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Patients with Antibodies to Both PmScl and dsDNA

NATALYA Z. WARNER and ERIC L. GREIDINGER

ABSTRACT.

Objective.
To determine the significance of dsDNA antibodies in patients with antibodies to PmScl.

Methods. All patients testing positive for PmScl and/or dsDNA antibodies at an academic medical center between 1977 and 2002 were identified. Charts for the PmScl-positive patients were reviewed for manifestations of lupus, scleroderma, or polymyositis/dermatomyositis. Patients with antibodies to dsDNA were matched to each of the double-positive PmScl+/dsDNA+ patients on the basis of sex, race, age, and date of autoantibody testing. Standard classification criteria for lupus, scleroderma, and myositis were used (excluding dsDNA, PmScl, or antinuclear antibodies as criteria), and the number of subjects meeting classification criteria was recorded.

Results. Records were available for 38 out of 47 patients who were identified as PmScl-positive. The prevalence of dsDNA antibodies in this group was 42% (16/38). Patients with PmScl and dsDNA antibodies had a higher prevalence of systemic lupus erythematosus (8/16 vs 2/22; p = 0.008) and a lower rate of scleroderma or myositis (1/16 vs 9/22; p = 0.025) than dsDNA-negative patients with PmScl antibodies. The prevalence of systemic lupus erythematosus, myositis, and scleroderma in patients with PmScl and dsDNA antibodies was not different from the prevalences of these diseases in a matched cohort of patients who were dsDNA-positive.

Conclusion. Antibodies to PmScl are associated with scleroderma and myositis when dsDNA antibodies are not present. In the presence of dsDNA antibodies, PmScl antibodies do not appear to have clinical relevance. (J Rheumatol 2004;31:2169-74)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
SYSTEMIC SCLERODERMA
POLYMYOSITIS
AUTOANTIBODIES


From the Division of Immunology and Rheumatology, Department of Medicine, University of Missouri School of Medicine, Columbia, Missouri; and the Division of Rheumatology, Department of Medicine, University of Miami School of Medicine, Miami, Florida, USA.

Supported by the National Institutes of Health (award AI1842 to ELG) and the Arthritis National Research Foundation (ELG).

N.Z. Warner, MD, Postdoctoral Fellow, University of Missouri School of Medicine; E.L. Greidinger, MD, Assistant Professor, University of Miami School of Medicine.

Address reprint requests to Dr. E.L. Greidinger, 1400 NW 10th Avenue, Suite 602, Miami, FL 33136. E-mail: egreidinger@med.miami.edu

Submitted December 22, 2003; revision accepted June 8, 2004.




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