{"title":"糖皮质激素在中枢性浆液性脉络膜视网膜病变中的作用的完全相反的观点","authors":"F. Behar-Cohen","doi":"10.1016/j.mehy.2025.111777","DOIUrl":null,"url":null,"abstract":"<div><div>Central serous chorioretinopathy (CSCR) is traditionally linked to glucocorticoid (GC) excess. We propose the opposite: in predisposed individuals, subtle hypothalamic–pituitary–adrenal (HPA) axis suppression—triggered by systemic GC exposure or maladaptive stress responses—lowers intraocular cortisol, shifts the glucocorticoid/mineralocorticoid receptor balance, and drives mineralocorticoid receptor (MR) overactivation in the retinal pigment epithelium–choroid complex. This cascade induces choroidal neuropathy, pachychoroid phenotype, and retinal pigment epithelium (RPE) barrier breakdown. Experimental models, biomarker studies, and metabolomic data support this mechanism, reconciling why systemic but not intraocular GCs are associated with CSCR. If confirmed, this paradigm shift would favor cautious GC tapering, local ocular GC supplementation, and MR antagonism as targeted therapeutic strategies.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"204 ","pages":"Article 111777"},"PeriodicalIF":0.8000,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A diametrically opposed view of the role of glucocorticoids in central serous chorioretinopathy\",\"authors\":\"F. Behar-Cohen\",\"doi\":\"10.1016/j.mehy.2025.111777\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Central serous chorioretinopathy (CSCR) is traditionally linked to glucocorticoid (GC) excess. We propose the opposite: in predisposed individuals, subtle hypothalamic–pituitary–adrenal (HPA) axis suppression—triggered by systemic GC exposure or maladaptive stress responses—lowers intraocular cortisol, shifts the glucocorticoid/mineralocorticoid receptor balance, and drives mineralocorticoid receptor (MR) overactivation in the retinal pigment epithelium–choroid complex. This cascade induces choroidal neuropathy, pachychoroid phenotype, and retinal pigment epithelium (RPE) barrier breakdown. Experimental models, biomarker studies, and metabolomic data support this mechanism, reconciling why systemic but not intraocular GCs are associated with CSCR. If confirmed, this paradigm shift would favor cautious GC tapering, local ocular GC supplementation, and MR antagonism as targeted therapeutic strategies.</div></div>\",\"PeriodicalId\":18425,\"journal\":{\"name\":\"Medical hypotheses\",\"volume\":\"204 \",\"pages\":\"Article 111777\"},\"PeriodicalIF\":0.8000,\"publicationDate\":\"2025-09-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical hypotheses\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0306987725002166\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical hypotheses","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306987725002166","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
A diametrically opposed view of the role of glucocorticoids in central serous chorioretinopathy
Central serous chorioretinopathy (CSCR) is traditionally linked to glucocorticoid (GC) excess. We propose the opposite: in predisposed individuals, subtle hypothalamic–pituitary–adrenal (HPA) axis suppression—triggered by systemic GC exposure or maladaptive stress responses—lowers intraocular cortisol, shifts the glucocorticoid/mineralocorticoid receptor balance, and drives mineralocorticoid receptor (MR) overactivation in the retinal pigment epithelium–choroid complex. This cascade induces choroidal neuropathy, pachychoroid phenotype, and retinal pigment epithelium (RPE) barrier breakdown. Experimental models, biomarker studies, and metabolomic data support this mechanism, reconciling why systemic but not intraocular GCs are associated with CSCR. If confirmed, this paradigm shift would favor cautious GC tapering, local ocular GC supplementation, and MR antagonism as targeted therapeutic strategies.
期刊介绍:
Medical Hypotheses is a forum for ideas in medicine and related biomedical sciences. It will publish interesting and important theoretical papers that foster the diversity and debate upon which the scientific process thrives. The Aims and Scope of Medical Hypotheses are no different now from what was proposed by the founder of the journal, the late Dr David Horrobin. In his introduction to the first issue of the Journal, he asks ''what sorts of papers will be published in Medical Hypotheses? and goes on to answer ''Medical Hypotheses will publish papers which describe theories, ideas which have a great deal of observational support and some hypotheses where experimental support is yet fragmentary''. (Horrobin DF, 1975 Ideas in Biomedical Science: Reasons for the foundation of Medical Hypotheses. Medical Hypotheses Volume 1, Issue 1, January-February 1975, Pages 1-2.). Medical Hypotheses was therefore launched, and still exists today, to give novel, radical new ideas and speculations in medicine open-minded consideration, opening the field to radical hypotheses which would be rejected by most conventional journals. Papers in Medical Hypotheses take a standard scientific form in terms of style, structure and referencing. The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific communication, which ideas must eventually enter if they are to be critiqued and tested against observations.