Abstract

Purpose To explore the disease progression of primary open-angle glaucoma (POAG) in individuals with different degrees of VF defects by analyzing the trends in retinal nerve fiber layer (RNFL) changes at each stage. Methods A total of 39 patients (77 eyes) were divided into three groups based on the severity of glaucomatous visual field (VF) loss: the first group included patients with mild baseline VF defects (mild group; n = 21 eyes). The second group included patients with moderate VF defects (moderate group; n = 18 eyes). The third group included patients with severe baseline VF defects (severe group; n = 38 eyes). For all patients, slit-lamp biomicroscopy of the anterior and posterior segments and detailed fundus and optic disc inspections were performed, the intraocular pressure (IOP) was measured by Goldman tonometry, best-corrected visual acuity (BCVA) was measured, the RNFL thickness was measured by OCT, and the VF was assessed by the Octopus perimeter. All the groups were followed up postoperatively for 18 months. Results The mean RNFL thickness was recorded for all the visits. Using simple linear regression analysis, we found that the R2 values of the three groups were 0.988, 0.982, and 0.814, respectively, and the slopes of mean RNFL thickness changes for mild, moderate, and severe baseline VF defects were −0.088, −0.082, and −0.015, respectively. Moreover, we used simple linear regression analysis to explore whether and how the speed of RNFL thinning differs across groups. The R2 values of the three groups were 0.982, 0.978, and 0.805, respectively, and the slopes for mild, moderate, and severe baseline VF defects were 0.089, 0.085, and 0.017, respectively. Conclusion The rate of RNFL thinning is linear; RNFL thinning is the fastest in individuals with mild baseline VF defects, followed by those with moderate baseline VF defects. In individuals with severe VF defects, changes in the RNFL thickness do not appropriately reflect the progression of the disease. The clinical trial is registered with ChiCTR2000028975.

Highlights

  • Primary open-angle glaucoma (POAG) is a common clinical eye disease that is irreversible and causes blindness; it is a type of optic neuropathy characterized by the loss of retinal ganglion cells and their axons [1]

  • E maximum, minimum, and average intraocular pressure (IOP) of the three groups after 18 months of follow-ups are presented in Figure 1. e mean retinal nerve fiber layer (RNFL) thickness changes in patients with mild, moderate, and severe baseline visual field (VF) defects are shown in Figures 2–4, respectively, and the mean thickness of the

  • RNFL thickness in combination with other indicators to diagnose and follow up patients, but they did not systematically study the changes in RNFL over time [13,14,15]. e slope of the RNFL changes differed across POAG patients with different severities of VF defects, and this result was mainly caused by the different structural characteristics of the eye in individuals with different VF defects

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Summary

Clinical Study

Received 3 January 2020; Revised 8 March 2020; Accepted 24 March 2020; Published 13 April 2020. E third group included patients with severe baseline VF defects (severe group; n 38 eyes). Using simple linear regression analysis, we found that the R2 values of the three groups were 0.988, 0.982, and 0.814, respectively, and the slopes of mean RNFL thickness changes for mild, moderate, and severe baseline VF defects were −0.088, −0.082, and −0.015, respectively. We used simple linear regression analysis to explore whether and how the speed of RNFL thinning differs across groups. E R2 values of the three groups were 0.982, 0.978, and 0.805, respectively, and the slopes for mild, moderate, and severe baseline VF defects were 0.089, 0.085, and 0.017, respectively. In individuals with severe VF defects, changes in the RNFL thickness do not appropriately reflect the progression of the disease. In individuals with severe VF defects, changes in the RNFL thickness do not appropriately reflect the progression of the disease. e clinical trial is registered with ChiCTR2000028975

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