Caccavale Antonio, Romanazzi Filippo, Imparato Manuela, Negri Angelo, Morano Anna, Ferentini Fabio
Department of Ophthalmology, Neuropthalmology and Ocular Immunology Service.
Clin Ophthalmol. 2011;5:239-43. doi: 10.2147/OPTH.S17182. Epub 2011 Feb 20.
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-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-α2- 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 (75-100 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.
尽管有大量研究主要描述了中心性浆液性脉络膜视网膜病变（CSCR）的人口统计学和临床病程，但该疾病的许多方面仍不明确。或许寻找有效治疗方法的主要障碍在于难以开展足够大规模队列的研究，这意味着临床医生更多地关注治疗，而非对疾病发病机制的深入理解。关于CSCR发病机制的假说范围广泛，从脉络膜的基本改变到视网膜色素上皮（RPE）的参与。从受影响的受试者常表现出易应激的性格且垂体 - 下丘脑轴反应（HPA）改变，以及他们血清和尿皮质醇及儿茶酚胺水平高于健康受试者的证据出发，我们推测了一系列可能通过高凝状态和血小板聚集增强导致CSCR的事件。特别是我们研究了组织型纤溶酶原激活剂、纤溶酶原激活剂抑制剂1（PAI - 1）增加以及纤溶酶 - α2 - 纤溶酶抑制剂复合物的作用。我们回顾了不同的治疗方法，包括肾上腺素能拮抗剂、碳酸酐酶抑制剂、米非司酮、酮康唑、激光光凝、玻璃体内注射贝伐单抗以及维替泊芬光动力疗法（PDT），并且我们的发病机制模型似乎与这些治疗所获得的临床效果一致。根据我们的论点，我们开始用低剂量阿司匹林（75 - 100毫克）治疗一组受CSCR影响的患者，这是因为它在其他血管疾病中有效，且长期使用时眼部和全身毒性较低。CSCR病因模型的构建使我们明白治疗方法不能基于通用疗法，而应针对每个患者个体化，有时需要联合治疗策略。此外，对该疾病的全面了解将有助于识别易患最持久形式CSCR的患者，从而有助于找到治疗方法。
