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Antiendothelial Cell Antibodies in Patients with Wegener's Granulomatosis: Prevalence and Correlation with Disease Activity and Manifestations
JODI K. SEBASTIAN, ALFRED D. MAHR, SOHAIL S. AHMED, JOHN H. STONE, ZURINA ROMAY-PENABAD, JOHN C. DAVIS, GARY S. HOFFMAN, W. JOSEPH McCUNE, E. WILLIAM ST. CLAIR, ULRICH SPECKS, ROBERT SPIERA, SILVIA PIERANGELI, and PETER A. MERKEL
ABSTRACT. Methods. Serum from subjects with WG who participated in a clinical therapeutic trial was collected at baseline, when all subjects had active disease. Clinical manifestations and disease activity were documented using the Birmingham Vasculitis Activity Score for WG (BVAS/WG). Serum AECA (IgG) was measured by cyto-ELISA using unfixed human umbilical vein endothelial cells (HUVEC). The AECA positivity cutoff was determined using 71 healthy control samples. Statistical analyses utilized Student's t test, chi-square and Fisher's exact tests, and linear regression. Results. AECA were detected in 34 of 173 (20%) evaluated serum samples. Mean BVAS/WG did not differ between patients with (7.3 ± 3.2) or without AECA (7.0 ± 3.3) (p = 0.58). Among the 34 patients positive for AECA, the antibody titer did not correlate with disease activity (BVAS/WG; r = 0.09, p = 0.60). There were no statistically significant differences in the frequency of major clinical manifestations between patients with or without AECA. Conclusion. AECA, as measured using HUVEC, are not highly prevalent among patients with active WG, are not associated with specific clinical manifestations, and do not correlate with level of disease activity. (J Rheumatol First Release April 15 2007) Key Indexing Terms:
ANTIENDOTHELIAL CELL ANTIBODIES From Boston University, Boston, Massachusetts; Johns Hopkins University, Baltimore, Maryland; University of Texas Medical Branch, Galveston, Texas; University of California, San Francisco, California; Cleveland Clinic, Cleveland, Ohio; University of Michigan, Ann Arbor, Michigan; Duke University, Durham, North Carolina; Mayo Clinic, Rochester, Minnesota; and Hospital for Special Surgery, New York, New York, USA. The WGET trial was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH N01-AR92240 and the Office of Orphan Products, FDA (grant FD-R-001652), General Clinical Research Center Grants M01-RRO-00533 (Boston University), M01-RRO-0042 (The University of Michigan), MO1-RR-30 (Duke University), and M01-RRO-2719 (Johns Hopkins University School of Medicine), from the National Center for Research Resources/NIH. Drs. Stone, Merkel, and St. Clair were supported by NIAMS grants K24 AR049185-01, K24 AR2224-01A1, and K24 AR02126-04. This work was also supported by a NIAMS Multidisciplinary Clinical Research Center Grant 2 P60 AR047785-06 (Boston University). Dr Pierangeli's laboratory is additionally supported by NIH grants G12-RR-03034 and SO2-GMM-08248. J.K. Sebastian, MD; A.D. Mahr, MD, MPH; S.S. Ahmed, MD; P.A. Merkel, MD, MPH, Boston University; J.H. Stone, MD, MPH, Johns Hopkins University; Z. Romay-Penabad, PhD; S. Pierangeli, PhD, University of Texas Medical Branch; J.C. Davis, MD, MPH, University of California, San Francisco; G.S. Hoffman, MD, MS, Cleveland Clinic; W.J. McCune, MD, University of Michigan, Ann Arbor; E.W. St. Clair, MD, Duke University; U. Specks, MD, Mayo Clinic; R. Spiera, MD, Hospital for Special Surgery. Address reprint requests to Dr. P.A. Merkel, Section of Rheumatology and the Clinical Epidemiology Unit, Vasculitis Center, E533, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118. E-mail: pmerkel@bu.edu Accepted for publication January 23, 2007.
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