A 22-year-old man was examined at a local clinic for visual deterioration in both eyes, and widespread multiple chorioretinal lesions were found in both fundi (Fig. 2a). Fundus autofluorescence demonstrated increase in central hypoautofluorescence within the lesions corresponding to the outer retinal atrophy and RPE hyperplasia (Fig. 2b). FA demonstrated hyperfluorescence of the lesions in late phase (Fig. 2c), and indocyanine green angiography showed hypofluorescence in the area coincide with the clinical legions (Fig. 2d). Similar to the previous case, laboratory work-up, including complete blood count, erythrocyte sedimentation rate, C-reactive protein, kidney function tests, and liver function test were within normal limits, and serology for syphilis and HIV were negative. Normal chest computed tomography, negative purified-protein derivative reaction, and negative T-SPOT.TB. denied sarcoidosis and tuberculosis. Oral prednisolone at 20 mg/day and oral cyclosporine at 300 mg/day were started. One month later, at the initial visit to our hospital, BCVA was 20/60 (OD) and 20/20 (OS). No inflammatory signs were observed. Thus, oral prednisolone prescription was gradually tapered.
Six months later (oral prednisolone: 11 mg/day, oral cyclosporine: 150 mg/day), relapse with new chorioretinal exudative changes occurred in the left eye. A diagnosis of RPC was made and oral prednisolone was increased to 15 mg/day. Once ocular inflammatory changes had subsided, adalimumab (40 mg/2 weeks) was started and cyclosporine was discontinued. Since then, no recurrence occurred over an 9-month period, and oral prednisolone was successfully tapered to 5 mg/day. No complications related to the use of adalimumab was noted. BCVA recovered to 20/20 (OD) and 20/16 (OS). Change in OCT findings are shown in Figure 3. Small amount of subretinal hyperreflective materials, focal outer retinal disruption, and subfoveal RPE hyperplasia were observed at the first visit (Fig. 3a). Nine months after the administration of adalimumab, the recession of RPE hyperplasia according to the inactivation of inflammation was detected, albeit partial hyperplasia remained. Ellipsoid zone was rarefied at the site of prior hyperplasia (Fig. 3b).