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Viviane Mayumi Sakata, Carlos E. HIrata, Maria Kiyoko Oyamada, Smairah F. Abdallah, Ever E. Rodriguez, Celso Morita, Joyce H Yamamoto; Multimodal evaluation of Vogt-Koyanagi-Harada disease: A 12-month prospective longitudinal study from the acute onset. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2075.
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© ARVO (1962-2015); The Authors (2016-present)
To describe Vogt-Koyanagi-Harada disease (VKHD) course during a 12-month follow-up from the acute onset concerning clinical, morphological and functional aspects.
Nine VKHD patients, diagnosed according to Revised Diagnostic Criteria, were included from the acute onset following a predefined protocol: 3-day pulsetherapy with methylprednisolone followed by slow tapering of oral prednisone over at least 1 y; folow up protocol included clinical exam, imaging exams (autofluorescence, indocyanine green and fluorescein angiography-FA- and enhanced depth-optical coherence tomography-OCT) performed with Spectralis HRA+OCT and ERG (RETI-port system; Roland Consult, Germany). The following disease activity signs defined “flare": anterior chamber cells (ACC), choroidal neovascular membrane, perivascular or optic disc leakage on FA, dark dots (DD), fuzzy vessels, increase in choroidal thickness (CT≥30%) or worsening of ERG parameters (≥30%) in two consecutive visits, after 2 mo of quiescence, without change in scheduled treatment. After 6 mo from disease onset, three patterns of disease evolution were characterized: A: no flare, B: subclinical flare or C: clinical flare (ACC and/or FA signs). Two trained readers analyzed autofluorescence patterns. The study protocol followed the statements of the Declaration of Helsinki and was approved by local Institutional Review Board.
Nine patients (7F/2M) median age of 33 y/o and median time to treatment of 12 d (3-46) were included. At day 30, all eyes had visual acuity ≥ 1,0 (logMar) and 12/18 eyes resolved retinal detachment. At 12th mo, DD were attenuated, though still observed in all eyes. Concerning disease pattern of evolution: 1 eye had no flare (A), 5 eyes had only subclinical (B) and 12 eyes had clinical flare (C). In 17/18 eyes (94%) at least one sign of inflammation was observed at 8 mo with a median prednisone dose of 0.3mg/kg/d. 16/17 eyes had ≥2 inflammatory signs. CT and autofluorescence pattern at one mo were related to chronic evolution with clinical flares (p=0.03; kappa=0.7, CI95%0.3-1.0).
8/9 VKHD patients had subclinical or clinical flares during the 12-mo follow up even when treated with early high-dose corticosteroids. Oral prednisone dose around 0.3mg/kg/d was a critical point when flares were observed. Autofluorescence pattern and CT analysis at 1 mo can help to identify more severe cases.
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