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Jennifer Sim, Kapil Kapoor; Mineralocorticoid antagonist effects on choroidal thickness in central serous chorioretinopathy. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5940.
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© ARVO (1962-2015); The Authors (2016-present)
Central serous chorioretinopathy (CSCR) is characterized by increased choroidal thickness (CT), and subretinal fluid (SRF) accumulation that can lead to vision loss. Despite the increased risk of visual morbidity, definitive treatment and pathogenesis remain elusive. Recently, overactivation of mineralcorticoid receptors (MR) in choroidal vessels has been implicated in the pathophysiology of CSCR. Though the use of MR antagonists has been described clinically, their anatomic effects on CT has not yet been quantified. The purpose of this study is to quantify the effect of MR antagonists on CT in CSCR.
A retrospective chart review of CSCR patients treated with spironolactone (S) and eplerenone (E) for at least 4 months’ follow up was conducted. CT from optical coherence tomography images was computed by using the Zen linear measuring tool. CT was measured from the outer edge of the hyperreflective RPE to the inner sclera, nasal to temporal at 500μm intervals to span 3000μm per scan. The baseline for each individual and overall average was compared to each follow up measurement using a T-test.
A total of 19 patients (5S and 14E) were included in the study. Average baseline CT for S-OD was 226.30µm and OS was 167.77µm. Average baseline CT for E-OD was 188.80µm and OS was 185.10µm. There was no significant decrease in CT from baseline for all individuals in the study throughout the treatment for both E and S (p>0.05). There was no significant decrease in overall averaged CT from baseline compared to each follow up for both E and S (p>0.05).
In this treatment series, patients on MR antagonists did not have a statistically significant decrease in overall CT (p>0.05). These results differ from previous results with rat eyes that found MR antagonists to inhibit choroidal thickening promoted by retinal vasodilation from inappropriate MR activation. MR antagonists have clinical effects of SRF resolution and visual acuity improvements, but the measurements of CT taken throughout these treatment groups may show the actual anatomic effects of MR antagonists in CSCR. These results may suggest that MR antagonists work differently in humans due to potential differences of anatomy and physiology. In light of these results, the role and mechanism of MR antagonists in the treatment of CSCR need to be further researched and better defined.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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