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Arthritis Care Res (Hoboken). 2019 Jun 14. doi: 10.1002/acr.24003. [Epub ahead of print]

American Indians Have A Higher Risk Of Sjögren's Syndrome And More Disease Activity Than Caucasians And African-Americans.

Author information

Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Department of Veterans Affairs Medical Center, Oklahoma City, OK, USA.
Department of Neurology, University of Arkansas for Medical Sciences, Little Rock, AR.
Department of Oral Diagnosis and Radiology, University of Oklahoma College of Dentistry, Oklahoma City, OK, USA.
Department of Oral Pathology, University of Oklahoma College of Dentistry, Oklahoma City, OK, USA.
Department of Oral Surgery, University of Minnesota School of Dentistry, Minneapolis, MN, USA.
Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Department of Oral Medicine, Carolinas Medical Center, Charlotte, NC, USA.
Molecular Biology and Genomic Medicine Unit, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, CDMX, Mexico.



To describe the clinical and serological manifestations of Sjögren's syndrome (SS) in ethnic groups of the United States.


Cross-sectional study of 648 patients with primary SS: 20 African-American (AA), 164 American Indian (AI), 426 European-American (EA) and 38 of other races evaluated in a multi-disciplinary sicca research clinic.


AA subjects comprised 3.1% of the SS cohort, much lower than the percentage of AA in the State of Oklahoma (p=3.01xE-05), the United States (p=2.24E-13) or a lupus cohort at the same institution (p=4.26x10E-27). In contrast, the percentage of AI in the SS cohort (25.3%) was much higher than expected (p=3.17E-09 vs. SLE; p=6.36-26 vs. Oklahoma and p=8.14E-96 vs. USA population). The SS classification criteria were similar between AA and EA, but subjects of AI ancestry had lower rates of abnormal tear and salivary flow as well as anti-Ro/SSA and anti-La/SSB antibodies. Paradoxically, AI had higher levels of disease activity (mean±SD ESSDAI 3.77±4.78) in comparison to whites (2.90±4.12; p=0.011) and more extraglandular manifestations affecting mainly the articular and glandular domains. Meanwhile, AA patients were characterized by higher rates of hypergammaglobulinemia (OR 1.39, 95%CI 1.39-8.65, p=0.01), elevated ESR (OR 3.95, 95%CI 1.46-9.95, p=0.009), and parotid enlargement (OR 4.40, 95%CI 1.49-13.07, p=0.02).


American Indians are affected at high rates with SS but present with few classical features, potentially preventing timely diagnosis. In contrast to SLE, SS is infrequent and not more severe amongst AA, but the triad of hypergammaglobulinemia, increased ESR and parotid enlargement warrants extra vigilance for lymphomagenesis. This article is protected by copyright. All rights reserved.


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