Pentraxin-3 and Lipocalin-2 are decreased in patients with uveal effusion syndrome
Caroline Havertz1, Benedikt Schworm2, Jakob Siedlecki2,3
1Department of Ophthalmology, LMU University Hospital, Ludwig Maximilians-University Munich, Mathildenstrasse 8, 80336, Munich, Germany. caroline.havertz@med.uni-muenchen.de.
Purpose:
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.
Design:
A randomized prospective case-control study was performed at the Ludwig Maximilians University, Department of Ophthalmology.
Methods:
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.
Results:
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.
Conclusion:
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.
