Adverse effect of corticosteroid therapy: Central serous chorioretinopathy

Geoffroy, M.; Afriat, Mickael; Fauconier, Marion; Eschard, J. P.; Salmon, Jessica

doi:10.1016/j.jbspin.2017.02.001

Cited by 4 publications

(1 citation statement)

References 9 publications

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“…However, in contrast to the other GCs-induced side effects, the route of GCs administration influences the risk of CSCR. The nasal, articular, oral and dermal routes favor CSCR [12][13][14][15][16][17][18][19][20][21] but not the high and sustained intraocular GCs [22,23]. This clinical observation led us to hypothesize that it is not the increase in ocular GCs levels but rather a consequence of systemic corticosteroids on ocular corticosteroids that may be the link between CSCR and corticosteroid therapy.…”

Section: Introductionmentioning

confidence: 99%

Chronic Systemic Dexamethasone Regulates the Mineralocorticoid/Glucocorticoid Pathways Balance in Rat Ocular Tissues

Zola

Mejlachowicz

Arribada

et al. 2022

IJMS

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Central serous chorioretinopathy (CSCR) is a retinal disease affecting the retinal pigment epithelium (RPE) and the choroid. This is a recognized side-effect of glucocorticoids (GCs), administered through nasal, articular, oral and dermal routes. However, CSCR does not occur after intraocular GCs administration, suggesting that a hypothalamic-pituitary-adrenal axis (HPA) brake could play a role in the mechanistic link between CSCR and GS. The aim of this study was to explore this hypothesis. To induce HPA brake, Lewis rats received a systemic injection of dexamethasone daily for five days. Control rats received saline injections. Baseline levels of corticosterone were measured by Elisa at baseline and at 5 days in the serum and the ocular media and dexamethasone levels were measured at 5 days in the serum and ocular media. The expression of genes encoding glucocorticoid receptor (GR), mineralocorticoid receptors (MR), and the 11 beta hydroxysteroid dehydrogenase (HSD) enzymes 1 and 2 were quantified in the neural retina and in RPE/ choroid. The expression of MR target genes was quantified in the retina (Scnn1A (encoding ENac-α, Kir4.1 and Aqp4) and in the RPE/choroid (Shroom 2, Ngal, Mmp9 and Omg, Ptx3, Plaur and Fosl-1). Only 10% of the corticosterone serum concentration was measured in the ocular media. Corticosterone levels in the serum and in the ocular media dropped after 5 days of dexamethasone systemic treatment, reflecting HPA axis brake. Whilst both GR and MR were downregulated in the retina without MR/GR imbalance, in the RPE/choroid, both MR/GR and 11β-hsd2/11β-hsd1 ratio increased, indicating MR pathway activation. MR-target genes were upregulated in the RPE/ choroid but not in the retina. The psychological stress induced by the repeated injection of saline also induced HPA axis brake with a trend towards MR pathway activation in RPE/ choroid. HPA axis brake causes an imbalance of corticoid receptors expression in the RPE/choroid towards overactivation of MR pathway, which could favor the occurrence of CSCR.

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