# Pentraxin-3 and Lipocalin-2 are decreased in patients with uveal effusion syndrome

## TL;DR

This study found that patients with uveal effusion syndrome have lower levels of two proteins linked to fluid regulation, suggesting a shared mechanism with a similar eye condition.

## Contribution

The study is the first to measure Lipocalin-2 and Pentraxin-3 levels in uveal effusion syndrome patients.

## Key findings

- UES patients had significantly thicker choroidal layers compared to controls.
- LCN2 and PTX3 levels were lower in UES patients, though not statistically significant.
- The findings suggest a possible shared pathophysiology between UES and CSCR.

## Abstract

Uveal effusion syndrome (UES) is characterized by exudative detachments of choroid, ciliary body and retina. Like central serous chorioretinopathy (CSCR) it is associated with scleral thickening inhibiting fluid outflow. Recently, decreased levels of Lipocalin-2 (LCN2) and Pentraxin-3 (PTX3) were found in CSCR. The aim of this study was to measure these parameters in patients with UES to evaluate a possible pachychoroid continuum with UES as the maximum form.

A randomized prospective case–control study was performed at the Ludwig Maximilians University, Department of Ophthalmology.

In patients with UES and in an age- BMI- and sex-matched control group, subfoveal choroidal thickness (SFCT) on optical coherence tomography imaging and the serum levels of PTX3 and LCN2 were measured.

12 patients were included in each group. SFCT was significantly thicker in the UES group compared to the normal controls (p = 0.0003). LCN2 and PTX3 values tended to be lower in patients with UES (LCN2: 65.74 ± 33.81 (33.7 − 165.4) ng/ml vs. 108.8 ± 67.1 (40.8 − 261.9, p = 0.133) ng/ml PTX3: 0.82 ± 0.52 (0.13 − 2.1) ng/ml vs. 1.23 ± 0.77 (0.3 − 1.86, p = 0.260) ng/ml.

Lipocalin-2 and Pentraxin-3 values, which are known to be induced by glucocorticoids, tend to be lower in patients with UES. The results suggest an impairment in the glucocorticoid receptor pathway and underline the hypothesis of a common pathophysiological pathway of CSCR and UES.