This Article  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on Web of Science (1)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Retinal/ Chorioretinal Disorders  • Drug Therapy  • Adverse Effects  • Alert me on articles by topic  Social Bookmarking   What's this?

Arch Ophthalmol. 2004;122:784-786.

Central serous chorioretinopathy (CSCR) is a common disease characterized by the accumulation of subretinal fluid at the posterior pole of the fundus; it typically affects young and middle-aged adults, with men affected more commonly than women. The exact pathogenic mechanism of CSCR remains unclear. There is accumulating evidence that both endogenous and exogenous glucocorticoids may be implicated in the pathogenesis of the disease.^1-2 Regarding the role of exogenous glucocorticoids, CSCR has been reported as a complication of intravenous, intramuscular, oral, epidural, inhaled, and intranasal glucocorticoid administration.² We describe 2 patients who developed CSCR after prolonged treatment with glucocorticoids applied locally to the skin for dermatological indications.

Report of Cases.
Case 1. A 32-year-old man complained of decreased vision and metamorphopsia in the right eye. Best-corrected visual acuity was 20/25 OD and 20/20 OS. Fundus examination results were normal in the left eye but in the right eye revealed a well-circumscribed, shallow, serous detachment of the sensory retina. The clinical appearance was consistent with CSCR, and the diagnosis was confirmed by means of fluorescein angiography, which showed a leakage point at the superior macula, spreading slowly in an inkblot configuration into the subretinal space (Figure 1).

View larger version (71K): [in this window] [in a new window] Figure 1. In case 1, the fluorescein angiogram of the right eye shows pinpoint leakage at the superior macula (A) that spreads to the subretinal space (B) at later phases.

The medical history of the patient was remarkable for seborrheic dermatitis involving the central face, eyebrows, eyelids, and scalp. The disease had been diagnosed 2 years earlier, and 1% hydrocortisone acetate cream was prescribed for topical application. After the initial prescription, the patient used the cream without further medical consultation when symptoms were exacerbated. The 1% hydrocortisone acetate cream was used for 4 weeks, 3 to 4 times daily, before the development of CSCR.

Case 2. A 37-year-old man was referred to us for blurred vision in the left eye of 1 week's duration. He had a history of CSCR in the contralateral eye, 5 years previously, for which he had been treated with laser photocoagulation at another institution. Best-corrected visual acuity was 20/20 OU. Funduscopy of the right eye revealed scars from previous laser photocoagulation at the superior macula. In the left eye, there was a well-delineated area of serous detachment temporal to the fovea. Small yellowish precipitates were visible at the posterior aspect of the detached retina. Fluorescein angiography revealed a leakage point at the upper pole of the detachment (Figure 2).

View larger version (51K): [in this window] [in a new window] Figure 2. In case 2, the red-free photograph of the left eye shows serous retinal detachment (A), and the fluorescein angiogram of the left eye demonstrates the leakage point (B).

The medical history of the patient was remarkable for pityriasis versicolor, for which he was treated with local application of 0.1% diflucortolone valerate cream in combination with 1% isoconazole nitrate. The patient used the cream occasionally and was being treated for 3 weeks before symptoms began. Notably, the patient was also being treated with 0.1% diflucortolone valerate cream during the first episode of CSCR.

Comment.
We describe 2 patients who developed CSCR during treatment with glucocorticoids applied locally to the skin for dermatological disorders. Notably, 1 had a history of CSCR in the contralateral eye, which had also developed while he was being treated with glucocorticoid cream applied locally.

The exact pathogenic mechanism of CSCR is unclear and is the subject of considerable controversy. Accumulating evidence suggests that glucocorticoids may contribute to the pathogenesis of CSCR. The development of CSCR has been described in association with conditions characterized by endogenous hypercortisolism such as pregnancy, stress, and endogenous Cushing syndrome.¹ It has also been described as a complication of exogenous glucocorticoids administered via various routes—oral, intravenous, intramuscular, inhaled, intranasal, and epidural.²

To our knowledge, this is the first report of patients developing CSCR after local application of glucocorticoids to the skin for the treatment of dermatological disorders. Percutaneous absorption of glucocorticoids applied locally to the skin is well described in the dermatological literature.^3-5 Application of glucocorticoids may result in systemic absorption sufficient to cause hypercortisolism, adrenal suppression, and reduced glucose tolerance.^3-5 Therefore, although a coincidental association cannot be excluded, the development of CSCR in our patients may be related to the local skin application of glucocorticoids. Even if this report does not prove that topical steroids cause CSCR, it provides evidence that raises this suspicion and suggests that further study of this potential association is warranted. The exact pathogenic mechanism by which glucocorticoids may be implicated in the development of CSCR is unknown and remains speculative. Proposed theories incriminate the effect of glucocorticoids either to the choroidal vasculature or to the function of the retinal pigment epithelium.²

In conclusion, local skin application of glucocorticoids may be complicated by the development of CSCR. In such cases, discontinuation of glucocorticoid treatment should be considered whenever possible.

The authors have no relevant financial interest in this article.

AUTHOR INFORMATION

Panagiotis Karadimas, MD; Anastasios Kapetanios, MD; Evrydiki A. Bouzas, MD
Athens, Greece

Corresponding author: Panagiotis Karadimas, MD, Medical Retina Unit, First Department of Ophthalmology, Henry Dunant Hospital, 107 Mesogion Ave, 11526 Athens, Greece (e-mail: t_karadimas{at}yahoo.com).

REFERENCES
1. Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, Kaiser-Kupfer MI. Central serous chorioretinopathy in endogenous hypercortisolism. Arch Ophthalmol. 1993;111:1229-1233. FREE FULL TEXT 2. Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy and glucocorticoids. Surv Ophthalmol. 2002;47:431-448. FULL TEXT | ISI | PUBMED 3. Aalto-Korte K, Turpeinen M. Pharmacokinetics of topical hydrocortisone at plasma level after applications once or twice daily in patients with widespread dermatitis. Br J Dermatol. 1995;133:259-263. FULL TEXT | ISI | PUBMED 4. Cook LJ, Freinkel RK, Zugerman C, Levin DL, Radtke R. Iatrogenic hyperadrenocorticism during topical steroid therapy: assessment of systemic effects by metabolic criteria. J Am Acad Dermatol. 1982;6:1054-1060. FULL TEXT | ISI | PUBMED 5. Garden JM, Freinkel RK. Systemic absorption of topical steroids: metabolic effects as an index of mild hypercortisolism. Arch Dermatol. 1986;122:1007-1010. FREE FULL TEXT

SECTION EDITOR: W. Richard Green, MD

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?