Characterization of Subretinal Fluid Leakage in Central Serous Chorioretinopathy

Pryds, Anders; Sander, Birgit; Larsen, Michael

doi:10.1167/iovs.09-4830

Cited by 26 publications

(18 citation statements)

References 25 publications

(22 reference statements)

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“…A role of choroidal vascular exudation in CSC is suggested by the prominent smoke‐stack leakage seen through ruptured retinal pigment epithelium detachments (Pryds et al. 2010).…”

Section: Discussionmentioning

confidence: 99%

Choroidal thickness following extrafoveal photodynamic treatment with verteporfin in patients with central serous chorioretinopathy

Pryds

Larsen

2011

Acta Ophthalmologica

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ABSTRACT.Purpose: To evaluate the effect of verteporfin photodynamic treatment (PDT) on choroidal thickness in patients with central serous chorioretinopathy (CSC). Methods: Choroidal thickness was measured with enhanced depth imaging-optical coherence tomography (EDI-OCT) before and after verteporfin PDT (fulldose verteporfin, half-light dose) in 16 eyes in 16 patients with serous detachment of the fovea secondary to extrafoveal angiographic fluorescein leakage. Treatment was confined to the area of leakage, whereas choroidal thickness before and after treatment was assessed over a larger area of the fundus using OCT. Results: Complete resolution of the serous detachment was seen in all 16 eyes within 1 month of extrafoveal PDT, while choroidal thickness in the area where PDT was applied decreased from 407 lm [mean; 95% confidence interval (CI 95 ) 356-458 lm] to 349 lm (mean; CI 95 300-399 lm; p < 0.0001), and subfoveal choroidal thickness was reduced from 421 lm (mean; CI 95 352-489 lm) to 346 lm (mean; CI 95 278-414 lm; p = 0.0001). Initially, subfoveal choroidal thickness was significantly increased in the treated eye compared with the healthy fellow eye (mean 324 lm; CI 95 273-376 lm; p = 0.0003), but after treatment, the difference was not significant. Discussion: Photodynamic therapy of active CSC was followed by choroidal thickness reduction, not only locally but also at considerable distance from the treated area. Thus, the process that causes choroidal thickening in CSC appears to spread laterally within the choroid.

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“…A role of choroidal vascular exudation in CSC is suggested by the prominent smoke‐stack leakage seen through ruptured retinal pigment epithelium detachments (Pryds et al. 2010).…”

Section: Discussionmentioning

confidence: 99%

Choroidal thickness following extrafoveal photodynamic treatment with verteporfin in patients with central serous chorioretinopathy

Pryds

Larsen

2011

Acta Ophthalmologica

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“…Anti-VEGF and photodynamic therapy to target choroidal vessels are currently under evaluation for CSCR treatment, but their efficacy remains unclear (7). The mechanisms underlying CSCR are not fully understood; angiographic findings indicate that the disease may start in the choroidal vessels (8,9). Optical coherence tomography (OCT), a noninvasive method of in vivo retinal imaging, has shown substantial thickening of the choroid in eyes affected by CSCR (10) and in the unaffected contralateral eye (11), which suggests that patients present a diffuse choroidal vasculopathy.…”

Section: Introductionmentioning

confidence: 99%

Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy

Zhao

Célérier²,

Bousquet³

et al. 2012

J. Clin. Invest.

335

296

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Central serous chorioretinopathy (CSCR) is a vision-threatening eye disease with no validated treatment and unknown pathogeny. In CSCR, dilation and leakage of choroid vessels underneath the retina cause subretinal fluid accumulation and retinal detachment. Because glucocorticoids induce and aggravate CSCR and are known to bind to the mineralocorticoid receptor (MR), CSCR may be related to inappropriate MR activation. Our aim was to assess the effect of MR activation on rat choroidal vasculature and translate the results to CSCR patients. Intravitreous injection of the glucocorticoid corticosterone in rat eyes induced choroidal enlargement. Aldosterone, a specific MR activator, elicited the same effect, producing choroid vessel dilation -and leakage. We identified an underlying mechanism of this effect: aldosterone upregulated the endothelial vasodilatory K channel KCa2.3. Its blockade prevented aldosterone-induced thickening. To translate these findings, we treated 2 patients with chronic nonresolved CSCR with oral eplerenone, a specific MR antagonist, for 5 weeks, and observed impressive and rapid resolution of retinal detachment and choroidal vasodilation as well as improved visual acuity. The benefit was maintained 5 months after eplerenone withdrawal. Our results identify MR signaling as a pathway controlling choroidal vascular bed relaxation and provide a pathogenic link with human CSCR, which suggests that blockade of MR could be used therapeutically to reverse choroid vasculopathy.

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“…It is currently believed that CSC is primarily an exudative choroidal vasculopathy since indocyanine-green (ICG) angiography has revealed choroidal vascular hyperpermeability and staining of choroidal vessels [Spaide et al, 1996;Yannuzzi et al, 2003;Pryds et al, 2010]. This is supported by enhanced depth-imaging optical coherence tomography (EDI-OCT) having demonstrated increased thickness of the choroid in patients with CSC and reduction of choroidal thickness after photodynamic therapy [Imamura et al, 2009;Pryds and Larsen, 2012].…”

Section: Introductionmentioning

confidence: 99%

Cadherin 5 is Regulated by Corticosteroids and Associated with Central Serous Chorioretinopathy

et al. 2014

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Central serous chorioretinopathy (CSC) is characterized by leakage of fluid from the choroid into the subretinal space and, consequently, loss of central vision. The disease is triggered by endogenous and exogenous corticosteroid imbalance and psychosocial stress and is much more prevalent in men. We studied the association of genetic variation in 44 genes from stress response and corticosteroid metabolism pathways with the CSC phenotype in two independent cohorts of 400 CSC cases and 1,400 matched controls. The expression of cadherin 5 (CDH5), the major cell–cell adhesion molecule in vascular endothelium, was downregulated by corticosteroids which may increase permeability of choroidal vasculature, leading to fluid leakage under the retina. We found a significant association of four common CDH5 SNPs with CSC in male patients in both cohorts. Two common intronic variants, rs7499886:A>G and rs1073584:C>T, exhibit strongly significant associations with CSC; P = 0.00012; odds ratio (OR) = 1.5; 95%CI [1.2;1.8], and P = 0.0014; OR = 0.70; 95%CI [0.57;0.87], respectively. A common haplotype was present in 25.4% male CSC cases and in 35.8% controls (P = 0.0002; OR = 0.61, 95% CI [0.47–0.79]). We propose that genetically predetermined variation in CDH5, when combined with triggering events such as corticosteroid treatment or severe hormonal imbalance, underlie a substantial proportion of CSC in the male population.

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Characterization of Subretinal Fluid Leakage in Central Serous Chorioretinopathy

Cited by 26 publications

References 25 publications

Choroidal thickness following extrafoveal photodynamic treatment with verteporfin in patients with central serous chorioretinopathy

Choroidal thickness following extrafoveal photodynamic treatment with verteporfin in patients with central serous chorioretinopathy

Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy

Cadherin 5 is Regulated by Corticosteroids and Associated with Central Serous Chorioretinopathy

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