Central serous chorioretinopathy in primary hyperaldosteronism

Abstract

PurposeTo describe ophthalmological characteristics of 13 patients with primary hyperaldosteronism (PA).MethodsCross-sectional study. All patients underwent extensive ophthalmological examination.ResultsThirteen PA patients (9 male, 4 female) were diagnosed with arterial hypertension for 11.0 ± 11.2 years. Ophthalmological imaging revealed macular serous subretinal fluid (SRF) on optical coherence tomography in 2 patients (15 %). In one of these patients, bilateral chronic central serous chorioretinopathy (CSC) with polypoidal choroidal neovasculopathy was diagnosed, which was effectively treated with full-dose photodynamic therapy. In the other patient with SRF and bilateral diffuse hyperfluorescent areas on fluorescein angiography, the SRF had decreased spontaneously after 6 weeks of follow-up. In 5 of the remaining patients (38 %), retinal pigment epithelium alterations resembling findings characteristic for CSC were seen on multimodal imaging. The mean subfoveal choroidal thickness was 290.2 ± 65.0 μm.ConclusionsRetinal abnormalities resembling (subclinical) CSC are common in patients with PA. These findings indicate that mineralocorticoid-mediated pathways are involved in the pathogenesis of CSC. In CSC patients with hypertension of unknown origin, a diagnosis of PA should be considered.

The association of primary aldosteronism with glaucoma-related fundus abnormalities

“…reported that retinal abnormalities resembling central serous chorioretinopathy were frequently observed in PA patients, and speculated the potential involvement of the mineralocorticoid receptor-mediated pathway in the pathogenesis of the disease [8]. In our present cases, no eyes showed any apparent fundus abnormalities indicative of central serous chorioretinopathy.…”

Non-resolving, recurrent and chronic central serous chorioretinopathy: available treatment options

“…In particular, MR receptor pathway activation causes choroidal vasodilation and leakage, due to upregulation of the vasodilator potassium channel KCa2.3 (calciumdependent channel) and smooth muscle cells relaxation in the choroidal vasculature [66]. These evidences have also been supported by ophthalmologic findings within patient with primary hyperaldosteronism [67].…”

The Effect of Corticosteroids on Human Choroidal Endothelial Cells: A Model to Study Central Serous Chorioretinopathy

“…Furthermore, the finding of CSC(-like) changes in primary hyperaldosteronism indicate a role for the MR in the pathogenesis of CSC. 11 Zhao et al 12 have proposed an underlying mechanism of this association: aldosterone could lead to transcriptional upregulation of the endothelial vasodilatory potassium channel KCa2.3, and blockade of this channel prevents aldosterone-induced choroidal thickening (pachychoroid), 38 which is typical for CSC and which has led to the introduction of MR antagonists for CSC in clinical practice. Nonetheless, the variation in the KCa2.3 channel was very small at the protein level, suggesting the involvement of other mechanisms in inducing the observed choroidal changes in the rat model.…”

“…8,9 Because corticosteroids bind to both the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), it has been hypothesized that both are involved in the pathogenesis of CSC. 5,[9][10][11][12] Because of the plausible role of the choroidal endothelium in the pathophysiology of CSC, culturing of human choroidal endothelial cells (CECs) is of particular interest. [13][14][15][16] Endothelial cells (ECs) are heterogenic cells that show substantial sitespecific structural and biochemical variation due to their interaction with their surroundings.…”