Unintentional secondary exogenous corticosteroid exposure and central serous chorioretinopathy

Thinda, Sumeer; Lam, K. M.; Park, Susanna Soon Chun

doi:10.1038/eye.2014.328

Cited by 4 publications

(2 citation statements)

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“…Glucocorticoids efficiently reduce macular edema of many origins, even when associated with subretinal fluid (Noma et al, 2012;Ossewaarde-van Norel et al, 2011), but glucocorticoids can aggravate subretinal fluid accumulation in CSCR patients. Even exposure to low-dose non-ocular corticosteroids has been associated with the occurrence of CSCR (Bouzas et al, 2002;Thinda et al, 2015). But high-dose intraocular injection of glucocorticoids, routinely administered for the treatment of macular edema, has not been associated with increased incidence of CSCR.…”

Section: Introductionmentioning

confidence: 97%

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Daruich

Matet

Dirani

et al. 2015

Progress in Retinal and Eye Research

800

996

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Central serous chorioretinopathy (CSCR) is a major cause of vision threat among middle-aged male individuals. Multimodal imaging led to the description of a wide range of CSCR manifestations, and highlighted the contribution of the choroid and pigment epithelium in CSCR pathogenesis. However, the exact molecular mechanisms of CSCR have remained uncertain. The aim of this review is to recapitulate the clinical understanding of CSCR, with an emphasis on the most recent findings on epidemiology, risk factors, clinical and imaging diagnosis, and treatments options. It also gives an overview of the novel mineralocorticoid pathway hypothesis, from animal data to clinical evidences of the biological efficacy of oral mineralocorticoid antagonists in acute and chronic CSCR patients. In rodents, activation of the mineralocorticoid pathway in ocular cells either by intravitreous injection of its specific ligand, aldosterone, or by over-expression of the receptor specifically in the vascular endothelium, induced ocular phenotypes carrying many features of acute CSCR. Molecular mechanisms include expression of the calcium-dependent potassium channel (KCa2.3) in the endothelium of choroidal vessels, inducing subsequent vasodilation. Inappropriate or over-activation of the mineralocorticoid receptor in ocular cells and other tissues (such as brain, vessels) could link CSCR with the known co-morbidities observed in CSCR patients, including hypertension, coronary disease and psychological stress.

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Section: Introductionmentioning

confidence: 97%

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Daruich

Matet

Dirani

et al. 2015

Progress in Retinal and Eye Research

800

996

View full text Add to dashboard Cite

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“…High endogenous serum cortisol levels [12] or corticosteroid administration in any form, systemic or topical on skin or on oral, nasal and conjunctival mucosae, are two important promoters of CSCR, as shown in numerous studies [13][14][15][16][17][18][19]. A relation was found between high cortisol levels in Cushing's syndrome and thickening of the choroid and between intravitreal dexamethasone and pachychoroid and CSCR development [20,21], indicating that the role played by corticosteroids in the development of CSCR was through choroidal thickening.…”

mentioning

confidence: 99%

Central serous chorioretinopathy in uveitis patients after corticosteroid therapy: a report of 6 cases

Skvortsova

Papasavvas

Херборт

2021

Rossijskij oftalʹmologičeskij žurnal

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Purpose. To report central serous chorioretinopathy (CSCR) in uveitis patients.Material and methods. A retrospective chart review of uveitis patients seen in a time frame of 20 years at the Centre for Ophthalmic Specialised Care, Lausanne, Switzerland. The ophthalmic and systemic features are presented.Results. Out of 1793 uveitis patients followed at the Centre for Ophthalmic Specialised Care, 6 patients (0.3%) developed CSСR following corticosteroid therapy due to uveitis. The mean age of patients was 40 ± 13.4 years, disease incidence was not associated with gender. In all 6 patients’ clinical disease was unilateral but subclinical signs were present in all fellow eyes. The mean duration of corticosteroid therapy before CSCR had occurred was 4.95 ± 4.0 months. The mean best-corrected visual acuity at the moment of CSCR was 0.6 ± 0.26 and 0.8 ± 0.17 after discontinuation of corticosteroids. Neurosensory retinal detachment and pigment epithelium detachment were observed in 3 eyes, respectively. During fluorescein angiography (FA), focal dye leakage and areas of alteration of RPE were observed in 6 out of 10 eyes. Diffuse hyperfluorescence of choroidal vessels observed by ICGA was detected in all eyes.Conclusion. Central serous chorioretinopathy should be suspected when functional and morphological deterioration occurs in uveitis patients receiving corticosteroid therapy with no signs of inflammation reactivation. This complication is extremely rare but serious condition which needs a prompt tapering and discontinuing of corticosteroids.

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Unintentional secondary exogenous corticosteroid exposure and central serous chorioretinopathy

Cited by 4 publications

References 8 publications

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Central serous chorioretinopathy in uveitis patients after corticosteroid therapy: a report of 6 cases

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