Most African-American Patients with Rheumatoid Arthritis Do Not Have the Rheumatoid Antigenic Determinant (Epitope)

1 August 1995 | Volume 123 Issue 3 | Pages 181-187

Objective: To evaluate the relation between the presence of the "rheumatoid epitope," defined by a sequence motif in the HLA-DRB1 alleles, and disease severity in African-American patients with rheumatoid arthritis.

Design: Cross-sectional study.

Setting: Rheumatology outpatient clinics at two university medical centers.

Patients: 86 African-American patients with rheumatoid arthritis (66 seropositive and 20 seronegative for the rheumatoid factor) attending the clinics and 88 healthy African-American persons.

Measurements: HLA-DRB1 alleles were determined by restriction fragment length polymorphism and by allele-specific oligonucleotide typing of polymerase chain reaction-amplified HLA-DRB1 second exons.

Results: With the exception of an increased frequency of HLA-DRB1*04 alleles in seropositive patients with rheumatoid arthritis (27.3%) compared with controls (13.1%) (P = 0.02), the frequencies of HLA-DRB1 alleles were similar in patients and controls. Most seropositive (48 of 66) and seronegative (15 of 20) patients were HLA-DR4 negative, but some (7 of 48 seropositive patients and 3 of 15 seronegative persons) inherited the rheumatoid epitope on a non-DR4 allele. Disease features, including severity, were similar for patients without the epitope and for those with either a single or a double dose of an epitope-positive allele. Positivity for rheumatoid factor, but not for the rheumatoid epitope, was weakly associated with severity in these patients.

Conclusion: Most African-American patients with rheumatoid arthritis did not express the rheumatoid epitope. The predisposition to and severity of rheumatoid arthritis in African-Americans appears to be independent of the presence and dose of the shared rheumatoid epitope.

Author and Article Information

From the University of Alabama at Birmingham, Birmingham, Alabama, and the University of Texas Health Science Center, Houston, Texas.
Requests for Reprints: John D. Reveille, MD, The University of Texas Health Science Center, Division of Rheumatology and Clinical Immunogenetics, PO Box 20708, Houston, TX 77225.
Acknowledgments: The authors thank Dr. William J. Koopman of the University of Alabama at Birmingham and Dr. Kenneth J. Hardy of the University of Mississippi for their helpful comments; the Clinical Faculty and Associates of the Division of Rheumatology and Clinical Immunology of the University of Alabama at Birmingham and the Division of Rheumatology and Clinical Immunogenetics of the University of Texas Health Science Center at Houston for allowing us to study their patients; and Ms. Ella Henderson for expert secretarial assistance.
Grant Support: By National Institutes of Health grants PO-AR 20614 and AR39325.