Conjunctival histopathological changes associated with netarsudil 0.02

与奈他舒地尔0.02相关的结膜组织病理学变化

阅读:1

Abstract

OBJECTIVE: To investigate histopathological conjunctival changes associated with topical netarsudil 0.02%. METHODS: Observational comparative case series. Histopathological analysis of conjunctival specimens taken from adult patients undergoing glaucoma surgery. Inflammation score was graded by three independent pathologists. RESULTS: 29 samples were included for analysis. Mean age was 72.4 years and 44.8% were female. Most patients underwent trabeculectomy with mitomycin C (22/29, 76%) while the remainder underwent tube shunt surgery, and one patient underwent insertion of an experimental NT-501 intravitreal implant. All patients were taking ≥2 topical IOP lowering medications, and 12 patients (41.3%) were using topical netarsudil, with mean duration 26.8 months. Compared to those on other glaucoma medications, patients taking netarsudil had significantly thicker conjunctival epithelium (mean 90.1 µm vs 43.2 µm, p = 0.03) and a trend toward higher epithelial cell thickness count (mean 7.7 cells thick vs. 4.9 cells thick, p = 0.07), both of which remained significant and trending respectively when adjusted for confounders (p = 0.02 and p = 0.06). All netarsudil treated samples demonstrated inflammation (graded score ≥0.5) compared to 64.7% of those not on netarsudil (p = 0.03). There were no significant differences in any histopathological parameters in patients who had ceased netarsudil prior to analysis (n = 7) compared to those who had never taken netarsudil (p > 0.05 for all). CONCLUSION: Conjunctiva treated with netarsudil may be more likely to demonstrate inflammation compared to those treated with other combinations of glaucoma medications. These findings may have surgical implications and additional studies correlating clinical outcomes are required.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。