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Anti-aquaporin-5 and anti-poly-U-binding-factor-60kDa protein antibodies in primary Sjögren's disease patients: preliminary data and correlation with disease activity indices


1, 2, 3, 4, 5, 6, 7

 

  1. Rheumatology Unit DiPReMeJ, University of Bari, Italy.
  2. Rheumatology Unit DiPReMeJ, University of Bari, Italy.
  3. Rheumatology Unit DiPReMeJ, University of Bari, Italy.
  4. Rheumatology Unit DiPReMeJ, University of Bari, Italy.
  5. Barts and The London School of Medicine and Dentistry, Queen Mary University of London, UK.
  6. Rheumatology Unit DiPReMeJ, University of Bari, Italy.
  7. Rheumatology Unit DiPReMeJ, University of Bari, Italy. florenzo.iannone@uniba.it

CER17751
2024 Vol.42, N°12
PI 2420, PF 2426
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PMID: 39699867 [PubMed]

Received: 08/04/2024
Accepted : 18/06/2024
In Press: 19/12/2024
Published: 19/12/2024

Abstract

OBJECTIVES:
In primary Sjögren’s disease (pSjD), in addition to glandular inflammation and atrophy, functional secretion impairment may contribute to dryness. Altered protein distribution and antibodies against aquaporin-5 (anti-AQP5) and poly-U-binding factor 60kDa protein (anti-PUF60) have been reported in pSjD and may be specifically implicated in the glandular secretive processes. This study aimed to assess the occurrence of serum anti-AQP5 and anti-PUF60 antibodies and their correlations with clinical and laboratory features of pSjD.
METHODS:
Blood samples from pSjD patients and healthy donors (HD) were collected, and anti-AQP5 and anti-PUF60 antibodies were detected using an enzyme-linked immunosorbent assay. Differences between groups were evaluated using appropriate statistical tests, and odds ratios (OR) of high disease activity were assessed by multivariate stepwise backward multiple regression and adjusted for clinical covariates.
RESULTS:
Serum samples from 36 pSjD patients and 8 HD were analysed, and anti-AQP5 and anti-PUF60 antibody levels were not significantly different between groups. However, pSjD patients with high disease activity (n. 10) had significantly higher levels of anti-AQP5 antibodies compared to those with low-moderate disease activity (p<0.001). At logistic regression analysis, variables associated with high disease activity were anti-AQP5 (OR 128.9, 95% CI 2.7–615), C-reactive protein (OR 12.9, 95% CI 1.2–137.2), and C4 <10 mg/dl (OR 60, 95% CI 1.1–318.9).
CONCLUSIONS:
Our pilot study confirms that anti-AQP5 antibodies may discriminate pSjD patients with high disease activity. These findings offer valuable clinical implications for managing pSjD patients, potentially identifying patients at high risk of glandular deterioration.

DOI: https://doi.org/10.55563/clinexprheumatol/ku7y1q

Rheumatology Article