Prosthetic Replacement of the Ocular Surface Ecosystem Scleral Lens Therapy for Patients With Ocular Symptoms of Chronic Stevens-Johnson Syndrome

2014 ◽  
Vol 158 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Martin Heur ◽  
Dianne Bach ◽  
Christos Theophanous ◽  
Gloria B. Chiu
Keyword(s):  
Ocular Surface ◽  
Stevens Johnson Syndrome ◽  
Prosthetic Replacement ◽  
Ocular Symptoms ◽  
Johnson Syndrome

Long-term Progression of Ocular Surface Disease in Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

Cornea ◽  
2020 ◽  
Vol 39 (6) ◽  
pp. 745-753
Author(s):  
Yamato Yoshikawa ◽  
Mayumi Ueta ◽  
Hideki Fukuoka ◽  
Tsutomu Inatomi ◽  
Isao Yokota ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Ocular Surface ◽  
Ocular Surface Disease ◽  
Stevens Johnson Syndrome ◽  
Johnson Syndrome

scholarly journals Autologous Blood Products: When, Where, and How?

2021 ◽  
Vol 8 (1) ◽  
pp. 1-9
Author(s):  
Alfonso L Sabater ◽  
Keyword(s):  
Ocular Surface ◽  
Keratoconjunctivitis Sicca ◽  
Therapeutic Option ◽  
Autologous Blood ◽  
Stevens Johnson Syndrome ◽  
Eye Drops ◽  
Corneal Epithelial ◽  
Johnson Syndrome ◽  
Ocular Surface Diseases ◽  
Persistent Epithelial Defects

Autologous blood eye drops have become an interesting, well-known, and widely used therapeutic option for many ocular surface diseases since their introduction into the ophthalmologic field forty-six years ago. The foundation for their use in the treatment of pathologies such as severe keratoconjunctivitis sicca, persistent epithelial defects, ocular chemical burns, recurrent epithelial erosions, Stevens-Johnson syndrome, ocular graft versus host disease, and, lately, in many other ocular surface conditions, relies on the fact that they contain proteins, vitamins, cytokines, and growth factors that participate in the signaling pathways of corneal epithelial healing in similar amounts to those found in normal, healthy tear films

scholarly journals Drugs causing severe ocular surface involvements in Japanese patients with Stevens–Johnson syndrome/toxic epidermal necrolysis

2015 ◽  
Vol 64 (4) ◽  
pp. 379-381 ◽  
Author(s):  
Nahoko Kaniwa ◽  
Mayumi Ueta ◽  
Ryosuke Nakamura ◽  
Yoshimi Okamoto-Uchida ◽  
Emiko Sugiyama ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Ocular Surface ◽  
Japanese Patients ◽  
Stevens Johnson Syndrome ◽  
Johnson Syndrome

scholarly journals Pathogenesis of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis With Severe Ocular Complications

2021 ◽  
Vol 8 ◽  
Author(s):  
Mayumi Ueta
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Ocular Surface ◽  
Acute Stage ◽  
Stevens Johnson Syndrome ◽  
Prostaglandin E ◽  
Ocular Complications ◽  
Chronic Stage ◽  
Snp Association ◽  
Johnson Syndrome ◽  
Burn Units

Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is an acute inflammatory vesiculobullous reaction of the mucosa of the ocular surface, oral cavity, and genitals, and of the skin. Severe ocular complications (SOC) are observed in about half of SJS/TEN patients diagnosed by dermatologists and in burn units. Ophthalmologists treat SOC, and they tend to encounter the patients not only in the acute stage, but also in the chronic stage. Our investigation of the pathogenesis of SJS/TEN with SOC led us to suspect that abnormal innate mucosal immunity contributes to the ocular surface inflammation seen in SJS/TEN with SOC. We confirmed that cold medicines such as NSAIDs and multi-ingredient cold medications are the main causative drugs for SJS/TEN with SOC. Single nucleotide polymorphism (SNP) association analysis of cold medicine-related SJS/TEN with SOC showed that the Toll-like receptor 3 (TLR3)-, the prostaglandin-E receptor 3 (PTGER3)-, and the IKZF1 gene were significantly associated with SNPs and that these genes could regulate mucocutaneous inflammation including that of the ocular surface. We also examined the tear cytokines of SJS/TEN with SOC in the chronic stage and found that IL-8, IL-6, IFN-γ, RANTES, eotaxin, and MIP-1β were significantly upregulated in SJS/TEN with SOC in the chronic stage. Only IP-10 was significantly downregulated in SJS/TEN with SOC in the chronic stage. This mini-review summarizes the pathological mechanisms that we identified as underlying the development of SJS/TEN with SOC.

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