Contributions of tissue‐specific pathologies to corneal injuries following exposure to SM vapor. Issue 1 (16th June 2016)

• Record Type: Journal Article
• Authors: McNutt, Patrick M.; Tuznik, Kaylie M.; Glotfelty, Elliot J.; Nelson, Marian R.; Lyman, Megan E.; Hamilton, Tracey A.
• Other Names: Laskin Jeffrey D. guestEditor.
• Is Part Of: Annals of the New York Academy of Sciences. Volume 1374:Issue 1(2016)
• Page Start: 132
• Page End: 143
• Publication Date: 2016-06-16
• Subjects: sulfur mustard -- cornea -- corneal epithelium -- limbal stem cell; Medical sciences -- Periodicals; Medicine -- Periodicals; Science -- Periodicals; 610
• DOI: 10.1111/nyas.13105
• Languages: English
• ISSNs: 0077-8923

Abstract

Abstract : Corneal injuries resulting from ocular exposure to sulfur mustard (SM) vapor are the most prevalent chemical warfare injury. Ocular exposures exhibit three distinct, dose‐dependent clinical trajectories: complete injury resolution, immediate transition to a chronic injury, or apparent recovery followed by the subsequent development of persistent ocular manifestations. These latter two trajectories include a constellation of corneal symptoms that are collectively known as mustard gas keratopathy (MGK). The etiology of MGK is not understood. Here, we synthesize recent findings from in vivo rabbit SM vapor studies, suggesting that tissue‐specific damage during the acute injury can decrement the regenerative capacities of corneal endothelium and limbal stem cells, thereby predisposing the cornea to the chronic or delayed forms of MGK. This hypothesis not only provides a mechanism to explain the acute and MGK injuries but also identifies novel therapeutic modalities to mitigate or eliminate the acute and long‐term consequences of ocular exposure to SM vapor.