High Levels of C-Reactive Protein with Low Levels of Pentraxin 3 as Biomarkers for Central Serous Chorioretinopathy

To investigate the association between the 2 acute phase proteins, C-reactive protein (CRP) and pentraxin 3 (PTX3) with central serous chorioretinopathy (CSCR), as PTX3 is a glucocorticoid-induced protein. Cross-sectional multicenter study. Patients with CSCR compared with age- and sex-matched healt...

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Veröffentlicht in:Ophthalmology science (Online) 2023-09, Vol.3 (3), p.100278-100278, Article 100278
Hauptverfasser: Bousquet, Elodie, Chenevier-Gobeaux, Camille, Jaworski, Thara, Torres-Villaros, Héloïse, Zola, Marta, Mantel, Irmela, Kowalczuk, Laura, Matet, Alexandre, Daruich, Alejandra, Zhao, Min, Yzer, Suzanne, Behar-Cohen, Francine
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Sprache:eng
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Zusammenfassung:To investigate the association between the 2 acute phase proteins, C-reactive protein (CRP) and pentraxin 3 (PTX3) with central serous chorioretinopathy (CSCR), as PTX3 is a glucocorticoid-induced protein. Cross-sectional multicenter study. Patients with CSCR compared with age- and sex-matched healthy participants. Patients with CSCR from 3 centers in Europe were included in the study. The clinical form of CSCR was recorded. Blood samples from patients with CSCR and healthy participants were sampled, and high-sensitivity CRP and PTX3 levels were measured in the serum. C-reactive protein and PTX3 serum level comparison between patients with CSCR with age- and sex-matched healthy participants. Although CRP levels were higher in patients with CSCR (n = 216) than in age- and sex-matched controls (n = 130) (2.2 ± 3.2 mg/l vs. 1.5 mg/l ± 1.4, respectively, P = 0.037), PTX3 levels were lower in patients with CSCR (10.5 ± 19.9 pg/ml vs. 87.4 ± 73.2 pg/ml, respectively, P < 0.001). There was no significant difference in CRP or PTX3 levels between patients with acute/recurrent and chronic CSCR. In patients with CSCR, high CRP and low PTX3 levels suggest a form of low-grade systemic inflammation together with a lack of glucocorticoid pathway activation, raising new hypotheses on the pathophysiology of CSCR. The author(s) have no proprietary or commercial interest in any materials discussed in this article.
ISSN:2666-9145
2666-9145
DOI:10.1016/j.xops.2023.100278