Egyptian Retina Journal

: 2014  |  Volume : 2  |  Issue : 2  |  Page : 79--82

Chronic alcoholism and central serous chorioretinopathy

Vishal Katiyar, Sanjiv K Gupta, Arun Kumar Sharma, Vinita Singh 
 Department of Ophthalmology, K.G.M.U, Lucknow, Uttar Pradesh, India

Correspondence Address:
Dr. Vishal Katiyar
Department of Ophthalmology, K.G.M.U, Lucknow, Uttar Pradesh - 226 003


A 36-year-old alcoholic male suffered from central serous chorioretinopathy (CSCR). Morning serum cortisol was 293.3 ng/ml (normal range: 50-250 ng/ml), which was elevated. After 1-week of treatment with mineralo-corticoid antagonist eplerenone at 25 mg/day, patients witnessed visual acuity in the left eye increased to 6/12, which corroborated with optical coherence tomography showing substantial decrease of sub-retinal fluid. It is first documented case of CSCR associated with chronic use of alcohol that exhibited response to mineralo-corticoid antagonist eplerenone. In this study, though the exact role of alcohol intake in the pathogenesis could not be established, a disturbed the hypothalamic-pituitary-adrenal axis as a connecting link between the two conditions are observed. This will pave the way for larger, controlled studies directed to establish an association between alcohol intake and CSCR.

How to cite this article:
Katiyar V, Gupta SK, Sharma AK, Singh V. Chronic alcoholism and central serous chorioretinopathy.Egypt Retina J 2014;2:79-82

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Katiyar V, Gupta SK, Sharma AK, Singh V. Chronic alcoholism and central serous chorioretinopathy. Egypt Retina J [serial online] 2014 [cited 2022 May 20 ];2:79-82
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Full Text


Central serous chorioretinopathy (CSCR) is characterized by subretinal serous fluid accumulation and retinal detachment. Systemic and/or loco-regional glucocorticoids use and conditions characterized by endogenous hypercortisolism are the main risk factors reported for CSCR. [1] The pathophysiology of CSCR remains obscure, although disorders in both the choroidal circulation and retinal pigment epithelium are implicated. [2] Alcohol has considerable influence on the release of glucocorticoids. Acute and chronic intake of ethanol, as well as withdrawal, in both humans and rodents markedly increases plasma glucocorticoid levels and with chronic use, produces a disturbed pattern of hypothalamic-pituitary-adrenal (HPA) axis dysfunction. [3] There are very few case reports on the association of CSCR with alcoholism. [4,5] We are first to report cases of CSCR in chronic alcoholic patient which responded to mineralo-corticoid antagonist eplerenone and showed visual improvement.

 Case Report

A 36-year-old male had suffered from impaired, blurred vision in the left eye since 1-month. On the basis of ophthalmologic evaluation including best-corrected visual acuity (VA) assessment, fundoscopy and spectral domain-optical coherence tomography (OCT, Zeiss, USA), he was diagnosed as having CSCR. At the time of diagnosis best corrected VA was 6/24 in the left eye (involved eye) and 6/6 in the right eye. OCT of the left eye showed serous detachment of the neurosensory retina including the macular area, with a small retinal pigment epithelial (RPE) detachment. The fundus fluorescein angiography (FFA) showed a characteristic leak and smoke stack pattern [Figure 1]a. The extent of retinal detachment is presented on [Figure 1] a-c. The right eye was unaffected.{Figure 1}

Patient accepted that he was an alcoholic for last 4 years, with an average alcohol intake of about 60 ml/day of rum (40% w/w alcohol content). Among systemic factors associated with CSCR, type A personality, glucocorticoid use and hypertensions were excluded. Patient did not show any signs or symptoms of depressive mood disorder or alcohol withdrawal in psychiatric evaluation. The details of the blood investigations are given in [Table 1]. The liver function test reports were within normal limits. Helicobacter pylori infection test was (13C urea kit, Otsuka pharmaceutical Co., Ltd.) was negative at the time of diagnosis of CSCR. Serum sample for cortisol level estimation (Globe Diagnostics SRL, Milan, Italy) was 293.3 ng/ml (normal range: 50-250 ng/ml), which was elevated. Endogenous hypercortisolism (Cushing's syndrome) was excluded on the basis of the test with 1 mg of dexamethasone given at night (serum cortisol after oral administration of 1 mg of dexamethasone - 221 ng/ml), which was abnormal. Serum testosterone was 2.13 nmol/l and 2.17 nmol/l (normal range: 0.198-2.68) tested 1-month apart. As there were no clinical signs and symptoms of the excess of aldosterone, such as hypertension and general anasarca, the concentration of aldosterone was not tested. Serum adrenocorticotrophic hormone (ACTH) was observed to be 35.6 pg/ml (normal range: 18-59 pg/ml).{Table 1}

The clinical course of the disease had been monitored with OCT, with patient on eye drop Bromfenac, in the expectation of resolution. No improvement of VA or OCT findings were observed even after 3 months of onset of symptoms, treatment with mineralo-corticoid antagonist eplerenone at 25 mg/day (Eplecard, Cadilla pharmaceuticals Ltd.,) was started. The treatment was started on the bases of the positive report of Bousquet et al. [6] and Gruszka; [7] in which authors suggested that the blockage of mineralocorticoid receptors (MR) could be effective in the treatment of CSCR. After 1-week of treatment, patients witnessed VA in the left eye increased to 6/12, which corroborated with OCT showing significant decrease of subretinal fluid as shown in [Figure 2]a-c. The treatment was continued for next 1-month when patient showed significant resolution of corporate social responsibility (CSR) on OCT and FFA, but vision did not improve beyond 6/12. After 1½ months of treatment, serum cortisol level was estimated (Globe Diagnostics SRL, Milan, Italy) was found to be normal (113.2 ng/ml).{Figure 2}


The abnormality in the hypothalamic-pituitary-adrenal functions is commonly seen following chronic ethanol use. Elevated serum ACTH and cortisol, higher urinary levels of metabolites of glucocorticoids, and positive dexamethasone suppression test that is, cortisol nonsuppression were also observed. [8] several other factors besides excess alcohol use were implicated. Depressive mood changes commonly observed in alcoholism, stress as manifested by alcohol withdrawal states could also cause HPA activation. [9]

In the present patient abnormality in the HPA functions were evident by elevated serum cortisol and a positive cortisol nonsuppression test. This abnormality was associated with a valid history of long-term alcohol intake in the absence of any other identifiable cause. Though the associated depression and alcoholic withdrawal could not be diagnosed in this patient, this could also have a contribution to the observed abnormality in the HPA functions. In many patients with an acute form of CSCR, spontaneous resolution of retinal detachment is observed within 1.5-3 months without any treatment. [10] Therefore, in several cases, including the presented one, the course of the disease is monitored in expectation of spontaneous resolution. If retinal detachment persists for > 3-4 months, laser photocoagulation directed at foci of RPE leakage should be considered. In a study concerning chronic CSCR, median lesion height assessed with OCT remained unchanged during 4 weeks of treatment with ketoconazole and decreased after 8 weeks. [11] In another small study in patients with acute CSCR, the treatment with ketoconazole did not result in a significantly better outcome. [11] Glucocorticoid receptor antagonist mifepristone had a beneficial effect in 14/16 patients with chronic CSCR. [12] In the presented case spontaneous remission cannot be excluded. However, the improvement in the involved eye was seen relatively late after the onset of CSCR. Our findings, together with the other recent studies [4,5] suggest that excessive glucocorticoid-dependent choroidal MR activation may be involved in the pathogenesis of CSCR, and blockade of MR could result in resorption of sub-retinal fluid and retinal reattachment in patients with nonresolved CSCR.

To our knowledge, is first documented case of CSR associated with chronic use of alcohol that showed resolution and visual recovery with mineralo-corticoid antagonist eplerenone. In this study, the exact role of alcohol intake in the pathogenesis could not be established but a disturbed HPA axis as a connecting link between the two conditions is observed. This will pave the way for larger, controlled studies directed to establish an association between alcohol intake and CSCR.


1Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy and glucocorticoids. Surv Ophthalmol 2002;47:431-48.
2Liew G, Quin G, Gillies M, Fraser-Bell S. Central serous chorioretinopathy: A review of epidemiology and pathophysiology. Clin Experiment Ophthalmol 2013;41:201-14.
3Rasmussen DD, Boldt BM, Bryant CA, Mitton DR, Larsen SA, Wilkinson CW. Chronic daily ethanol and withdrawal: 1. Long-term changes in the hypothalamo-pituitary-adrenal axis. Alcohol Clin Exp Res 2000;24:1836-49.
4Gkotsi D, Gupta M, Lascaratos G, Syrogiannis A, Dhillon B. Alcoholic liver disease and bilateral multifocal central serous retinopathy: A case report. J Med Case Rep 2013;7:43.
5Haimovici R, Koh S, Gagnon DR, Lehrfeld T, Wellik S, Central Serous Chorioretinopathy Case-Control Study Group. Risk factors for central serous chorioretinopathy: A case-control study. Ophthalmology 2004;111:244-9.
6Bousquet E, Beydoun T, Zhao M, Hassan L, Offret O, Behar-Cohen F. Mineralocorticoid receptor antagonism in the treatment of chronic central serous chorioretinopathy: A pilot study. Retina 2013;33:2096-102.
7Gruszka A. Potential involvement of mineralocorticoid receptor activation in the pathogenesis of central serous chorioretinopathy: Case report. Eur Rev Med Pharmacol Sci 2013;17:1369-73.
8Cronholm T, Curstedt T, Schmidt DN, Sjövall J. Steroid profiles in urine and plasma of alcoholics during withdrawal. Alcohol 1985;2:677-82.
9de La Fuente JR, Rosenbaum AH, Morse RM, Niven RG, Abboud CF, Jiang NS, et al. The hypothalamic-pituitary- adrenal axis in alcoholics. Alcohol Clin Exp Res 1983;7:35-7.
10Carvalho-Recchia CA, Yannuzzi LA, Negrão S, Spaide RF, Freund KB, Rodriguez-Coleman H, et al. Corticosteroids and central serous chorioretinopathy. Ophthalmology 2002;109:1834-7.
11Meyerle CB, Freund KB, Bhatnagar P, Shah V, Yannuzzi LA. Ketoconazole in the treatment of chronic idiopathic central serous chorioretinopathy. Retina 2007;27:943-6.
12Nielsen JS, Jampol LM. Oral mifepristone for chronic central serous chorioretinopathy. Retina 2011;31:1928-36.