A narrower, distinctly studied outcome of Stevens-Johnson syndrome and toxic epidermal necrolysis: cases triggered by cold medicine that go on to cause severe eye damage. An ethnicity-specific study in Japanese and Korean cohorts found a variant near REC114 — a different gene from this site's general SJS/TEN page.
This catalogue already has a page for drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) generally, built around the common trigger drugs — allopurinol, certain anticonvulsants, some antibiotics. This page is about something more specific: cases triggered by cold medicine (in Japan, most often acetaminophen-containing remedies and NSAIDs) that go on to cause severe eye complications — scarring, corneal damage, and vision loss from the mucous membrane damage SJS/TEN can cause.
That specific outcome is severe and distinct enough that Japanese and Korean ophthalmology and genetics groups have studied it as its own research question, rather than treating it as automatically explained by SJS/TEN genetics generally.
Ueta et al. 2017 used the Japonica array, an ethnicity-specific genotyping array with imputation based on whole-genome sequences from 1,070 Japanese individuals — a design built specifically to catch variants that an array designed for European populations would miss. They identified two new susceptibility loci, on chromosomes 15 and 16, validated in further Japanese samples and replicated in Korean samples.
The variant on this page, rs16957893, sits near REC114 — a different gene from HCP5, the locus behind this site's general drug-induced SJS/TEN page. That difference is itself part of the case for treating this as a distinct question: the more specific trigger (cold medicine) and the more specific outcome (severe ocular complications) are tracked by a different genetic signal, not simply a subset of the general finding.
Any suspected SJS/TEN reaction — skin blistering, peeling, mucous membrane involvement, especially after starting a new medicine — needs emergency care. Early ophthalmology involvement specifically improves eye outcomes when mucous membranes are affected; this is established clinical practice and does not depend on genotype.
The mucous membranes lining the eyelids and eye surface are among the tissues SJS/TEN can damage, and the resulting scarring is a leading cause of the vision loss survivors experience — which is why this specific outcome, distinct from the skin reaction itself, has been studied as its own question.
Drug-induced SJS/TEN generally has its own page and its own genetics (HCP5). This page is deliberately kept separate rather than merged into it, because the specific trigger, the specific outcome, and the genetic signal found for each are not the same.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Cold Medicine-Related SJS/TEN with Severe Ocular Complications comes down to these specific, well-studied positions — not a diagnosis.
REC114 · rs16957893
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No. That page covers drug-induced SJS/TEN broadly and is built around a different gene (HCP5). This page is specifically about cases triggered by cold medicine that go on to cause severe eye complications — a narrower, separately studied outcome with its own genetic signal.
Seek emergency care immediately — skin blistering, peeling, or mucous membrane involvement after starting a medicine needs urgent evaluation. Early ophthalmology involvement specifically improves eye outcomes when the eyes are affected, regardless of genotype.
It used a genotyping array built for the Japanese population specifically, rather than a standard array designed around European genetic variation — a reminder that genetic studies built for one population can miss variants that matter in another.
No single variant works that way. This is one locus from one study, shifting risk of a rare, serious reaction — it is not used as a screening test before taking cold medicine.
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