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Low serum lipocalin-2 in pregnant women with systemic lupus erythematosus


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

 

  1. Norwegian National Advisory Unit on Pregnancy and Rheumatic diseases, Department of Rheumatology, St. Olavs University Hospital, Trondheim, and Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. tina.pedersen@stolav.no
  2. Department of Immunology and Transfusion Medicine, St. Olavs University Hospital, Trondheim, Norway.
  3. Norwegian National Advisory Unit on Pregnancy and Rheumatic diseases, Department of Rheumatology, St. Olavs University Hospital, Trondheim, and Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
  4. Department of Mathematical Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
  5. Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
  6. Department of Mathematical Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
  7. Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim; Centre of Molecular Inflammation Research (CEMIR), NTNU, Trondheim; and Department of Infectious Diseases, St. Olavs University Hospital, Trondheim, Norway.

CER16274
2023 Vol.41, N°9
PI 1838, PF 1846
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PMID: 37246773 [PubMed]

Received: 11/10/2022
Accepted : 11/01/2023
In Press: 24/05/2023
Published: 17/08/2023

Abstract

OBJECTIVES:
Systemic lupus erythematosus (SLE) pregnancies are considered high-risk due to risk of disease flare and pregnancy complications. A more in-depth understanding of the immunological alterations in SLE patients during pregnancy and identification of predictive biomarkers may help to achieve stable disease and to avoid pregnancy complications. Lipocalin-2 (LCN2) has been implicated as a potential biomarker for rheumatic diseases and preeclampsia, but remains unexplored in SLE pregnancies.
METHODS:
We measured LCN2 levels in serum samples from SLE pregnancies (n=25) at seven different time points. Samples were taken preconception, in each trimester, at 6 weeks, 6 months and 12 months postpartum. Serum LCN2 levels were compared to samples from rheumatoid arthritis (RA) (n=27) and healthy (n=18) pregnancies at each time point using t-test, and for all time points using a linear mixed effects model. In addition, we investigated the association between LCN2 levels and disease activity, CRP, kidney function, BMI, treatment regimen and adverse pregnancy outcome for SLE and RA patients.
RESULTS:
We found significantly lower serum LCN2 levels throughout pregnancy in SLE patients with quiescent disease compared to RA and healthy pregnancies. We did not find an association between serum LCN2 and disease activity or adverse pregnancy outcome in SLE pregnancies.
CONCLUSIONS:
In a population of SLE women with low disease activity we have not found evidence that serum LCN2 levels predict disease activity or adverse pregnancy outcomes. Further studies are needed to elucidate a possible biological role of low LCN2 levels in SLE pregnancies.

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

Rheumatology Article