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Progranulin-autoantibodies in sera of rheumatoid arthritis patients negative for rheumatoid factor and anti-citrullinated peptide antibodies

1, 2, 3, 4, 5, 6

 

  1. Department of Internal Medicine I, José Carreras Center for Immuno- and Gene Therapy, Saarland University Medical School, Homburg/Saar, Germany. gunter.assmann@uks.eu
  2. Outpatient Rheumatology Center Berlin-Lichtenberg, Berlin, Germany.
  3. Department of Internal Medicine, Klinikum Bremerhaven, Germany.
  4. Department of Internal Medicine I, José Carreras Center for Immuno- and Gene Therapy, Saarland University Medical School, Homburg/Saar, Germany.
  5. Department of Internal Medicine I, José Carreras Center for Immuno- and Gene Therapy, Saarland University Medical School, Homburg/Saar, Germany.
  6. Department of Internal Medicine I, José Carreras Center for Immuno- and Gene Therapy, Saarland University Medical School, Homburg/Saar, Germany.

CER12094
2020 Vol.38, N°1
PI 0094, PF 0098
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PMID: 31074725 [PubMed]

Received: 19/01/2019
Accepted : 01/04/2019
In Press: 10/05/2019
Published: 06/02/2020

Abstract

OBJECTIVES:
Previously we discovered antibodies against progranulin (PGRN-abs) in a protein array-based screening of sera from various rheumatic diseases. Here we conducted a study to evaluate the prevalence of PGRN-abs in seropositive and seronegative rheumatoid arthritis (RA).
METHODS:
PGRN-abs were determined in the sera from 257 RA patients being seropositive for RF-IgM and/or ACPA-IgG and from 224 seronegative RA patients who were prospectively included in this study (total RA cohort n=481). All serum samples from the included participants were tested for RF-IgM as well as for ACPA-IgG, and PGRN-abs were determined using a previously described ELISA. Statistics was performed using the χ2 test for evaluating differences in clinical data; to evaluate independent statistical effects on the frequency of PGRN-abs status a logistic regression model with Wald-test was performed.
RESULTS:
PGRN-abs were detected in 25.3% from seropositive RA and in 21.0% from RF- and ACPA-negative RA resulting in a prevalence of 23.7% for both cohorts together. Comparing mean DAS28 values in the PGRN-abs positive cohort with the PGRN-abs negative cohort, the DAS28 value was significantly higher in PGRN-abs positive RA patients (3.81 vs. 3.50, p=0.038). A trend for higher frequencies of PGRN-abs in sera of RA patients with unfavourable characteristics such as erosive disease or requiring TNFi medication was observed.
CONCLUSIONS:
These data suggest that the determination of PGRN-abs in seronegative RA patients may reduce their seronegative status. Further studies are required to evaluate PGRN-abs as a potential diagnostic marker in RA.

Rheumatology Article