UNLABELLED: Acute syphilitic posterior placoid chorioretinitis (ASPPC) has been described as a rare chorioretinal manifestation in patients with secondary syphilis. The fundus changes may simulate other chorioretinal disorders and thus delay an accurate diagnosis and initiation of appropriate pharmacological therapy. PATIENT: A 54-year-old male patient presented with severely impaired visual acuity in both eyes. Yellowish geographic lesions were noted at the posterior pole. Scanning laser ophthalmoscopy showed corresponding areas of increased fundus autofluorescence. On fluorescein angiography hypofluorescent lesions were noted in the early phase, which became hyperfluorescent in later frames. Indocyanine green agiography demonstrated hypofluorescent lesions both during the early and late frames. Serological examinations were positive for secondary lues (TPHA, FTA-IgM, cardiolipin antibody). Treatment with penicillin was introduced, resulting in complete functional and morphological recovery. CONCLUSION: Fundus and angiographic changes in ASPPC may mimic other chorioretinal diseases, including acute posterior multifocal placoid pigmentepitheliopathy (APMPPE). The angiographic findings suggest that inflammation-associated perfusion abnormalities of the choriocapillaris contribute to the pathophysiological process. Accurate diagnosis of ASPPC as a presenting sign of secondary lues is especially important for the prompt initiation of systemic antibiotic treatment.
UNLABELLED: Acute syphilitic posterior placoid chorioretinitis (ASPPC) has been described as a rare chorioretinal manifestation in patients with secondary syphilis. The fundus changes may simulate other chorioretinal disorders and thus delay an accurate diagnosis and initiation of appropriate pharmacological therapy. PATIENT: A 54-year-old male patient presented with severely impaired visual acuity in both eyes. Yellowish geographic lesions were noted at the posterior pole. Scanning laser ophthalmoscopy showed corresponding areas of increased fundus autofluorescence. On fluorescein angiography hypofluorescent lesions were noted in the early phase, which became hyperfluorescent in later frames. Indocyanine green agiography demonstrated hypofluorescent lesions both during the early and late frames. Serological examinations were positive for secondary lues (TPHA, FTA-IgM, cardiolipin antibody). Treatment with penicillin was introduced, resulting in complete functional and morphological recovery. CONCLUSION: Fundus and angiographic changes in ASPPC may mimic other chorioretinal diseases, including acute posterior multifocal placoid pigmentepitheliopathy (APMPPE). The angiographic findings suggest that inflammation-associated perfusion abnormalities of the choriocapillaris contribute to the pathophysiological process. Accurate diagnosis of ASPPC as a presenting sign of secondary lues is especially important for the prompt initiation of systemic antibiotic treatment.