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      Advances in the treatment of central serous chorioretinopathy

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          Abstract

          Central serous chorioretinopathy is a disease that is partly understood. Novel advancements have led to further understanding of the disease, and have identified choroidal dysfunction as the principal element in CSCR development. New imaging tools have aided in better monitoring disease response to various treatment models. Enhanced depth imaging optical coherence tomography, in particular, has helped in observing choroidal thickness changes after various treatment models. To date, photodynamic therapy and focal laser remain the main stay of treatment. More understanding of disease pathophysiology in the future will help in determining the drug of choice and the best management option for such cases.

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          Most cited references128

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          Enhanced depth imaging optical coherence tomography of the choroid in central serous chorioretinopathy.

          The purpose of the study was to evaluate the choroidal thickness in patients with central serous chorioretinopathy, a disease attributed to increased choroidal vascular hyperpermeability. Patients with central serous chorioretinopathy underwent enhanced depth imaging spectral-domain optical coherence tomography, which was obtained by positioning a spectral-domain optical coherence tomography device close enough to the eye to acquire an inverted image. Seven sections, each comprising 100 averaged scans, were obtained within a 5 degrees x 30 degrees rectangle to encompass the macula. The subfoveal choroidal thickness was measured from the outer border of the retinal pigment epithelium to the inner scleral border. The mean age of subjects undergoing enhanced depth imaging spectral-domain optical coherence tomography was 59.3 years (standard deviation, 15.8 years). Seventeen of 19 patients (89.5%) were men, and 12 (63.2%) patients had bilateral clinical disease. The choroidal thickness measured in 28 eligible eyes of the 19 patients was 505 microm (standard deviation, 124 microm), which was significantly greater than the choroidal thickness in normal eyes (P < or = 0.001). Enhanced depth imaging spectral-domain optical coherence tomography demonstrated a very thick choroid in patients with central serous chorioretinopathy. This finding provides additional evidence that central serous chorioretinopathy may be caused by increased hydrostatic pressure in the choroid.
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            Central serous chorioretinopathy in younger and older adults.

            The purpose of the study is to investigate the demographic characteristics and clinical findings of central serous chorioretinopathy (CSC). This study examined a consecutive series of 130 patients with CSC seen over an 18-month period. The mean age of the patients when examined was 51 years, and the male-to-female ratio was 2.6:1.0. A total of 62 patients were older than 50 years of age when first examined. Although the patients shared some clinical and angiographic similarities, the older patients had a lower mean visual acuity and were more likely to have diffuse retinal pigment epitheliopathy, bilateral involvement, and secondary choroidal neovascularization than were the younger patients. With ophthalmoscopic and angiographic examination results, it was possible to differentiate CSC in older adults from choroidal neovascularization. This study expands the clinical concept of CSC. The male-to-female ratio was much lower, and the range of ages of the patients was much greater than in previous studies. Disease manifestations in older adults differed somewhat from those seen in younger adults. In older patients, CSC can be distinguished from other exudative maculopathies, particularly that of choroidal neovascularization secondary to age-related macular degeneration.
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              Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy.

              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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                Author and article information

                Contributors
                Journal
                Saudi J Ophthalmol
                Saudi J Ophthalmol
                Saudi Journal of Ophthalmology
                Elsevier
                1319-4534
                24 January 2015
                Oct-Dec 2015
                24 January 2015
                : 29
                : 4
                : 278-286
                Affiliations
                King Saud University, Riyadh, Saudi Arabia
                Author notes
                [* ]Address: Department of Ophthalmology, College of Medicine, King Saud University, P.O. Box 245, Riyadh 11411, Saudi Arabia. Tel.: +966 505476426; fax: +966 14775724. dr.abouammoh@ 123456gmail.com
                Article
                S1319-4534(15)00023-5
                10.1016/j.sjopt.2015.01.007
                4625218
                26586979
                f212cf9f-59eb-4988-b004-89eadbc5a0e0
                © 2015 Production and hosting by Elsevier B.V. on behalf of Saudi Ophthalmological Society, King Saud University.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 27 October 2014
                : 18 January 2015
                : 19 January 2015
                Categories
                Review Article

                cscr,central serous chorioretinopathy,central serous retinopathy,photodynamic therapy,corticosteroids,treatment

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