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Tytuł pozycji:

The Role of Genetics in Clinically Suspect Arthralgia and Rheumatoid Arthritis Development: A Large Cross-Sectional Study.

Tytuł:
The Role of Genetics in Clinically Suspect Arthralgia and Rheumatoid Arthritis Development: A Large Cross-Sectional Study.
Autorzy:
Maurits MP; Department of Rheumatology, Leiden University Medical Center, The Netherlands.
Wouters F; Department of Rheumatology, Leiden University Medical Center, The Netherlands.
Niemantsverdriet E; Department of Rheumatology, Leiden University Medical Center, The Netherlands.
Huizinga TWJ; Department of Rheumatology, Leiden University Medical Center, The Netherlands.
van den Akker EB; Department of Biomedical Data Sciences Leiden, Leiden University Medical Center, The Netherlands.
Le Cessie S; Department of Medical Statistics, Leiden University Medical Center, The Netherlands.
van der Helm-van Mil AHM; Department of Rheumatology, Leiden University Medical Center, The Netherlands.
Knevel R; Department of Rheumatology, Leiden University Medical Center, The Netherlands, and Translational & Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK.
Źródło:
Arthritis & rheumatology (Hoboken, N.J.) [Arthritis Rheumatol] 2023 Feb; Vol. 75 (2), pp. 178-186. Date of Electronic Publication: 2022 Dec 13.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Malden, MA : Wiley, [2014]-
MeSH Terms:
Autoantibodies*
Arthritis, Rheumatoid*/epidemiology
Arthritis, Rheumatoid*/genetics
Humans ; Cross-Sectional Studies ; HLA-DRB1 Chains/genetics ; Arthralgia/epidemiology ; Arthralgia/genetics ; Epitopes/genetics
References:
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Substance Nomenclature:
0 (Autoantibodies)
0 (HLA-DRB1 Chains)
0 (Epitopes)
Entry Date(s):
Date Created: 20221214 Date Completed: 20230201 Latest Revision: 20230419
Update Code:
20240105
PubMed Central ID:
PMC10107764
DOI:
10.1002/art.42323
PMID:
36514807
Czasopismo naukowe
Objective: To investigate whether established genetic predictors for rheumatoid arthritis (RA) differentiate healthy controls, patients with clinically suspect arthralgia (CSA), and RA patients.
Methods: Using analyses of variance, chi-square tests, and mean risk difference analyses, we investigated the association of an RA polygenic risk score (PRS) and HLA shared epitope (HLA-SE) with all participant groups, both unstratified and stratified for anti-citrullinated protein antibody (ACPA) status. We used 3 separate data sets sampled from the same Dutch population (1,015 healthy controls, 479 CSA patients, and 1,146 early classified RA patients). CSA patients were assessed for conversion to inflammatory arthritis over a period of 2 years, after which they were classified as either CSA converters (n = 84) or CSA nonconverters (n = 395).
Results: The PRS was increased in RA patients (mean ± SD PRS 1.31 ± 0.96) compared to the complete CSA group (1.07 ± 0.94) and compared to CSA converters (1.12 ± 0.94). In ACPA- strata, PRS distributions differed strongly when comparing the complete CSA group (mean ± SD PRS 1.05 ± 0.94) and CSA converters (0.97 ± 0.87) to RA patients (1.20 ± 0.94), while in the ACPA+ strata, the complete CSA group (1.25 ± 0.99) differed clearly from healthy controls (1.05 ± 0.94) and RA patients (1.41 ± 0.96). HLA-SE was more prevalent in the RA group (prevalence 0.64) than the complete CSA group (0.45), with small differences between RA patients and CSA converters (0.64 versus 0.60) and larger differences between CSA converters and CSA nonconverters (0.60 versus 0.42). HLA-SE prevalence differed more strongly within the ACPA+ strata as follows: healthy controls (prevalence 0.43), CSA nonconverters (0.48), complete CSA group (0.59), CSA converters (0.66), and RA patients (0.79).
Conclusion: We observed that genetic predisposition increased across pre-RA participant groups. The RA PRS differed in early classified RA and inflammatory pre-disease stages, regardless of ACPA stratification. HLA-SE prevalence differed between arthritis patients, particularly ACPA+ patients, and healthy controls. Genetics seem to fulfill different etiologic roles.
(© 2022 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.)

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