Vogt-Koyanagi-Harada Disease

@article{Cunningham2014VogtKoyanagiHaradaD,
  title={Vogt-Koyanagi-Harada Disease},
  author={Emmett T. Cunningham and Sivakumar R. Rathinam and İlknur Tuğal-Tutkun and Cristina Muccioli and Manfred Zierhut},
  journal={Ocular Immunology and Inflammation},
  year={2014},
  volume={22},
  pages={249 - 252}
}
Department of Ophthalmology, California Pacific Medical Center, San Francisco, CA, USA, Department of Ophthalmology, Stanford University School of Medicine, Stanford, CA, USA, The Francis I. Proctor Foundation, UCSF School of Medicine, San Francisco, CA, USA, Aravind Eye Hospital, Madurai, Tamil Nadu, India, Department of Ophthalmology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey, Department of Ophthalmology, Universidade Federal de São Paulo, São Paulo, Brazil, and… 
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References

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TLDR
The disease is incomplete and acute in half of the patients and has a quite good visual prognosis and seems to have increased during the last few years in Turkey.
Vogt-Koyanagi-Harada disease.
TLDR
Experimental data continue to support an autoimmune etiology for VKH disease, directed most probably against an antigenic component of the melanocyte, possibly tyrosinase or a tyros inase-related protein.
Vogt-Koyanagi-Harada Disease in Thailand
TLDR
Cataract and glaucoma represented the common ocular complications of VKH and were not associated with a specific treatment regimen but with an early withdrawal of systemic corticosteroids.
The spectrum of Vogt-Koyanagi-Harada disease in Turkey
TLDR
It is concluded that the majority of patients with VKH in Turkey do not have the complete form of the disease and are likely to be late referrals.
Retinal pigment epithelium folds as a diagnostic finding of Vogt-Koyanagi-Harada disease
TLDR
The detection of the folds of the RPE on OCT is a simple and effective method to help diagnose VKH disease at its acute stage which does not require pupil dilation.
Frequency of distinguishing clinical features in Vogt-Koyanagi-Harada disease.
Suboptimal therapy controls clinically apparent disease but not subclinical progression of Vogt-Koyanagi-Harada disease
TLDR
Submaximal doses of inflammation suppressive therapy are sufficient to suppress clinically apparent disease but not the underlying lesion process, which explains the propensity for sunset glow fundus in seemingly controlled disease.
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