Severe bilateral central serous chorioretinopathy in a black patient: 16 years follow-up

Katsimpris, J. M.; Pournaras, Constantin J.; Sehgelmeble, Carlos W.; Petropoulos, Ioannis K.

doi:10.1007/s00417-006-0342-2

Cited by 13 publications

(7 citation statements)

References 7 publications

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“…Whether uncomplicated acute CSCR can evolve into chronic CSCR with diffuse RPE disease, or whether they are two different entities, is still debated. Evidence of this connection relies on illustrative case reports and case series (Bujarborua, 2001;Katsimpris et al, 2007). In one report, 8 of 50 patients demonstrate three years after initial evaluation a more extended surface of RPE defects on FA (Castro-Correia et al, 1992).…”

Section: Clinical Presentation: Forms and Definitionsmentioning

confidence: 95%

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Daruich

Matet

Dirani

et al. 2015

Progress in Retinal and Eye Research

798

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: Clinical Presentation: Forms and Definitionsmentioning

confidence: 95%

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Daruich

Matet

Dirani

et al. 2015

Progress in Retinal and Eye Research

798

996

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“…The relation to acute CSC is documented by published cases of long‐term follow‐up (Castro‐Correia et al. 1992; Bujarborua 2001; Katsimpris et al. 2006).…”

Section: Course and Complications Stagingmentioning

confidence: 99%

Central serous chorioretinopathy

Wang

Munch

Hasler

et al. 2008

Acta Ophthalmologica

576

521

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ABSTRACT.Central serous chorioretinopathy (CSC) is a disease of the retina characterized by serous detachment of the neurosensory retina secondary to one or more focal lesions of the retinal pigment epithelium (RPE). CSC occurs most frequently in mid-life and more often in men than in women. Major symptoms are blurred vision, usually in one eye only and perceived typically by the patient as a dark spot in the centre of the visual field with associated micropsia and metamorphopsia. Normal vision often recurs spontaneously within a few months. The condition can be precipitated by psychosocial stress and hypercortisolism. Ophthalmoscopic signs of CSC range from mono-or paucifocal RPE lesions with prominent elevation of the neurosensory retina by clear fluid -typical of cases of recent onset -to shallow detachments overlying large patches of irregularly depigmented RPE. The spectrum of lesions includes RPE detachments. Granular or fibrinous material may accumulate in the subretinal cavity. Serous detachment often resolves spontaneously. From first contact, counselling about the potential relation to stress and glucocorticoid medication is warranted. After 3 months without resolution of acute CSC or in chronic CSC, treatment should be considered. Resolution of detachment can usually be achieved in acute CSC by focal photocoagulation of leaking RPE lesions or, in chronic CSC, by photodynamic therapy. The effect of therapy on long-term visual outcome is insufficiently documented. Reattachment within 4 months of onset is considered a relevant therapeutic target because prolonged detachment is associated with photoreceptor atrophy. This suggests that the value of treatment depends upon proper selection of cases that will not resolve without therapy. Chronic CSC may be difficult to differentiate from occult choroidal neovascularization secondary to CSC. Patients with chronic CSC who receive glucocorticoid treatment for systemic disease can often be managed without having to discontinue this medication.

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“…People of African descent seem to be affected notably less frequently according to some authors, although it has been discussed that this conception might be wrong and derived from the reduced availability of medical infrastructure in poor countries for adequately diagnosing this condition [24]. Some authors also report on more aggressive courses of the disease in Black people [25,26]. …”

Section: Epidemiologymentioning

confidence: 99%

Central Serous Chorioretinopathy

Liegl¹,

Ulbig²

2014

Ophthalmologica

133

115

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The pathogenesis of central serous chorioretinopathy (CSC) is still not fully understood. The involvement of corticosteroids is undisputed, although their exact role has not been clarified; other parts of the underlying mechanism of CSC have been mainly elucidated by imaging techniques such as fluorescein and indocyanine green angiography. Even though most cases of CSC are self-limiting, severe as well as recurrent courses exist, and for these patients only a limited number of treatment options are available: laser photocoagulation, with a risk of scotoma and choroidal neovascularization, and photodynamic therapy. In this review article, we give an overview of its epidemiology, the current understanding of its pathogenesis as well as systemic and ocular risk factors. We illuminate modern diagnostic tools as well as current treatment options in the context of CSC, particularly in the light of a better understanding of corticosteroids and their receptors involved in its pathogenesis.

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Severe bilateral central serous chorioretinopathy in a black patient: 16 years follow-up

Cited by 13 publications

References 7 publications

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis

Central serous chorioretinopathy

Central Serous Chorioretinopathy

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