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论文范文
1. Introduction Central serous chorioretinopathy (CSC) is a posterior segment disease characterized by the serous detachment of the neurosensory retina in the macular area [1]. CSC occurs in 9.9 per 100,000 men and 1.7 per 100,000 women, six times more frequently in men than in women [2]. This disease can be classified as acute (less than three to six months in duration) or chronic (longer term) [3]. As a benign and self-limiting disease, most acute CSC cases last only between two and three months [4]; however, CSC recurs in approximately one-third of recovered patients [5]. The symptoms of acute CSC are related to the localization of the subretinal detachment around the macular area and limited focal or multifocal retinal pigment epithelium (RPE) alterations. Chronic CSC may also cause severe loss of visual acuity and decreased light sensitivity [6]. Advances in imaging techniques, such as fluorescein fundus angiography (FFA) and indocyanine green angiography (ICGA), have enabled researchers to obtain a better understanding of the anatomical structural alterations occurring in CSC. They include disturbed choroidal circulation and retinal pigment epithelium (RPE) which are the primary changes associated with this disease. The current understanding of the pathophysiology of CSC involves choroidal vascular hyperpermeability, which leads to increased tissue hydrostatic pressure beneath the RPE and discontinuity of the RPE [7]. ICGA findings showed staining of the inner choroid in the midphase of the angiogram, suggesting that choroidal vascular hyperpermeability may arise from venous congestion and ischemia [8]. Some studies found that patients affected by CSC often have higher levels of serum and urinary cortisol and catecholamines than do healthy subjects and therapies with local or systemic steroids can cause the disease [9–11]. Glucocorticoid elevations were also identified as the primary risk factor for the onset of CSC [12–14]. However, some regions of the retina may show signs of increased choroidal hyperpermeability but are not linked to manifestations of CSC [8]. Additionally, Turkcu et al. found that the antioxidant capacity decreased significantly in CSC cases, which implies that the oxidative process is involved in the pathogenesis of CSC [15]. Because the choroidal vessels contribute greatly to CSC pathophysiology and the ophthalmic artery supplies the retinal circulation, this study investigated whether altered retinal circulation was also related to CSC. Noninvasive spectrophotometric retinal oximetry has been used to measure oxygen saturation in retinal arterioles and venules [16]. This method was applied to determine whether there is an association between changes in retinal vessel oxygen saturation and the vessel diameter around the macular region in patients with CSC. In this study, we used a noninvasive retinal oximeter to measure oxygen saturation in retinal vessels in patients with CSC to detect retinal oxygen metabolic changes. 2. Materials and Methods The study protocol was reviewed and approved by the Sun Yat-sen University Medical Ethics Committee (Zhongshan Ophthalmic Center Medical Ethics (2013) number 07). The protocol strictly adhered to the principles of the World Medical Association’s Declaration of Helsinki. Informed consent was obtained from all subjects before examinations were performed. 
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