1. Corticosteroid-induced central serous chorioretinopathy in patients with Ocular Toxoplasmosis Merih Soylu, MD, Prof. Ophthalmology, Füsun Uzunoğlu, MD World Eye Hospital, TURKEY Development of central serous chorioretinopathy (CSC) following the administration of corticosteroids is a well-known fact. Especially in patients with uveitis in whom corticocosteroids are widely used, it is very important to make the differential diagnosis between a new inflammatory episode or another pathology like CSCR. In these patients discontinuation of steroids is mandatory, and it should be done with careful monitorisation of the disease activity. In the present study, two cases with ocular toxoplasmosis who developed CSCR during treatment is presented. The symptoms appeared concurrently during treatment with antibiotic/steroid treatment of the underlying disease, and resolved after cessation of steroids. This study is undertaken in order to emphasize the importance of monitoring patients under treatment with steroids.

2. CASE 1 Fig 1 –RE a. Healing chorioretinal scar and old scars. b. Early phase FFA with hypofluorescent foci c. Late phase FFA with hyperfluorescent borders of the lesion and window defects on the posterior pole Fig 2-LE a, b. Serous detachment of the macula. Fundus photo and OCT c. FFA, showing pinpoint hyperfluorescence and minimal leakage c 27 y/old F Decrease of vision in the left eye while receiving therapy for toxoplasmic chorioretinitis in her RE. She has been under Clindamycine and prednisolone treatment for the last two months, and having gastrointestinal problems. Upon admission, she was diagnosed as CSCR in the LE. The therapy was stopped, a single dose of peribulbar depot betamethasone was injected to the RE, and sulfadiazine- trimethoprim combination was started. After 3 months, vision was improved, and CSCR resolved. No recurrences were detected during 18 months of follow-up.

3. CASE 2 37 y/o M Visual detoriation in the normal eye, started during antitoxoplasmosis treatment for the activation in the fellow eye. Before admission, he stopped taking daraprim by himself because of side effects, and continued treatment only with steroids. On admission, he had CSCR in his RE and focal chorioretinal scar in the LE. VA was 0.16 OU. Acetozolamide with topical and systemic NSAID was started, systemic steroids were tapered and discontinued. His VA returned to 1.0 in his RE, after cessation of steroids. He has been followed for a year and no recurrences were detected during this period.

4. Fig. 3- FAF and FFA at presentation. Note the hypoautofluororescence in the LE in the areas of chorioretinal scarring, and hyperautofluororescen spots in both eyes. In FFA, there is a 2 spots of pinpoint leakage on the upper side of the fovea in RE, whereas hyperfluorescence in the borders of the scar in the LE. Fig. 4-There is a serous elevation in the macula in RE and multipl reverbaration echoing in the LE due to scarring at presentation. Central macular thickness was 640 mμ in the RE. CASE 2

5. Fig. 5- 10 days after tapering off steroids and starting acetozolamide and non-steroid antiinflammory treatment. CMT was 411 mμ. Note the hyperreflective spots in the retina. Fig. 6- 30 days after presentation, there is still some serous fluid in the macula (CMT 278 mμ). BCVA was 1.0. Fig. 7- Two months after presentation, macula is on without any residual fluid, and anatomical recovery is good, without any change in outer retinal layers.

6. DISCUSSION In clinical practice, corticosteroids are usually given in combination with antiparasitic drugs to reduce the inflammatory reaction during active chorioretinitis and to minimize tissue damage in ocular toxoplasmosis. Besides causing ocular side effects, corticosteroids increases fragility and hyperpermeability of capillaries, increases free radicals, inhibit collagen production, changes ion and water transportation. Clearly the chance of significant side effects increases with dose and duration of treatment, therefore minimum dose necessary to control the disease should be given and tapered slowly in order to prevent rebound effect. In our first visit with the patient, besides her declining vision, complained about irritability, gastrointestinal symptoms, weight gain and fatigue. After stopping the medications and switching to a single dose depot steroid, the steroid side effects resolved. We added sulfadiazine- trimetoprim to the regimen, thus providing a cover for the continuing slow release of steroids, with fewer side effects and well tolerated by the patient. CSCR is a relatively common chorio-retinal disease characterized by the accumulation of subretinal fluid at the posterior pole, creating a circumscribed area of serous retinal detachment. CSCR has been described in patients with endogenous hypercorticolism. Toxoplasmic chorioretinitis treatment or any treatment protocol with corticosteroids can cause CSCR, not related to dosage and duration of therapy. Presentation of CSCR due to toxoplasmic chorioretinitis therapy is very rare. However, the potential side effects of corticosteroids, favoring CSC, are well-known. When an unexpected clinical and angiographic change compatible with CSC develops in a patient under antitoxoplasmic therapy, overuse or improper use of steroids should be kept in mind as a causative agent. This report emphasizes the necessity of thorough evaluation and close follow-up, and monitoring treatment agents in patients under toxoplasma treatment.