Vestnik oftalmologii · 2020
[The influence of long-term retinal protective therapy on glaucoma progression according to structural and functional tests].
СтатьяРандомизированное исследованиеНазвание и аннотация: Оригинал на русском
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Strakhov V V, Egorov E A, Erichev V P, Yartsev A V, Petrov S Yu, Dorofeev D A
Аннотация
PURPOSE: To evaluate the influence of prolonged neuroprotective therapy on disease progression in patients with primary open-angle glaucoma (POAG) with compensated intraocular pressure (IOP).
MATERIAL AND METHODS: The study included 147 patients with stages I-II POAG (249 eyes) who were randomized into the main (69 patients, 119 eyes) and control groups (78 patients, 130 eyes). Patients of the main group underwent retinalamin treatment course every 6 months. Patients were examined before enrolling and then every 3 months during the 24-months follow-up including optical coherence tomography (OCT; RNFL - retinal nerve fiber layer, NRR - neuroretinal rim, GCL - ganglion cell layer) and static perimetry (MD - mean deviation, PSD - pattern standard deviation).
RESULTS: Visual acuity and refraction did not change in either group (p>0.05). IOP increased in the control group (p=0.033). There was no difference between the groups by the 24th month (p=0.87). No MD changes were noted in the main (p=0.45) and control groups (p=0.27). PSD changed in the main (4.84±3.21 and 6.01±2.584 dB in the beginning and the end, respectively, p=0.0004) and the control groups (3.46±2.23 and 5.86±2.26 dB, respectively; p<0.0001). The groups differed in MD and PSD initially (p=0.15; p=0.02) and became equal by the end (p=0.59; p=0.53). RNFL did not change significantly in the main group (p=0.078) and decreased from 83.5±22.47 to 76.7±20.7 µm in the control group (p=0.001); no differences between the groups were noted in the beginning (p=0.276) or in the end of the study (p=0.524). NRR increased in the main group from 222±88.94 to 231±99.3 (p=0.012), and decreased in the control group from 248±87.09 to 234±96.2 (p=0.0006); no differences were found between groups in the beginning or in the end of the study (p=0.109; p=0.909). GCL thickness did not change either in the main, or in the control group (p=0.211; p=0.16), with no difference between the group noted in the beginning or the end of the study (p=0.44; p=0.51).
CONCLUSION: Regular treatment with retinalamin arrests the development of glaucomatous optic neuropathy. Longer-term research is required to study its influence on the visual function and the quality of life.
MATERIAL AND METHODS: The study included 147 patients with stages I-II POAG (249 eyes) who were randomized into the main (69 patients, 119 eyes) and control groups (78 patients, 130 eyes). Patients of the main group underwent retinalamin treatment course every 6 months. Patients were examined before enrolling and then every 3 months during the 24-months follow-up including optical coherence tomography (OCT; RNFL - retinal nerve fiber layer, NRR - neuroretinal rim, GCL - ganglion cell layer) and static perimetry (MD - mean deviation, PSD - pattern standard deviation).
RESULTS: Visual acuity and refraction did not change in either group (p>0.05). IOP increased in the control group (p=0.033). There was no difference between the groups by the 24th month (p=0.87). No MD changes were noted in the main (p=0.45) and control groups (p=0.27). PSD changed in the main (4.84±3.21 and 6.01±2.584 dB in the beginning and the end, respectively, p=0.0004) and the control groups (3.46±2.23 and 5.86±2.26 dB, respectively; p<0.0001). The groups differed in MD and PSD initially (p=0.15; p=0.02) and became equal by the end (p=0.59; p=0.53). RNFL did not change significantly in the main group (p=0.078) and decreased from 83.5±22.47 to 76.7±20.7 µm in the control group (p=0.001); no differences between the groups were noted in the beginning (p=0.276) or in the end of the study (p=0.524). NRR increased in the main group from 222±88.94 to 231±99.3 (p=0.012), and decreased in the control group from 248±87.09 to 234±96.2 (p=0.0006); no differences were found between groups in the beginning or in the end of the study (p=0.109; p=0.909). GCL thickness did not change either in the main, or in the control group (p=0.211; p=0.16), with no difference between the group noted in the beginning or the end of the study (p=0.44; p=0.51).
CONCLUSION: Regular treatment with retinalamin arrests the development of glaucomatous optic neuropathy. Longer-term research is required to study its influence on the visual function and the quality of life.