Spectral-Domain Optical Coherence Tomography Features of Acute Syphilitic Posterior Placoid Chorioretinitis: The Role of Autoimmune Response in Pathogenesis

• Published in: Case reports in ophthalmology Vol. 2; no. 1; pp. 39 - 44
• Main Authors: Brito, Pedro, Penas, Susana, Carneiro, Ângela, Palmares, Jorge, Reis, F.Falcão
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 25.01.2011; Karger Publishers
• Subjects: Beta2 glycoprotein; Chorioretinitis; Placoid; Published: January 2011; Spectral-domain optical coherence tomography; Syphilis; Beta2 glycoprotein; Chorioretinitis; Syphilis; Spectral-domain optical coherence tomography; Placoid
• ISSN: 1663-2699; 1663-2699
• DOI: 10.1159/000324086

Purpose: Syphilis is an infectious disease that can cause a wide variety of ocular signs. One of the rarest manifestations of ocular syphilis is acute syphilitic posterior placoid chorioretinitis (ASPPC). We report on the spectral-domain optical coherence tomography (SD-OCT) features of a case diagnosed with unilateral ASPPC. Methods: A 64-year-old man presented with a sudden loss of visual acuity (VA) in the right eye. His only clinical sign was a large, geographic, yellow-white lesion centered on the right fovea. Our patient was studied with SD-OCT on presentation and during follow-up, as well as with fluorescein and indocyanine green angiography, electrophysiological study, and serologic and autoimmune screening. Results: Laboratory workup revealed positive serology for active syphilis and elevated anti-beta2 glycoprotein I antibodies. SD-OCT showed a marked distortion of both the choroidal and outer retinal architecture. After treatment, best-corrected VA improved to 20/25. Pattern electroretinography displayed a severe reduction of P50 amplitude, which improved in late follow-up. Six months after presentation, VA was 20/25 and anti-beta2 glycoprotein I antibodies returned to normal levels. Conclusions: Our findings are compatible with immunologically mediated temporary physiological impairment of the neuroretina, since the changes seen by SD-OCT could not have normalized if they were due to anatomical injury. The results of our study provide clues to understanding the pathogenesis of this disease and allow us to define a characteristic temporal sequence of events in ASPPC.