G P Williams1, H S Mudhar, M Leyland. 1. Department of Ophthalmology, Royal Berkshire NHS Foundation Trust, Reading, Berkshire, UK. gpwilliams@doctors.net.uk
Abstract
AIM: To describe the early pathological changes in the cornea during toxic epidermal necrolysis (TEN). METHOD: Demonstration of histological features of sequential corneal samples taken during management of complications of TEN in a young adult. RESULTS: Early vacuolation of basal keratinocytes and late infiltration of the cornea with CD 8 lymphocytes were observed. These changes are similar to those found in cutaneous TEN and may represent weakening of the stromal-epithelium interface with resultant recurrent erosion and chronic inflammation. CONCLUSIONS: Similar changes were found in avascular corneal tissue to those previously described in skin. The initial insult may be traumatic. We propose that a cytokine-mediated response contributes to the initial insult, either in response to and/or by accelerating severe inflammation. This precedes a cytotoxic infiltration which may exacerbate episodes of recurrent erosion. This provides a new insight into the mechanism of disease in the cornea following TEN.
AIM: To describe the early pathological changes in the cornea during toxic epidermal necrolysis (TEN). METHOD: Demonstration of histological features of sequential corneal samples taken during management of complications of TEN in a young adult. RESULTS: Early vacuolation of basal keratinocytes and late infiltration of the cornea with CD 8 lymphocytes were observed. These changes are similar to those found in cutaneous TEN and may represent weakening of the stromal-epithelium interface with resultant recurrent erosion and chronic inflammation. CONCLUSIONS: Similar changes were found in avascular corneal tissue to those previously described in skin. The initial insult may be traumatic. We propose that a cytokine-mediated response contributes to the initial insult, either in response to and/or by accelerating severe inflammation. This precedes a cytotoxic infiltration which may exacerbate episodes of recurrent erosion. This provides a new insight into the mechanism of disease in the cornea following TEN.
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