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Role of Dendritic Cells and Inflammatory Cells in Herpetic Endotheliitis: Analysis Using In Vivo Confocal Microscopy.
Cornea 2018 June
PURPOSE: To observe the pathological changes in dendritic cells (DCs) and inflammatory cells in the corneal epithelium and endothelium using in vivo confocal microscopy during the management of herpetic endotheliitis.
METHODS: A total of 110 eyes with herpetic endotheliitis were included. All patients were treated with antiviral agents combined with glucocorticoids. Changes in corneal edema were observed using slit-lamp microscopy and anterior segment optical coherence tomography. DCs and inflammatory cells in the epithelium and endothelium were detected using in vivo confocal microscopy before treatment and at 1 to 2 weeks and 1 and 3 months after treatment. Recurrence was monitored for 2 years. The contralateral normal eyes were evaluated as controls.
RESULTS: Mean density of DCs decreased at 1 month after treatment (100 ± 14 cells/mm) compared with before treatment (148 ± 26 cells/mm, P < 0.001). At 3 months, DCs returned to small and dendritiform reflective corpuscular cells at a density of 44 ± 11 cells/mm (P < 0.001), and the mean density of endothelial cells (2011 ± 173 cells/mm) was significantly lower than in controls (2472 ± 233 cells/mm, P = 0.002). Inflammatory cells residing in the epithelium were significantly reduced in number and disappeared at 1 to 2 weeks, and those at the endothelial surface almost disappeared at 1 month. There was no relapse during the follow-up evaluation.
CONCLUSIONS: DCs and inflammatory cells in the epithelial and endothelial cell layers of the cornea changed constantly in density, morphology, and distribution during the therapeutic process of herpetic endotheliitis. Adequate understanding of these alterations may help to guide the management of this disease.
METHODS: A total of 110 eyes with herpetic endotheliitis were included. All patients were treated with antiviral agents combined with glucocorticoids. Changes in corneal edema were observed using slit-lamp microscopy and anterior segment optical coherence tomography. DCs and inflammatory cells in the epithelium and endothelium were detected using in vivo confocal microscopy before treatment and at 1 to 2 weeks and 1 and 3 months after treatment. Recurrence was monitored for 2 years. The contralateral normal eyes were evaluated as controls.
RESULTS: Mean density of DCs decreased at 1 month after treatment (100 ± 14 cells/mm) compared with before treatment (148 ± 26 cells/mm, P < 0.001). At 3 months, DCs returned to small and dendritiform reflective corpuscular cells at a density of 44 ± 11 cells/mm (P < 0.001), and the mean density of endothelial cells (2011 ± 173 cells/mm) was significantly lower than in controls (2472 ± 233 cells/mm, P = 0.002). Inflammatory cells residing in the epithelium were significantly reduced in number and disappeared at 1 to 2 weeks, and those at the endothelial surface almost disappeared at 1 month. There was no relapse during the follow-up evaluation.
CONCLUSIONS: DCs and inflammatory cells in the epithelial and endothelial cell layers of the cornea changed constantly in density, morphology, and distribution during the therapeutic process of herpetic endotheliitis. Adequate understanding of these alterations may help to guide the management of this disease.
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