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A 66-year-old male patient presented to the ophthalmology department with bilateral blurred vision, which had persisted for 1 week. Due to a pulmonary melanoma metastasis, the patient received a combination treatment with dabrafenib and trametinib. At the first presentation visual acuity was 1.2 on the right and 1.0 on the left. A normotensive intraocular pressure was measured in both eyes. Fundoscopy showed bilateral white, areolar alterations in the choroid and choroid folds and in the left eye a bullous choroidal detachment. Bilateral neurosensory detachment and subretinal fluid were found in optical coherence tomography (OCT). After reduction of the local treatment for pressure reduction and under local and systemic anti-inflammatory treatment, the choroidal swelling was progressive, the visual acuity dropped to 0.5 in the right and to 0.1 in the left eye. A significant regression of the findings occurred only after pausing the treatment with trametinib. Visual acuity rose to 1.0 (left) and 0.8 (right). The OCT showed a dry macula on the right and a small amount of residual subretinal fluid in the left eye.

Background: Interferon alpha, used in the treatment of different viral, autoimmune and malignant diseases, is known to induce a variety of side effects. Recently, induction of sarcoidosis during interferon therapy has been reported. We analyzed patients for uveitis, possibly induced by interferon alpha., Methods: We report on three patients who had developed typical signs of ocular sarcoidosis under treatment with interferon alpha for chronic hepatitis C virus infection. In two patients, conventional interferon alpha was used and in another one, pegylated interferon alpha-2b. All patients additionally received ribavirin., Results: In all three cases, panuveitis was diagnosed. The mean duration of interferon treatment before development of uveitis was 10 months. Clinically, all patients demonstrated granulomatous panuveitis with choroidal granulomas of various sizes. In one case, the uveitis developed together with renal failure, fever and malaise. In this patient, an elevated ACE level was detected. In another patient, the diagnosis of sarcoid induced uveitis was confirmed by positive chest CT scan. The intraocular inflammation was managed with a reduction of the interferon dosage. The therapy with ribavirin was not changed. All patients received topical steroids. Systemic steroids were applied only in the case with systemic disease manifestations., Conclusions: Uveitis can be a sign of sarcoidosis induced by interferon alpha. Further studies are required to support the observation that with early diagnosis the prognosis of uveitis seems to be good.

Background: This report describes a case of central serous chorioretinopathy following intravitreal triamcinolone acetonide injection., Methods: A 42-year-old man presented with a 4-month history of decreased visual acuity (0.4) in his left eye. The left eye demonstrated macular edema due to branch retinal vein occlusion. Triamcinolone acetonide 4 mg/ 0.1 mL was injected intravitreally to treat the macular edema., Results: Pigmentary retinal discoloration, retinal pigment epithelium leakage and a slight neurosensorial detachment with cystoid macular edema at the temporal macula were present prior to intravitreal triamcinolone injection. Three weeks after injection, visual acuity had decreased to 0.2 and metamorphopsies appeared in the left eye. A sharply demarcated serous macular elevation and a progressively increasing hyperfluorescence of the pre-existing leakage point led to the diagnosis of "exacerbation of the pre-existing asymptomatic central serous chorioretinopathy" following intravitreal triamcinolone injection. Macular elevation spontaneously resolved by the 4th month post-injection. At the 6th month, the patient experienced recurrence of a small serous detachment at the temporal macula., Conclusion: Central serous chorioretinopathy exacerbation may arise as a complication of intravitreal triamcinolone acetonide injection.

Purpose: To evaluate whether exposure to glucocorticoids represents a risk factor for the development of central serous chorioretinopathy (CSCR)., Methods: Prospective, case-control study. Thirty-eight consecutive patients with acute CSCR were asked to answer a specific questionnaire regarding the use of glucocorticoids, in any form, during the last month before the onset of the symptoms. An age- and sex-matched control group was also recruited. It consisted of patients attending the outpatient department for a condition other than CSCR, who were asked to answer the same questionnaire., Results: Use of glucocorticoids was recorded in 11 of 38 patients (28.9%) with CSCR; 8 of them were men and 3 women. In the control group, use of glucocorticoids was recorded in 2 of 38 patients (5.2%), 1 man and 1 woman. The difference between the two groups is statistically significant (odds ratio=7.33, 95% CI=1.49-35.85, P=0.006)., Conclusion: In this prospective, case-control study, we found that glucocorticoid use represents a risk factor for the development of CSCR.

Background: Solar retinopathy and central serous chorio-retinopathy are two well-defined clinical entities which affect the macular area. Their association has never been described. The relation of central serous chorioretinopathy with the exposure to glucocorticoids has been recently suggested., Case Report: Central serous chorioretinopathy developed in a patient who received corticosteroid therapy for solar retinopathy., Conclusion: This case report provides additional evidence that central serous chorioretinopathy may develop under the effect of glucocorticoids. Retinal damage resulting from a previous insult, such as solar retinopathy, may act as the permissive factor.

Background: The purpose of the study is to demonstrate the development of subretinal fibrotic scar formation in central serous chorioretinopathy (CSCR) that developed during systemic corticosteroid treatment., Methods: The clinical and photographic records of a patient in whom an unusual manifestation of severe central serous chorioretinopathy developed during systemic corticosteroid treatment were reviewed., Results: A 34-year-old man received high dosages of corticosteroids for several years because of severe asthma. There was no previous history of idiopathic CSCR. He developed three successive attacks of CSCR. On the third occasion, an unusual variant of severe CSCR was observed which presented as a bullous sensory retinal detachment with subretinal serofibrinous exudate followed by subretinal fibrosis and fibrotic scar formation with contracting bands. After tapering of the corticosteroid dosage to a low level the retinal detachment resolved without laser treatment., Conclusion: The finding suggests that during systemic corticosteroid treatment atypical manifestations of CSCR may develop with subretinal fibrosis and scar formation.

Background: The purpose of this study is to examine the relationship between pathological changes of the choriocapillaris (CC) and the finding of bright fluorescence on indocyanine green (ICG) angiography., Methods: An animal model was used, with chorioretinal lesions produced by injecting sodium iodate 3 h, 24 h, 7 days or 14 days previously. The ICG angiographic findings were compared with histology., Results: Three hours after injection, many spots of bright fluorescence were scattered at the posterior pole. Histologically, variable changes in CC endothelial cells were observed. In some regions, the cells remained almost normal morphologically. In other regions, the endothelial cytoplasm was thickened with decreased fenestrations, or precipitation of fibrin in the choroidal interstitium was observed. Twenty-four hours after injection, the area of bright fluorescence had extended beyond that observed after 3 h. Histologically, the cytoplasmic structure of CC endothelial cells was unclear, and the endothelial walls were detached from the basement membrane. When ferritin was administered as a tracer, many ferritin granules were observed in Bruch's membrane. Seven days after injection, the degree of bright fluorescence was reduced as compared with 3 and 24 h after injection. Histologically, the cytoplasm of CC endothelial cells was thinned, but contained few fenestrations. The endothelial walls were detached from the basement membrane. Fourteen days after injection, normal diffuse ICG fluorescence was observed. Histologically, CC endothelial cells exhibited almost normal structure., Conclusion: These findings indicate that changes in CC endothelial cells and bright fluorescence on ICG angiography are closely related. ICG angiography should enable clinical evaluation of increased permeability of CC endothelial cells to relatively large molecules.