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      The effect of eradicating Helicobacter pylori on idiopathic central serous chorioretinopathy patients

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          Abstract

          Purpose

          To evaluate the effect of Helicobacter pylori ( H. pylori) eradication on the remission of acute idiopathic central serous chorioretinopathy (ICSCR).

          Study design

          A prospective, randomized, placebo-controlled study of 53 participants.

          Main outcome measure

          Twenty-seven acute ICSCR patients tested positive for H. pylori were given an eradication H. pylori therapy, and another 26 patients with the same diagnosis received matching placebo medication. All participants were tested for the following items: (1) disappearance rate of subretinal fluid (SRF); (2) best-corrected visual acuity (BCVA); and (3) central retinal sensitivity at baseline, 2 weeks, 4 weeks, 8 weeks, and 12 weeks after treatment. The difference between the two groups was analyzed by PASW statistics version 18.0.

          Results

          At each follow-up, the disappearance rate of SRF in the active treatment group seemed slightly better than in the control group, but no statistically significant differences were observed ( P > 0.05 at each follow-up). The BCVA between the two groups also did not demonstrate statistically significant differences ( P > 0.05 at each follow-up). Unlike the BCVA and the disappearance rate of SRF, we compared the change in central retinal sensitivity at 12 weeks after treatment; a statistical difference was observed ( P = 0.042).

          Conclusion

          Our findings suggested that H. pylori eradication does not improve BCVA and the disappearance rate of SRF, but it could improve the central retinal sensitivity in acute ICSCR patients. We recommend that chronic ICSCR patients and more sensitive methods for H. pylori diagnosis should be involved in evaluating the effect of H. pylori eradication.

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          Most cited references 33

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          Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy.

          Central serous chorioretinopathy (CSCR) is a vision-threatening eye disease with no validated treatment and unknown pathogeny. In CSCR, dilation and leakage of choroid vessels underneath the retina cause subretinal fluid accumulation and retinal detachment. Because glucocorticoids induce and aggravate CSCR and are known to bind to the mineralocorticoid receptor (MR), CSCR may be related to inappropriate MR activation. Our aim was to assess the effect of MR activation on rat choroidal vasculature and translate the results to CSCR patients. Intravitreous injection of the glucocorticoid corticosterone in rat eyes induced choroidal enlargement. Aldosterone, a specific MR activator, elicited the same effect, producing choroid vessel dilation -and leakage. We identified an underlying mechanism of this effect: aldosterone upregulated the endothelial vasodilatory K channel KCa2.3. Its blockade prevented aldosterone-induced thickening. To translate these findings, we treated 2 patients with chronic nonresolved CSCR with oral eplerenone, a specific MR antagonist, for 5 weeks, and observed impressive and rapid resolution of retinal detachment and choroidal vasodilation as well as improved visual acuity. The benefit was maintained 5 months after eplerenone withdrawal. Our results identify MR signaling as a pathway controlling choroidal vascular bed relaxation and provide a pathogenic link with human CSCR, which suggests that blockade of MR could be used therapeutically to reverse choroid vasculopathy.
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            Systemic findings associated with central serous chorioretinopathy.

            To determine systemic factors associated with central serous chorioretinopathy. In a retrospective study, 230 consecutive patients with central serous chorioretinopathy examined in a referral setting were compared with a historical gender-matched and age-matched control group of 230 patients with ocular findings who were examined in the same referral setting. The median age of the patients was 49.8 years, and of the control subjects, 50.0 years. The male-female ratio for both groups was 2.7:1. Patients with central serous chorioretinopathy were more likely to use psychopharmacologic medications (odds ratio = 2.6; 95% confidence interval = 1.30 to 5.19; P = .0049) and corticosteroids (odds ratio = 3.17; 95% confidence interval = 1.30 to 7.70; P = .0067) and were more likely to have hypertension (odds ratio = 2.25; 95% confidence interval = 1.39 to 3.63; P = .0008) than were the control subjects. This study identified psychopharmacologic medication use, corticosteroid use, and hypertension as factors associated with central serous chorioretinopathy. These findings reinforce the concept that stress and adaptations to stress play a role in this disorder. The findings of possible associations between central serous chorioretinopathy and both hypertension and corticosteroid usage suggest that these modifiable factors may influence morbidity of central serous chorioretinopathy.
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              Corticosteroids and central serous chorioretinopathy.

              The purpose of this study is to investigate the relationship between corticosteroid use and central serous chorioretinopathy (CSC). A prospective, case-controlled study. A consecutive series of patients with acute manifestations of CSC and a control group matched for age, race, and gender were recruited between January 2000 and July 2000. A detailed clinical history was taken, and fundus examination with slit-lamp biomicroscopy was performed on all patients. Fluorescein angiography was obtained on the study patients. A total of 50 patients was recruited. Twenty-six patients (52%) had a history of exogenous steroid use, including oral, intravenous, intranasal, and intraarticular administration. Two additional patients had a history of endogenous hypercortisolism (Cushing's syndrome). In a matched control group, eight patients (18%) had a history of steroid use. The difference in corticosteroid exposure between study patients and controls was statistically significant (P < 0.0001). History of corticosteroid use or Cushing's syndrome. This study is consistent with previous reports associating steroid use with CSC. It identifies corticosteroids as a significant risk factor for the development of acute, exudative macular manifestation and implicates hypercortisolism as a factor in the pathogenesis of this disorder. Several forms of corticosteroid administration were observed to be a risk factor for CSC. Accordingly, susceptible patients in need of corticosteroids should be advised of the risk of developing acute manifestations of CSC.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2013
                2013
                02 September 2013
                : 9
                : 355-360
                Affiliations
                [1 ]Department of Ophthalmology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People’s Republic of China
                [2 ]Department of Ophthalmology and Visual Science, Yellow River Hospital of Henan University of Science and Technology, Sanmenxia City, Henan, People’s Republic of China
                [3 ]Department of Ophthalmology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang City, Henan, People’s Republic of China
                [4 ]Gu-Cheng Eye Hospital, Xi’an City, Shanxi, People’s Republic of China
                Author notes

                *These authors contributed equally to this work

                Correspondence: Yu Zhu, The First Affiliated Hospital of Zhengzhou University, Jianshe East road, Zhengzhou, Henan, People’s Republic of China, Tel +86 398 228 9268, Fax +86 398 282 3634, Email dr.dang@ 123456aol.com
                Article
                tcrm-9-355
                10.2147/TCRM.S50407
                3772708
                24043941
                © 2013 Dang et al. This work is published by Dove Medical Press Ltd, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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