Almost simultaneous onset of Vogt–Koyanagi–Harada syndrome in co-workers, friends, and neighbors

Hayasaka, Yoriko; Hayasaka, Seiji

doi:10.1007/s00417-004-0888-9

Cited by 18 publications

(8 citation statements)

References 5 publications

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“…One publication described six cases of patients who had had contact with each other and who presented with the initial stages of VKHS almost simultaneously. That report supports the hypothesis that an external factor, such as a viral infection, may be involved in the development of this disease [34].…”

Section: Infectious Hypothesissupporting

confidence: 88%

Vogt–Koyanagi–Harada syndrome

Greco

Fusconi

Gallo

et al. 2013

Autoimmunity Reviews

120

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Section: Infectious Hypothesissupporting

confidence: 88%

Vogt–Koyanagi–Harada syndrome

Greco

Fusconi

Gallo

et al. 2013

Autoimmunity Reviews

120

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Section: Etiology and Pathogenesissupporting

confidence: 78%

Síndrome de Vogt-Koyanagi-Harada e o seu acometimento multissistêmico

Mota¹,

Santos²

2010

Rev. Assoc. Med. Bras.

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Vogt-Koyanagi-Harada's syndrome is a rare disease that affects tissues containing melanocytes, such as the eyes, central nervous system, inner ear and skin. Some ethnic groups have a higher probability of developing the disease, including Asians, Indians and Latin Americans and females are affected more often. Methods: Literature was reviewed in books, articles published on the internet and papers available in the online databases MEDLINE, LILACS and SciELO. Texts were selected that focused on otorhinolaryngological symptoms. Literature review: The disease probably has autoimmune etiology, with aggression occurring on the surface of melanocytes by promoting inflammatory reaction in which T lymphocytes predominate. The allele most often found in association with this disease is HLA DRB1*0405. Clinical manifestations are divided into four stages: prodromal, uveitic, chronic and recurrent. Otorhinolaryngological symptoms occur during the uveitic stage and are characterized by bilateral sensorineural hearing loss, tinnitus and vestibular symptoms. Diagnosis is made according to the diagnostic criteria for the disease. Treatment is primarily with corticosteroids. Conclusions: It is important that professionals in other specialties are able to recognize Vogt-Koyanagi-Harada's syndrome, because late diagnosis can lead to ocular and cutaneous sequelae.

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“…In addition, DO analysis suggested that the immune DEGs were mainly involved in human immunodeficiency virus infectious disease. As VKH disease is an autoimmune inflammatory disorder with virus infection playing an important role in its pathogenesis ( 12 , 23 ), the results of the present DO analysis were consistent with those of previous studies. Since monocytes were thought to be significantly involved in the development of autoimmune diseases, peripheral blood mononuclear cells (PBMCs) have gradually become a breakthrough in studying the pathogenesis of VKH disease.…”

Section: Discussionsupporting

confidence: 92%

Identification of immune hub genes participating in the pathogenesis and progression of Vogt-Koyanagi-Harada disease

Wang

Ju²,

Wang³

et al. 2022

Front. Immunol.

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BackgroundVogt-Koyanagi-Harada (VKH) disease is an autoimmune inflammatory disorder characterized by bilateral granulomatous uveitis. The objective of this study was to identify immune hub genes involved in the pathogenesis and progression of VKH disease.MethodsHigh throughput sequencing data were downloaded from the Gene Expression Omnibus (GEO) and an immune dataset was downloaded from ImmPort. Immune differentially expressed genes (DEGs) were obtained from their intersection in the GEO and ImmPort datasets. Immune hub genes for VKH disease were selected through differential expression analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Disease Ontology (DO), protein-protein interaction (PPI) network, and clustering analyses. Confidence in the immune hub genes was subsequently validated using box plots and receiver operating characteristic (ROC) curves.ResultsA total of 254 DEGs were screened and after the intersection with ImmPort, 20 genes were obtained as immune DEGs. Functional enrichment analysis indicated that the key genes were mainly involved in several types of immune pathways (such as the lymphocyte mediated and leukocyte mediated immune responses, natural killer cell mediated cytotoxicity, and antigen binding) and immunodeficiency diseases. Following PPI network analysis, the top seven genes in cluster 1 were selected as potential immune hub genes in VKH. After evaluating the accuracy of the hub genes, one gene (GNLY) was excluded because its expression level was statistically similar in VKH patients and healthy controls. Finally, six immune hub genes, namely KLRC2, KLRC3 SH2D1B, GZMB, KIR2DL3, and KIR3DL2 were identified as playing important roles in the occurrence and development of VKH disease.ConclusionSix immune hub genes (KLRC2, KLRC3 SH2D1B, GZMB, KIR2DL3, and KIR3DL2) identified by our bioinformatics analyses may provide new diagnostic and therapeutic targets for VKH disease.

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Almost simultaneous onset of Vogt–Koyanagi–Harada syndrome in co-workers, friends, and neighbors

Abstract: Almost simultaneous onset of VKH syndrome in co-workers, friends, and neighbors may suggest an exogenous factor such as viral infection in the pathogenesis.

Cited by 18 publications

References 5 publications

Vogt–Koyanagi–Harada syndrome

Vogt–Koyanagi–Harada syndrome

Síndrome de Vogt-Koyanagi-Harada e o seu acometimento multissistêmico

Identification of immune hub genes participating in the pathogenesis and progression of Vogt-Koyanagi-Harada disease

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