Downregulation of interferon-γ-induced protein 10 in the tears of patients with Stevens-Johnson syndrome with severe ocular complications in the chronic stage

Objectives Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are acute inflammatory vesiculobullous reactions of the skin and mucosa such as the ocular surface, oral cavity and genitals. Severe ocular complications (SOC) arise in some patients with SJS/TEN diagnosed by dermatologists. To investigate the pathophysiology of ocular surface inflammation in SJS/TEN with SOC in the chronic stage, we examined cytokines in the tears of patients with ocular surface diseases and healthy controls. Participants SJS/TEN eyes in the chronic stage (n>30), healthy eyes (n>20, controls) and eyes (n>20) from patients with atopic keratoconjunctivitis representing different ocular surface inflammatory disorders. Primary outcome measures Tear samples were collected on Schirmer's measurement strips. To measure the level of various cytokines in the tears we used BD CBA Flex sets. Study design An observational study (case-control study). Results We recorded the level of interleukin (IL)-6, IL-8, eotaxin, macrophage inflammatory protein (MIP)-1β, RANTES (regulated on activation, normal T cell expressed and secreted), interferon gamma (IFN)-γ, monocyte chemoattractant protein-1, IFN-γ-induced protein 10 (IP-10) and total IgE. We found that compared with the controls, in SJS/TEN with SOC, IL-6, IL-8, eotaxin and MIP-1β were significantly upregulated while IP-10 was significantly downregulated. Compared with atopic keratoconjunctivitis, IP-10 was significantly downregulated in SJS/TEN with SOC; on the other hand, total IgE was significantly upregulated in atopic keratoconjunctivitis compared with SJS/TEN with SOC. Conclusions IP-10 in tears may be a biomarker to distinguish between chronic SJS/TEN with SOC and other ocular inflammatory disorders such as atopic keratoconjunctivitis.