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• W2023925443 abstract "Purpose: Central serous chorioretinopathy (CSCR) mostly affects middle-aged men and has been associated with stress and hypercortisolism. We hypothesized that some factors prone to inducing CSCR could also have a harmful effect on erectile function. This study aimed to investigate the risk of subsequent erectile dysfunction after CSCR using Taiwan National Health Insurance Research Database. Methods: The study cohort (n = 1220) consisted of newly diagnosed CSCR men aged 19–64 years between 1999 and 2007, and men matched for age, monthly income and time of enrolment were randomly selected as the control group (n = 10870). Cox proportional hazard regressions were performed to calculate the hazard ratios (HR) of clinically diagnosed erectile dysfunction (including organic origin and/or psychogenic origin) for the two groups. Erectile dysfunction-free survival analysis was assessed using a Kaplan–Meier method. Results: Twenty-five patients (2.0%) from the CSCR cohort and 103 (0.9%) from the control group were diagnosed erectile dysfunction clinically during a mean observation period of 4.3 years. Patients with CSCR had a significantly higher incidence of erectile dysfunction diagnosis than those without CSCR (p < 0.001). After adjusting for age, geographic location, chronic comorbidities and medication habits, patients with CSCR were found to have a 2.22-fold [95% confidence interval (CI), 1.42–3.46] higher hazard ratio of a subsequent erectile dysfunction diagnosis than the matched controls. The adjusted HR for organic and psychogenic erectile dysfunction were 2.14 (95% CI: 1.34–3.44) and 3.83 (95% CI: 1.47–10.01), respectively. Conclusions: Central serous chorioretinopathy was independently associated with an increased risk of being diagnosed with erectile dysfunction. Central serous chorioretinopathy (CSCR) is a common maculopathy characterized by serous neurosensory retinal detachment associated with focal lesions of retinal pigment epithelium and abnormalities of choroidal circulation (Iida et al. 1999; Kitaya et al. 2003). Central serous chorioretinopathy typically affects young and middle-aged adults, with the incidence approximately six times higher in men than in women (Kitzmann et al. 2008). With indocyanine green angiography (ICGA), delayed filling of the choroidal arteries and choriocapillaris, venous congestion and focal hyperfluorescence of the choroid have been observed in CSCR eyes (Iida et al. 1999; Kitaya et al. 2003). Decreased foveal choroidal blood flow in CSCR has also been demonstrated using laser Doppler flowmetry (Kitaya et al. 2003). The acute phase of CSCR often follows a self-limited course with good recovery of visual function. However, recurrences develop in about one-third to half of patients with CSCR and tend to reduce the final visual outcome (Ficker et al. 1988; Wang et al. 2008). Although the pathogenesis of CSCR is still under debate, it is generally accepted that a Type A or stressful personality, endogenous hypercortisolism and glucocorticoid medication have a significant impact on the pathophysiology of CSCR (Wakakura & Ishikawa 1984; Gelber & Schatz 1987; Yannuzzi 1987; Bouzas et al. 1993). Stress stimuli may activate hypothalamic–pituitary–adrenal (HPA) axis and subsequently increase cortisol secretion. Previous studies have demonstrated elevated values of plasma and urine cortisol in Type A persons (Williams et al. 1982; Chrousos & Gold 1992), as well as patients with CSCR (Garg et al. 1997; Haimovici et al. 2003). Glucocorticoids can modulate platelet aggregation and thrombus formation. Furthermore, there is a trend towards increased levels of plasma plasminogen activator inhibitor-1 (PAI-1), the major inhibitor of physiologic fibrinolysis, among patients with CSCR (Yamada et al. 1993; Iijima et al. 1999). These observations suggest that increased platelet aggregation and impaired fibrinolysis may play a role in the choroidal circulatory disturbance found in CSCR eyes (Caccavale et al. 2009). Erectile dysfunction, the consistent or recurrent inability to attain and keep a sufficient penile erection for satisfactory sexual performance (NIH Consensus Conference 1993), is a complex disorder with multiple aetiologies, which may be vascular, hormonal, neurologic and/or psychogenic in origin (Virag et al. 1985). This embarrassing sexual problem may not only reduce the quality of life and well-being but has also been recognized as a disease marker of cardiovascular diseases and stroke (Kirby et al. 2001; Chung et al. 2011a,b; Shin et al. 2011). A growing body of evidence has demonstrated that both organic erectile dysfunction and cardiovascular diseases share some pathogeneses in common and may be the consequences of endothelial dysfunction (Costa & Virag 2009; Shin et al. 2011). Stress is also a psychogenic factor of erectile dysfunction, and elevated levels of active forms of cortisol, the standard stress indicator, have been found in serum and saliva among men with erectile dysfunction (Kobori et al. 2009). These stress-related characteristics are found in patients with CSCR as well. Both the choroid and penis have a rich vasculature, and impaired microcirculation has been disclosed in the choroids of patients with CSCR and in the penises of men with erectile dysfunction. Apart from the common finding of elevated levels of circulating stress hormones in both patient groups, these similar attributes are suggestive of a possible association between CSCR and erectile dysfunction. However, to the best of our knowledge, no published study has investigated the risk of clinically diagnosed erectile dysfunction after a diagnosis of CSCR. We used the Taiwan National Health Insurance Research Database to conduct this nationwide population-based study with a retrospective longitudinal study design to evaluate the impact of CSCR on the risk of subsequent diagnosis of erectile dysfunction. The National Health Insurance (NHI) program in Taiwan, a mandatory, single-payer social health insurance system, has been operating since 1995 and currently has more than 22 million enrollees, representing nearly 99% of the entire population of Taiwan. The National Health Insurance Research Database (NHIRD), containing all the original claims data from the NHI program, is published annually by the Taiwan National Health Research Institute (NHRI) in an electronically encrypted form. It is one of the largest and most comprehensive nationwide population-based databases in the world and has been used extensively in epidemiological studies. A cohort data set composed of 1 000 000 randomly sampled beneficiaries covered by the NHI program in year 2000 was created by the NHRI for research purposes. These random samples were confirmed by the NHRI to be representative of the Taiwanese population under the NHI program, and all their claims data are available from 1996 onwards. Therefore, we analysed this representative cohort data set to identify the risk of clinically diagnosed erectile dysfunction among the patients with the diagnosis of CSCR. The Institutional Review Board of National Yang-Ming University Hospital approved this study and waived the requirement of informed consent because of analysing data sets in a database, which is devoid of identifiable personal information. This study adhered to the Declaration of Helsinki and all laws in Taiwan. In our study, both the CSCR cohort and control group were obtained from the aforementioned longitudinal data set. The CSCR cohort consisted of male patients who were of age 19–64 years and newly diagnosed as cases of CSCR [International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) code 362.41] from 1 January 1999 to 31 December 2007. Those who had been diagnosed with CSCR before 1999 were excluded to increase the likelihood of a purge of pre-existing patients with chronic or recurrent CSCR. The paediatric population was not included as CSCR and erectile dysfunction always occur in adults. Incident CSCR also occurs rarely in the elderly, so we excluded subjects aged 65 years or above to minimize the likelihood of inadvertently including patients with age-related maculopathies mimicking CSCR. Using stratified random sampling, the control group was selected from male enrollees without CSCR throughout the whole course of observation and was matched with the study cohort in terms of age, monthly income and the time of outpatient visits for the first CSCR diagnosis. In both groups, subjects who had received any organ transplantation (ICD-9-CM codes V42.xx) or had been diagnosed as cases of erectile dysfunction (302.72 or 607.84), spinal cord injury (344.1), systemic lupus erythematosus (710.0), malignancy (140.0–199.1) or major depression (296.2x, 296.3x) before enrolment were excluded. All of the subjects had been observed until being diagnosed as erectile dysfunction or the end of database review before 31 December 2007. The end-point of the study was defined as occurrence of clinically diagnosed erectile dysfunction (ICD-9-CM code 607.84 for organic impotence and 302.72 for psychogenic impotence) throughout the observation period. In our study, erectile dysfunction diagnosis was identified on the basis of the registry of erectile dysfunction by urologists as a principle diagnosis in the database rather than self-reporting questionnaires such as the International Index of Erectile Function. A similar method of identifying erectile dysfunction cases who sought ambulatory care by ICD registry has been accepted and used in other population-based epidemiological investigations (Chou et al. 2011; Chung et al. 2011a,b). microsoft sql server 2005 (Microsoft Corporation, Redmond, WA, USA) was used for data management and computing, and all statistical analyses were performed using spss software (Version 15.0, SPSS Inc., Chicago, IL, USA). All data were expressed as mean ± standard deviation (SD) or percentage. Differences between the two groups in terms of sociodemographic characteristics, pre-existing comorbidities [hypertension (ICD-9-CM codes 401.xx–405.xx), diabetes mellitus (250.xx), hyperlipidaemia (272.xx), coronary artery disease (410.xx–414.xx), dysrhythmia (427.xx, 785.0, 785.1), chronic lung disease (490.xx–496.xx) and chronic renal disease (580.xx–587.xx)] and drug exposure (alpha-1 adrenergic blockers and beta adrenergic blockers) were determined by the independent Student’s t-test or Pearson’s chi-square test as appropriate. Exposure to each drug category was defined as ever or never according to whether the subject had ever received the prescriptions for more than 6 months. Survival analysis was assessed using Kaplan–Meier method, with the significance based on the log-rank test. Multivariate regression analysis was carried out using Cox proportional hazard regression analysis with adjustment for age, geographic location and chronic comorbidities (hypertension, diabetes mellitus, hyperlipidaemia, coronary artery disease, dysrhythmia, chronic lung disease and chronic renal disease) and drug exposures (alpha-1 adrenergic blockers and beta adrenergic blockers). Statistical significance was inferred at a two-sided p-value of <0.05. A total of 1220 male patients (mean age 41.5 ± 9.8 years) with newly diagnosed CSCR were identified from the 1 000 000 sampling cohort data set between January 1999 and December 2007. Another 10 870 male patients matched for age, time of enrolment and monthly income were recruited as the control group. Table 1 shows the distributions of sociodemographic characteristics, pre-existing comorbidities and drug exposures for these two cohorts. Patients with CSCR were more likely to have chronic comorbidities of hypertension (p < 0.001), hyperlipidaemia (p < 0.001), chronic lung disease (p < 0.001), dysrhythmia (p = 0.001) and coronary artery disease (p < 0.001) at baseline as being compared with controls. The percentage of subsequent erectile dysfunction diagnosis among the patients with CSCR and controls is presented in Table 2. Of the total 12 090 sampled subjects, 128 patients (1.1%) were diagnosed with erectile dysfunction (organic and/or psychogenic origin) during an average of 4.3 ± 2.4 years of observation period, including 25 (2.0%) from the CSCR cohort and 103 (0.9%) from the control group. The log-rank test showed that the patients with CSCR had a significantly higher incidence of erectile dysfunction compared to those without CSCR diagnosis (p < 0.001). Figure 1 shows the results of the Kaplan–Meier analysis. Kaplan–Meier curves of freedom from diagnosis of erectile dysfunction (ED) in subjects with and without central serous chorioretinopathy (CSCR). There was a statistically significant difference between the two curves (log-rank test, p < 0.001). The distributions of organic and psychogenic erectile dysfunction diagnoses between the both cohorts were also analysed. Among all clinically diagnosed erectile dysfunction patients, 106 (82.8%), 13 (10.2%) and 9 (7.0%) patients suffered from organic origin, psychogenic origin and mixed type, respectively. In the CSCR cohort, 22 (1.8%) and 6 (0.5%). had the diagnosis of organic and psychogenic erectile dysfunction, respectively. In the control cohort, 93 (0.9%) and 16 (0.1%). had the diagnosis of organic and psychogenic erectile dysfunction, respectively. There were significantly higher incidences of organic and psychogenic erectile dysfunction in the CSCR cohort compared to the controls (p < 0.001 and p = 0.006, respectively). Table 2 also shows the crude and adjusted hazard ratios (HRs) for erectile dysfunction by cohort. After adjusting for covariates including age, geographic location, hypertension, diabetes mellitus, hyperlipidaemia, coronary artery disease, dysrhythmia, chronic lung disease, chronic renal disease, alpha-1 adrenergic blockers use and beta adrenergic blockers use, CSCR was independently associated with the increased risk of clinically diagnosed erectile dysfunction [HR, 2.22; 95% confidence interval (CI), 1.42–3.46; p < 0.001], organic erectile dysfunction (HR, 2.14; 95% CI, 1.34–3.44; p = 0.002) and psychogenic erectile dysfunction (HR, 3.83; 95% CI, 1.47–10.01; p = 0.006). The association between CSCR and erectile dysfunction has never been elucidated in the literature. Our current population-based study firstly identified CSCR as an independent risk factor for either organic or psychogenic erectile dysfunction diagnoses in an Asian population. We demonstrated that men with CSCR were more likely to suffer from subsequent diagnosis of erectile dysfunction than those without, after adjusting for age, geographic location, pre-existing comorbidities and drug exposures. Our novel findings demonstrated that there was a significant association between CSCR and increased risk of subsequent diagnosis of erectile dysfunction and suggested the hypothesis that some factors involved in the pathogenesis of CSCR could also have a harmful effect on erectile function. Although the exact mechanism of CSCR remains undetermined, glucocorticoids, which may affect the choroidal vasculature, Bruch’s membrane and the retinal pigment epithelium, are believed to play a critical role in the pathogenesis of CSCR (Bouzas et al. 2002). Excessive cortisol may facilitate capillary hyperpermeability and fragility and promote blood coagulation, giving rise to fluid leakage into the subretinal space and choroidal hypoperfusion (Bouzas et al. 2002). In addition, the production of local vasodilators, such as prostaglandins and nitric oxide (NO), can be suppressed by glucocorticoids (Worrall et al. 1996), which consequently leads to abnormalities in the regulation of choroidal blood flow (Mann et al. 1995). On the other hand, cortisol has been reported to play an inhibitory role in the mechanism of penile erection, suggesting the possible relationship between cortisol and erectile dysfunction (Granata et al. 1995; Uckert et al. 2003; Kobori et al. 2009). Uckert et al. 2003 demonstrated that serum levels of cortisol of healthy volunteers significantly decreased in the systemic circulation and cavernous blood with increasing sexual arousal, when the flaccid penis became rigid. Kobori et al. 2009 showed negative correlations between the active forms of cortisol and sexual function, indicating that erectile dysfunction occurs in patients with high levels of cortisol because of the relationship between cortisol and stress. Granata et al. 1995 disclosed a link between increased circulating cortisol and impaired erectile response to intracavernosal injections of prostaglandin E1 in men with erectile dysfunction. Taken together, it is reasonable to postulate that an abnormal elevation of cortisol levels would be a common risk factor shared by both CSCR and erectile dysfunction. Furthermore, a higher HR was observed between CSCR and psychogenic erectile dysfunction diagnosis in this study, further suggesting a possible connection between CSCR and erectile dysfunction through increased psychogenic stress. The disturbance of choroidal microcirculation in CSCR is thought to be related to the localized occlusion of choriocapillaris based on the findings of ICGA studies (Kitaya et al. 2003). Besides, reduced retinal flow circulation in CSCR has been found using retinal function imager (Beutelspacher et al. 2011). Although the mechanisms underlying these circulatory abnormalities have not been determined, the vascular endothelial injury and mircothrombus formation in CSCR are associated with impaired choroidal fibrinolysis, steroid-induced vasoconstriction, suppression of NO and prostacyclin and augmented platelet-mediated clotting (Yamada et al. 1993; Iijima et al. 1999; Haimovici et al. 2003; Caccavale et al. 2009, 2011). In addition, the enhanced HPA reactivity during stress is related to systemic hypertension induced by increased vascular resistance (Nyklicek et al. 2005; Caccavale et al. 2011). The penis is also a richly vascularized organ, and penile erections are considered to be a predominantly vascular event (Shin et al. 2011). Most organic erectile dysfunction has underlying vascular pathologies, especially atherosclerosis (Aversa et al. 2010). NO, produced and released by intact penile endothelium, promotes the relaxation of arterial and cavernosal smooth muscle via activation of guanylate cyclase and suppression of activator Ca2+, which in turn results in dilation of penile arteries and penile erection (Jeremy et al. 2000). It is widely accepted that endothelial dysfunction, in particular the release and actions of NO, is the basic initiator of atherosclerotic change and the main aetiologic factor in several vascular diseases, including erectile dysfunction (Costa & Virag 2009; Chung et al. 2011a,b; Shin et al. 2011). The major consequence of the impaired availability of NO is the increased adhesion and aggregation of platelets and neutrophils, and the release of vasoconstrictors, such as thromboxane A2 and serotonin (Jeremy et al. 2000). Because of the smaller diameter of vessels in the choroids than in the penis, we hypothesize that the same size of lumen obstruction has a greater and earlier effect on blood flow in the choroids. However, there is very limited knowledge regarding endothelial function among patients with CSCR. Further investigations to assess endothelial function with brachial artery flow-mediated dilation may be helpful to elucidate the relationship between endothelial dysfunction and CSCR. It is reported that erectile dysfunction affects an estimated 150 million men worldwide, and the prevalence continues to grow as the population ages (Ayta et al. 1999). On the basis of various definitions and methods in previous studies, the prevalence of erectile dysfunction has been reported to be between 2% and 13% for men aged 40–49 years and between 6% and 29% for those aged 50–59 years (Nicolosi et al. 2003, 2004; Inman et al. 2009). Compared with these studies that surveyed prevalent erectile dysfunction patients with self-reported questionnaires, the frequency of erectile dysfunction seemed to be low in our study, which used ICD-9-CM coding to identify incident erectile dysfunction cases. Sex has always been an embarrassing subject and a cultural taboo in Asian society, and men complaining of mild erectile dysfunction may be reluctant to admit to this disorder and seek medical attention. Those who are willing to visit urologists for evaluation and treatment may have more significant symptoms and disease severity. In addition, our study population was relatively young, and the incidence of erectile dysfunction in this age group is lower than in the elderly (Nicolosi et al. 2003, 2004; Inman et al. 2009). The strength of our study is that we retrospectively collected data from the NHIRD, which provides nationwide, population-based and randomized claims information of insured people in Taiwan. In addition, the longitudinal data enabled us to trace the differences between the CSCR cohort and controls and to measure the risk for subsequent diagnosis of erectile dysfunction more effectively than other study methods such as medical chart reviews and cross-sectional field investigations. However, several limitations to our study should be pointed out. First, the reliability and validity of secondary data should be considered. Diagnoses of CSCR, erectile dysfunction and other comorbidities that are based on the administrative database may be less accurate than those obtained individually through standardized procedures. Nevertheless, similar analysis methods to identify erectile dysfunction and other maculopathies have been used and proven valid in previous studies (Ho et al. 2009; Hu et al. 2009; Chou et al. 2011; Chung et al. 2011a,b). Second, personal information that might contribute to erectile dysfunction, such as body mass index and smoking habit, are not available in the administrative database, and this could have compromised our results. Third, CSCR may be asymptomatic if the fovea is not involved. Subjects with eccentric CSCR may have been undiagnosed and misclassified into the control group, which could have lead to misclassification bias in our study. However, this nondifferential misclassification might bias our results towards null hypothesis. Fourth, data regarding the clinical severity of CSCR, such as visual acuity or central fovea thickness, are not available in NHIRD, which hinders us from evaluating the dose–response relationship between CSCR severity and risk of erectile dysfunction. Fifth, the pathogenesis of CSCR is still poorly understood, and the aetiology of erectile dysfunction is multifactorial. It is possible that there are some unknown or unmeasured shared confounders that are not controlled in the regression analysis. Finally, the external validity of our findings may be a concern as our study subjects are of Chinese ethnicity. The generalizability of our results to other non-East Asian ethnic groups needs to be further evaluated. In conclusion, we demonstrated large-scale epidemiological evidence of a significantly increased hazard ratio for subsequent diagnosis of erectile dysfunction among patients with CSCR diagnosis. Although our results imply that some factors involved in the pathogenesis of CSCR may play a role in erectile dysfunction, the underlying mechanisms remain elusive. Further prospective studies are warranted to explore the underlying mechanism of this association. This study was partly supported by research grants from RD 2010-028 and RD2011-020 from National Yang-Ming University Hospital, Yilan, Taiwan; V99B1-011, V99C1-125 and V100B-013 from Taipei Veterans General Hospital, Taipei, Taiwan; CI-97-13 and CI-98-16 from the Yen Tjing Ling Medical Foundation, Taipei, Taiwan; NSC 100-2314-B-075-055 from the National Science Council and NSC-99-2911-I-009-101 from the UST-UCSD International Center of Excellence in Advanced Bio-engineering sponsored by the Taiwan National Science Council I-RiCE Program. The sponsor or funding organization had no role in the design or conduct of this research. All the authors declare that there is no potential conflict of interest." @default.
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• W2023925443 title "Increased risk of erectile dysfunction among males with central serous chorioretinopathy - a retrospective cohort study" @default.
• W2023925443 cites W1498511941 @default.
• W2023925443 cites W1580980304 @default.
• W2023925443 cites W1600505145 @default.
• W2023925443 cites W1669261011 @default.
• W2023925443 cites W1832887128 @default.
• W2023925443 cites W1931088434 @default.
• W2023925443 cites W1943838044 @default.
• W2023925443 cites W1965711370 @default.
• W2023925443 cites W1995557286 @default.
• W2023925443 cites W2011326884 @default.
• W2023925443 cites W2021282547 @default.
• W2023925443 cites W2021908078 @default.
• W2023925443 cites W2035395401 @default.
• W2023925443 cites W2035442658 @default.
• W2023925443 cites W2035928356 @default.
• W2023925443 cites W2038002179 @default.
• W2023925443 cites W2038448732 @default.
• W2023925443 cites W2045342919 @default.
• W2023925443 cites W2055363592 @default.
• W2023925443 cites W2063167222 @default.
• W2023925443 cites W2064810726 @default.
• W2023925443 cites W2065417670 @default.
• W2023925443 cites W2081299090 @default.
• W2023925443 cites W2085992983 @default.
• W2023925443 cites W2088818069 @default.
• W2023925443 cites W2091882382 @default.
• W2023925443 cites W2093177844 @default.
• W2023925443 cites W2093216792 @default.
• W2023925443 cites W2117467286 @default.
• W2023925443 cites W2123095204 @default.
• W2023925443 cites W2123591247 @default.
• W2023925443 cites W2130577608 @default.
• W2023925443 cites W2135099241 @default.
• W2023925443 cites W2136252004 @default.
• W2023925443 cites W2142229996 @default.
• W2023925443 cites W2152856257 @default.
• W2023925443 cites W2334432374 @default.
• W2023925443 cites W4243770305 @default.
• W2023925443 cites W4294184534 @default.
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