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Abnormal Antinuclear Antibody Titers Are Less Common Than Generally Assumed in Established Cases of Systemic Lupus Erythematosus CHRISTOPHER SJÖWALL, MARTIN STURM, CHARLOTTE DAHLE, ANDERS A. BENGTSSON, ANDREAS JÖNSEN, GUNNAR STURFELT, and THOMAS SKOGH
ABSTRACT. Methods. Sera from 50 patients with SLE and 65 patients with RA were analyzed regarding abnormal concentrations of F-ANA (serum dilution ≥ 1:200 = 95th percentile among 300 healthy blood donors). The sera were also analyzed with 2 commercial ANSA-EIA kits. Results. An abnormal F-ANA titer occurred in 76% of the SLE sera compared to 23% in RA, and was not related to present use of antirheumatic drugs. At dilution 1:50, 84% of the SLE sera were F-ANA-positive compared to 20% of healthy women. Forty percent and 56%, respectively, of the SLE sera tested positive in the 2 ANSA-EIA kits. By the most sensitive assay, 96% of the ANSA-positive SLE sera produced a homogenous (chromosomal) F-ANA staining pattern compared to 18% of the ANSA-negative SLE sera. Ten of the 15 F-ANA-positive RA sera (63%) generated homogenous F-ANA staining and 13 (20%) tested positive in the most sensitive ANSA-EIA, but with no correlation to the F-ANA staining pattern. Conclusion. The sensitivity of F-ANA at an abnormal titer was surprisingly low (76%) in established cases of SLE. ANSA occurred in 56% of the SLE sera, but also in a fair number (20%) of RA sera. Practically all ANSA-positive SLE sera were identified by chromosomal F-ANA staining. We conclude that the antigen-specific antinucleosomal EIA does not have high enough diagnostic specificity to justify use of this analysis for routine diagnostic purposes. (First Release Sept 1 2008; J Rheumatol 2008;35:1994–2000) Key Indexing Terms:
SYSTEMIC LUPUS ERYTHEMATOSUS
From the Division of Rheumatology; Autoimmunity and Immune Regulation unit (AIR) and Department of Clinical and Experimental Medicine, Division of Clinical Immunology, Faculty of Health Science, Linköping University, Linköping University Hospital, Linköping; and Department of Rheumatology, University Hospital of Lund, Lund, Sweden. Supported by grants from the Swedish Research Council (grants K2006-74X-14594-04-03 and 13489), The Swedish Society Against Rheumatism, King Gustaf V 80-year Foundation, the Siv Olsson and Karin Svensson Foundations, the County Council of Östergötland, Österlund's Foundation, and Greta and Johan Kock's Foundation. C. Sjöwall, MD, PhD, Division of Rheumatology; M. Sturm, MD, Division of Rheumatology, Division of Clinical Immunology; C. Dahle, MD, PhD, Division of Clinical Immunology, Faculty of Health Science, Linköping University; A.A. Bengtsson, MD, PhD; A. Jönsen, MD, PhD; G. Sturfelt, MD, PhD, Department of Rheumatology, University Hospital of Lund; T. Skogh, MD, PhD, Division of Rheumatology, Faculty of Health Science, Linköping University. Dr. Sjöwall and Dr. Sturm contributed equally to the study. Address reprint requests to Dr. T. Skogh, Molecular and Clinical Medicine, Rheumatology, AIR, Patologihuset pl.10, Linköping, SE-581 85 Sweden. E-mail: thomas.skogh@lio.se Accepted for publication May 26, 2008. |
