Genetic predisposition to Stevens-Johnson syndrome with severe ocular surface complications
Cornea, ISSN: 1536-4798, Vol: 34, Issue: Supplement 11, Page: S158-S165
2015
- 21Citations
- 17Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations21
- Citation Indexes21
- 21
- CrossRef14
- Captures17
- Readers17
- 17
Conference Paper Description
Stevens-Johnson syndrome (SJS) is an acute inflammatory vesiculobullous reaction of the skin and mucosa, including the ocular surface, oral cavity, and genitals. In patients with extensive skin detachment and a poor prognosis, the condition is termed toxic epidermal necrolysis (TEN). This review covers 4 topics: (1) ophthalmic SJS, (2) human leukocyte antigen (HLA) analysis, (3) genome-wide association studies, and (4) other pathogenic factors. Severe ocular complications (SOCs) develop in some SJS/TEN patients diagnosed by dermatologists. Cold medicine-related SJS/ TEN (CM-SJS/TEN) with SOCs is associated with HLA-A∗02:06 in Japanese and Koreans and HLA-B∗44:03 in Japanese, Indians, and Brazilian whites. We conducted a genome-wide association study for CM-SJS/TEN with SOCs and found that IKZF1 single-nucleotide polymorphisms (SNPs) were significantly associated with CM-SJS/ TEN with SOCs, and that the ratio of the Ik2/Ik1 isoforms might be influenced by these IKZF1 SNPs. Moreover, HLA-A∗02:06 with TLR3 polymorphisms and HLA-A∗02:06 with EP3 polymorphisms exerted additive effects in SJS/TEN with SOCs. EP3 is strongly downregulated in the conjunctival epithelium of SJS/TEN. Cold medicines including nonsteroidal antiinflammatory drugs, which are the main causative drugs for SJS/TEN with SOCs, downregulate the production of prostanoids, including PGE2. Because the PGE2-EP3 pathway suppresses the inflammation of the ocular surface, skin, and respiratory tract, downregulation of PGE by nonsteroidal antiinflammatory drugs or acetaminophen might significantly contribute to the onset of CM-SJS/TEN with SOCs. Cold medicines and infectious agents such as viruses or other microbes are both important in triggering the onset of SJS/TEN with SOCs.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84944070838&origin=inward; http://dx.doi.org/10.1097/ico.0000000000000605; http://www.ncbi.nlm.nih.gov/pubmed/26448174; http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00003226-201511001-00012; https://journals.lww.com/00003226-201511001-00012; https://dx.doi.org/10.1097/ico.0000000000000605; https://insights.ovid.com/article/00003226-201511001-00012
Ovid Technologies (Wolters Kluwer Health)
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