis, multivariable analyses were done to adjust for clinically relevant covariates. RESULTS: Of the 165 anti-CENP antibody positive patients, 21 (12.7%) also had anti-IFI-16 antibodies. Patients who were double-positive for anti-CENP and anti-IFI-16 antibodies were more likely to have had digital pits, ischemic digital ulcers, and/or gangrene (P = 0.03). After adjustment for clinically relevant covariates (age, cutaneous subtype, disease duration, and smoking), double-positive patients remained at significantly higher odds of having severe Raynaud's phenomenon (odds ratio 3.5 [95% confidence interval 1.1-11.1]; P = 0.03). CONCLUSION: Scleroderma patients who are double-positive for antibodies recognizing CENP and IFI-16 are significantly more likely to have significant digital vascular events during the course of their disease. This study provides further evidence that anti-CENP and anti-IFI-16 antibodies are disease biomarkers that may be used for risk stratification of vascular events in scleroderma.
OBJECTIVE: To evaluate whether sclerodermapatients who are double-positive for anti-interferon-inducible protein 16 (anti-IFI-16) antibodies and anticentromere (anti-CENP) antibodies are at increased risk for significant digital vascular events relative to patients positive for anti-CENP antibodies alone. METHODS: Sera from 165 sclerodermapatients who tested positive for anti-CENP antibodies upon clinical evaluation were reassayed for both anti-CENP and anti-IFI-16 antibodies using enzyme-linked immunosorbent assay testing. Patients who were positive for anti-CENP antibodies alone were then compared to patients who were double-positive for both anti-IFI-16 and anti-CENP antibodies. The association between a history of significant digital vascular events (digital pits, ischemic digital ulcers, and/or gangrene) and double-positive antibody status was examined using chi-square tests. After completion of univariate analysis, multivariable analyses were done to adjust for clinically relevant covariates. RESULTS: Of the 165 anti-CENP antibody positive patients, 21 (12.7%) also had anti-IFI-16 antibodies. Patients who were double-positive for anti-CENP and anti-IFI-16 antibodies were more likely to have had digital pits, ischemic digital ulcers, and/or gangrene (P = 0.03). After adjustment for clinically relevant covariates (age, cutaneous subtype, disease duration, and smoking), double-positive patients remained at significantly higher odds of having severe Raynaud's phenomenon (odds ratio 3.5 [95% confidence interval 1.1-11.1]; P = 0.03). CONCLUSION:Sclerodermapatients who are double-positive for antibodies recognizing CENP and IFI-16 are significantly more likely to have significant digital vascular events during the course of their disease. This study provides further evidence that anti-CENP and anti-IFI-16 antibodies are disease biomarkers that may be used for risk stratification of vascular events in scleroderma.
Authors: T A Medsger; A J Silman; V D Steen; C M Black; A Akesson; P A Bacon; C A Harris; S Jablonska; M I Jayson; S A Jimenez; T Krieg; E C Leroy; P J Maddison; M L Russell; R K Schachter; F A Wollheim; H Zacharaie Journal: J Rheumatol Date: 1999-10 Impact factor: 4.666
Authors: Y Kawaguchi; Y Nakamura; I Matsumoto; E Nishimagi; T Satoh; M Kuwana; T Sumida; M Hara Journal: Ann Rheum Dis Date: 2008-09-01 Impact factor: 19.103
Authors: K A Patterson; P J Roberts-Thomson; S Lester; J A Tan; P Hakendorf; M Rischmueller; J Zochling; J Sahhar; P Nash; J Roddy; C Hill; M Nikpour; W Stevens; S M Proudman; J G Walker Journal: Arthritis Rheumatol Date: 2015-12 Impact factor: 10.995
Authors: Scott H Visovatti; Oliver Distler; J Gerry Coghlan; Christopher P Denton; Ekkehard Grünig; Diana Bonderman; Ulf Müller-Ladner; Janet E Pope; Madelon C Vonk; James R Seibold; Juan-Vicente Torres-Martin; Martin Doelberg; Harbajan Chadha-Boreham; Daniel M Rosenberg; Vallerie V McLaughlin; Dinesh Khanna Journal: Arthritis Res Ther Date: 2014-12-10 Impact factor: 5.156
Authors: Christopher A Mecoli; Jamie Perin; Jennifer E Van Eyk; Jie Zhu; Qin Fu; Andrew G Allmon; Youlan Rao; Scott Zeger; Fredrick M Wigley; Laura K Hummers; Ami A Shah Journal: Clin Rheumatol Date: 2019-12-19 Impact factor: 2.980
Authors: Christopher A Mecoli; Ami A Shah; Francesco Boin; Fredrick M Wigley; Laura K Hummers Journal: Clin Rheumatol Date: 2018-05-26 Impact factor: 2.980
Authors: George Hung; Valentina Mercurio; Steven Hsu; Stephen C Mathai; Ami A Shah; Monica Mukherjee Journal: Curr Rheumatol Rep Date: 2019-12-07 Impact factor: 4.592