ReviewInternational ophthalmology2020
Genetic variations in autoimmune genes and VKH disease.
Review in International ophthalmology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- The effect of high-altitude exposure on Vogt-Koyanagi-Harada syndrome: a case report.BMC ophthalmology · 2025Article
- High prevalence of angle-closure glaucoma in Vogt-Koyanagi-Harada disease.International ophthalmology · 2022Observational
- Vogt-Koyanagi-Harada Disease with Oral Manifestations: A Rare Case Report.Contemporary clinical dentistryArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeVogt-Koyanagi-Harada (VKH) disease is a rare autoimmune disease. The autoimmune response in VKH disease is against the melanin-producing cells; therefore, in affected individuals melanocyte-containing organs manifest disease symptoms including eyes, ears, skin and nervous system. VKH is a multifactorial disease, and the precise cause of the VKH disease is unknown. Studies have suggested that both environmental and genetic factors are responsible for the VKH disease. In this review, the authors have collected all the available literature on the genetics of VKH to their knowledge and discussed the role of genetic variants in causing VKH disease.
methodsAn extensive literature search was performed in order to review all the published studies regarding VKH clinical phenotyping and genetic variants in VKH disease. Medline, PubMed, Cochrane library, and Scopus was searched using combination of keywords.
resultsIt was found that variants in HLA genes, IL-12b, TNFSF4, and miR-20-5p genes are significantly associated with VKH; however, variants in genes ATG10, TNIP1 and CLEC16A did not achieve significant genome-wide association threshold. Moreover, polymorphisms in TNIP1 and CLEC16A play a protective role against VKH.
conclusionThe authors conclude that increased sample size and a more homogeneous VKH patient population may reveal a significant association of variants in ATG10, TNIP1 and CLEC16A genes with VKH disease.
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