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Genetic predisposition to Stevens-Johnson syndrome with severe ocular surface complications

Cornea, ISSN: 1536-4798, Vol: 34, Issue: Supplement 11, Page: S158-S165
2015
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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.

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