Autoantibody Reactive with RNA Polymerase III in Systemic Sclerosis

15 November 1993 | Volume 119 Issue 10 | Pages 1005-1013

Objective: To determine the clinical significance of anti-RNA polymerase III antibody in systemic sclerosis (SSc).

Design: A point prevalence study of autoantibody to RNA polymerase III and longitudinal examination of its clinical significance in patients with SSc and in controls.

Setting: University medical center rheumatology practice.

Patients: Two hundred fifty-two consecutive new patients with SSc and 170 controls (150 patients with other connective tissue diseases and 20 normal volunteers).

Measurements: The presence of anti-RNA polymerase III antibody was determined by immunoprecipitation, immunoblotting, and immunodepletion studies.

Main Results: Serum specimens from 57 of the 252 patients with SSc (23%; 95% CI, 18% to 28%) reacted with RNA polymerase III, compared with none of the specimens from 170 controls (0%; 95% CI, 0% to 2%). In 40 of these 57 specimens, immunoprecipitation studies also showed the presence of RNA polymerase I or II, or both. Anti-RNA polymerase III antibody was detected in sera from 50 of the 111 patients (45%) who had SSc with diffuse cutaneous involvement (dcSSc), 7 of 114 patients (6%) who had SSc with limited cutaneous involvement, and none of 27 patients with an SSc overlap syndrome (P < 0.001). Among patients with dcSSc, anti-RNA polymerase III antibody was more common than antitopoisomerase I antibody (45% compared with 27%; P = 0.008). Patients with anti-RNA polymerase III antibody had a statistically significant higher mean maximum skin thickness score but statistically significant lower frequencies of telangiectasias, inflammatory myopathy, restrictive lung disease, and serious cardiac abnormalities than did patients with antitopoisomerase I antibody.

Conclusion: Anti-RNA polymerase III antibody is a new marker autoantibody for many patients who have SSc with diffuse or extensive cutaneous involvement.

Author and Article Information

From the University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Requests for Reprints: Thomas A. Medsger, Jr., MD, Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh School of Medicine, 985 Scaife Hall, Pittsburgh, PA 15261.
Acknowledgments: The authors thank Drs. R. Kovelman and R. G. Roeder (Rockefeller University School of Medicine) for providing the partially purified RNA polymerase III; Dr. M. Schmidt (University of Pittsburgh School of Medicine) for providing HeLa S100 extracts and pVA I DNA template; Colleen Thomas, Claudia Conte, and Noreen Fertig for providing technical assistance; and Joan Neitznick and Roberta Shope for secretarial assistance.
Grant Support: In part by The Arthritis Foundation, Western Pennsylvania Chapter (Shoemaker Fund), Pittsburgh, Pennsylvania; The Scleroderma Federation, New York, New York; The RGK Foundation, Austin, Texas; National Institutes of Health grant 5M01RR00056; and the Arthritis, Rheumatism and Aging Medical Information System (ARAMIS) National Institutes of Health grant AR21393.