Research on underlying mechanisms of Stevens-Johnson syndrome

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1. We enrolled 73 patients (138 eyes) with Stevens-Johnson syndrome at chronic stage. Complications were categorized as corneal-, conjunctival-, and eyelid complications and 13 components were evaluated and graded on a scale from 0 to 3 according to their severity. The most severe complication components were loss of the palisades of Vogt (114 eyes, 82.6%) and meibomian gland involvement (102 eyes, 73.9%). Visual acuity in 74 of the 138 eyes (53.6 %) was worse than 20/200. Multivariable regression analysis showed that corneal neovascularization, opacification, keratinization, and cataracts significantly affected logMAR (p<0.0001, p<0.0001, p=0.0142, and p=0.0375, respectively). 2. We examined the histocompatibility antigen genes HLA-A,-B, and-C of 40 Japanese SJS/TEN patients with ocular complications and 113 healthy Japanese volunteers. We clarified that HLA-A*0206 is strongly associated with SJS/TEN with ocular complications in the Japanese. 3. The Japanese single-nucleotide-polymorphism (JSNP) database reports 7 polymorphisms consisting of 7 SNPs in the human Toll-like receptor (TLR) 3 gene ; 3 of the 7 SNPs are coded in exon regions, and the other 4 are coded in intron regions. These 7 SNPs were analysed in 57 Japanese patients with SJS/TEN with ocular surface complications and in 160 Japanese healthy controls. SNP 299698T/G and the genotype patterns of 293248A/A and 299698T/T were strongly associated with SJS/TEN. The results suggested that polymorphisms in the TLR3 gene could be associated with SJS/TEN in the Japanese population. 4. We found that bacterial strains not only from different subjects but also from multiple ocular surface sites of the same subject exhibited different PFGE patterns. The data demonstrated the polyclonality of S. epidermidis on the healthy ocular surface.