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Marcelo Mendes Lavezzo, Viviane Mayumi Sakata, Ever Ernesto Caso Rodriguez, Smairah Frutuoso Abdallah, CELSO MORITA, Cleide Guimarães Machado, Mauro Goldbaum, Sérgio Luís Gianotti Pimentel, Maria Kiyoko Oyamada, Carlos Eduardo Hirata, Joyce H Yamamoto; Is there any choroidal inflammation in the non-acute stage of Vogt-Koyanagi-Harada disease (VKHD)?. Invest. Ophthalmol. Vis. Sci. 2016;57(12):No Pagination Specified. doi: https://doi.org/.
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To evaluate disease activity in the non-acute stage of VKHD.
Patients (P) within a minimum 12-mo period from disease onset (defined as non-acute) were prospectively evaluated over at least 1y. Follow-up protocol included every 3-mo clinical and imaging exams [indocyanince green and fluorescein angiographies (FA) and enhanced depth optical coherence tomography]. Full-field (ffERG) and multifocal electroretinograms (mfERG) were carried out at inclusion and at 12-mo follow-up. Imaging exams were read by 3 masked retina specialists. Disease activity signs were defined as clinical signs [anterior chamber cells (ACC), macular edema (ME) and choroidal neovascularization (CNV)] and as subclinical signs [perivascular or optic disc leakage on FA, dark dots and increase in choroidal thickness (CT≥30%)]. Treatment was tailored based on the presence of clinical signs. Patients with no clinical or subclinical signs were designed as pattern A; those with only subclinical signs, as pattern B, and those with both signs, as pattern C.
20P (17F/3M) with median disease duration of 55mo (12-144mo) were included. While CT increase, ME and CNV had a substantial to optimal reading concordance (kappa>0.8), other angiographic signs had poor concordance (kappa<0.2). During follow-up, cells were observed in 11 evaluations; subclinical posterior segment inflammation (PSI) was simultaneously observed in 64% of eyes. At inclusion, inflammation status was: none in 1P (5%); only subclinical signs in 10P (50%); and both clinical and subclinical in 9P (45%). The follow-up of pattern B patients showed that 2P converted to pattern C (ACC+); ERG parameters became stable in 4P and worsened in 3P (3P not done). Pattern C patients had ERG parameters stable in 2P and worsened in 4p. Treatment was incremented in 13P (65%) during follow-up.
1. Among PSI signs, those observed on OCT were the most reliable ones; 2. ACC was indicative of subclinical PSI in 2/3 of the patients; 3. 18 out of 25 eyes (72%) included as with no clinical sign of inflammation, had subclinical PSI; during follow-up, only 2 eyes remained with no clinical or subclinical signs of inflammation; 4. Half of the eyes showed retina function deterioration during follow-up, despite remaining with good visual acuity.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
Table 1 -Disease activity and electroretinogram parameters of patients with non-acute VKHD at inclusion and at 12-month follow-up.
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