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

高水平 C 反应蛋白和低水平 Pentraxin 3 作为中心性浆液性脉络膜视网膜病变的生物标志物

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作者:Elodie Bousquet, Camille Chenevier-Gobeaux, Thara Jaworski, Héloïse Torres-Villaros, Marta Zola, Irmela Mantel, Laura Kowalczuk, Alexandre Matet, Alejandra Daruich, Min Zhao, Suzanne Yzer, Francine Behar-Cohen

Conclusions

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. Financial disclosures: The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Methods

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. Main outcome measures: C-reactive protein and PTX3 serum level comparison between patients with CSCR with age- and sex-matched healthy participants.

Purpose

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. Design: Cross-sectional multicenter study. Participants: Patients with CSCR compared with age- and sex-matched healthy participants.

Results

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. Conclusions: 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. Financial disclosures: The author(s) have no proprietary or commercial interest in any materials discussed in this article.

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