Central serous chorioretinopathy: a pathogenetic model

Antonio Caccavale1, Filippo Romanazzi1, Manuela Imparato1, Angelo Negri2, Anna Morano3, Fabio Ferentini21Department of Ophthalmology, Neuropthalmology and Ocular Immunology Service, 2Department of Ophthalmology, Hospital &ldquo;C. Cant&ugrave;&rdquo;, Abbiategrasso, Milan, It...

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Autores principales:	et al, Manuela Imparato, Filippo Romanazzi, Antonio Caccavale
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2011
Materias:	Ophthalmology RE1-994
Acceso en línea:	https://doaj.org/article/20db36cb19634d2a8d05a49e62373bb0
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spelling	oai:doaj.org-article:20db36cb19634d2a8d05a49e62373bb02021-12-02T07:50:19ZCentral serous chorioretinopathy: a pathogenetic model1177-54671177-5483https://doaj.org/article/20db36cb19634d2a8d05a49e62373bb02011-02-01T00:00:00Zhttp://www.dovepress.com/central-serous-chorioretinopathy-a-pathogenetic-model-a6405https://doaj.org/toc/1177-5467https://doaj.org/toc/1177-5483Antonio Caccavale1, Filippo Romanazzi1, Manuela Imparato1, Angelo Negri2, Anna Morano3, Fabio Ferentini21Department of Ophthalmology, Neuropthalmology and Ocular Immunology Service, 2Department of Ophthalmology, Hospital &ldquo;C. Cant&ugrave;&rdquo;, Abbiategrasso, Milan, Italy; 3University Eye Clinic, Foundation IRCCS San Matteo Hospital, Pavia, ItalyAbstract: Despite numerous studies describing predominantly its demography and clinical course, many aspects of central serous chorioretinopathy (CSCR) remain unclear. Perhaps the major impediment to finding an effective therapy is the difficulty of performing studies with large enough cohorts, which has meant that clinicians have focused more on therapy than on a deeper understanding of the pathogenesis of the disease. Hypotheses on the pathogenesis of CSCR have ranged from a basic alteration in the choroid to an involvement of the retinal pigment epithelium (RPE). Starting from evidence that affected subjects often present a personality prone to stress with altered pituitary&ndash;hypothalamic axis response (HPA) and that they have higher levels of serum and urinary cortisol and catecholamines than healthy subjects, we hypothesize a cascade of events that may lead to CSCR through hypercoagulability and augmented platelet aggregation. In particular we investigated the role of tissue plasminogen activator, increasing plasminogen activator inhibitor 1 (PAI-1), and plasmin-&alpha;2- plasmin inhibitor complexes. We reviewed the different therapeutic approaches, including adrenergic antagonists, carbonic anhydrase inhibitors, mifepristone, ketoconazole, laser photocoagulation, intravitreal injection of bevacizumab, and photodynamic therapy with verteporfin (PDT) and our model of pathogenesis seems to be in agreement with the clinical effects obtained from these treatments. In accord with our thesis, we began to treat a group of patients affected by CSCR with low-dose aspirin (75&ndash;100 mg), because of its effectiveness in other vascular diseases and its low ocular and general toxicity with prolonged use. The formulation of a causative model of CSCR enables us to understand how the therapeutic approach cannot be based on a generalized therapy but should be individualized for each patient, and that sometimes a combined strategy of treatment is required. Moreover a complete knowledge of the disease will help to identify patients prone to the most persistent forms of CSCR, and thus help to find a treatment.Keywords: CSCR, aspirin, PAI-1, glucocorticoid, macula, pathogenesis&nbsp; et alManuela ImparatoFilippo RomanazziAntonio CaccavaleDove Medical PressarticleOphthalmologyRE1-994ENClinical Ophthalmology, Vol 2011, Iss default, Pp 239-243 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Ophthalmology RE1-994
spellingShingle	Ophthalmology RE1-994 et al Manuela Imparato Filippo Romanazzi Antonio Caccavale Central serous chorioretinopathy: a pathogenetic model
description	Antonio Caccavale1, Filippo Romanazzi1, Manuela Imparato1, Angelo Negri2, Anna Morano3, Fabio Ferentini21Department of Ophthalmology, Neuropthalmology and Ocular Immunology Service, 2Department of Ophthalmology, Hospital &ldquo;C. Cant&ugrave;&rdquo;, Abbiategrasso, Milan, Italy; 3University Eye Clinic, Foundation IRCCS San Matteo Hospital, Pavia, ItalyAbstract: Despite numerous studies describing predominantly its demography and clinical course, many aspects of central serous chorioretinopathy (CSCR) remain unclear. Perhaps the major impediment to finding an effective therapy is the difficulty of performing studies with large enough cohorts, which has meant that clinicians have focused more on therapy than on a deeper understanding of the pathogenesis of the disease. Hypotheses on the pathogenesis of CSCR have ranged from a basic alteration in the choroid to an involvement of the retinal pigment epithelium (RPE). Starting from evidence that affected subjects often present a personality prone to stress with altered pituitary&ndash;hypothalamic axis response (HPA) and that they have higher levels of serum and urinary cortisol and catecholamines than healthy subjects, we hypothesize a cascade of events that may lead to CSCR through hypercoagulability and augmented platelet aggregation. In particular we investigated the role of tissue plasminogen activator, increasing plasminogen activator inhibitor 1 (PAI-1), and plasmin-&alpha;2- plasmin inhibitor complexes. We reviewed the different therapeutic approaches, including adrenergic antagonists, carbonic anhydrase inhibitors, mifepristone, ketoconazole, laser photocoagulation, intravitreal injection of bevacizumab, and photodynamic therapy with verteporfin (PDT) and our model of pathogenesis seems to be in agreement with the clinical effects obtained from these treatments. In accord with our thesis, we began to treat a group of patients affected by CSCR with low-dose aspirin (75&ndash;100 mg), because of its effectiveness in other vascular diseases and its low ocular and general toxicity with prolonged use. The formulation of a causative model of CSCR enables us to understand how the therapeutic approach cannot be based on a generalized therapy but should be individualized for each patient, and that sometimes a combined strategy of treatment is required. Moreover a complete knowledge of the disease will help to identify patients prone to the most persistent forms of CSCR, and thus help to find a treatment.Keywords: CSCR, aspirin, PAI-1, glucocorticoid, macula, pathogenesis&nbsp;
format	article
author	et al Manuela Imparato Filippo Romanazzi Antonio Caccavale
author_facet	et al Manuela Imparato Filippo Romanazzi Antonio Caccavale
author_sort	et al
title	Central serous chorioretinopathy: a pathogenetic model
title_short	Central serous chorioretinopathy: a pathogenetic model
title_full	Central serous chorioretinopathy: a pathogenetic model
title_fullStr	Central serous chorioretinopathy: a pathogenetic model
title_full_unstemmed	Central serous chorioretinopathy: a pathogenetic model
title_sort	central serous chorioretinopathy: a pathogenetic model
publisher	Dove Medical Press
publishDate	2011
url	https://doaj.org/article/20db36cb19634d2a8d05a49e62373bb0
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Central serous chorioretinopathy: a pathogenetic model

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