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Objective:To evaluate the efficacy and safety of oral anisodine hydrobromide tablets in the treatment of nonarteritic anterior ischemic optic neuropathy (NAION).Methods:A multicenter nonrandomized controlled trial was conducted.A total of 282 acute NAION patients (282 eyes) were recruited from 16 hospitals in China from July 2020 to May 2021.Patients were divided into two groups according to treatment methods, which were control group (124 cases, 124 eyes) receiving regular treatment including citicoline sodium plus Ginkgo biloba leaf liquid extract or Ginkgo biloba leaf extract tablets plus mecobalamin, and experimental group (158 cases, 158 eyes) receiving treatment in control group plus oral anisodine hydrobromide tablets 1 mg, twice daily for 2 to 3 months.Best corrected visual acuity (BCVA), visual field index (VFI), peripapillary retinal nerve fiber layer (pRNFL) and radial peripapillary capillary vessel density (RPC) were assessed at 1, 2, 3, and 6 months after enrollment using the standard decimal visual acuity chart, 750i Humphery visual field analyzer, Cirrus HD-OCT 4000/Cirrus HD-OCT 5000, RTVue-XR optical coherence tomography respectively.The primary outcomes were BCVA and VFI, and the secondary outcomes were pRNFL, RPC, and the side effects during the follow-up.The study adhered to the Declaration of Helsinki.All patients were fully informed about the treatment and purpose of this study and voluntarily signed the informed consent form.The study protocol was approved by Chinese PLA General Hospital (No.S2020-021-01). Results:In all, 242 patients (242 eyes) completed the follow-up of BCVA, and 98 patients (98 eyes) completed the VFI follow-up.In terms of visual function, BCVA and VFI improved significantly over time in the two groups, and BCVA and VFI were better in experimental group than in control group at various follow-up time points (all at P<0.05). In terms of structure, pRNFL gradually decreased in both groups with the extension of treatment, and pRNFL was significanthy thinner in experimental group than in control group at various follow-up time points (all at P<0.05). There was no significant difference in RPC between the two groups at the last follow-up ( P>0.05). There were two cases with side effects and one case was discontinued due to side effects 25 days after enrollment. Conclusions:Oral anisodine hydrobromide can improve visual acuity and visual field in NAION and accelerate the regression of optic disc edema, with good safety.
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Objective:To explore the clinical and imaging features and prognoses of myelin oligodendrocyte glycoprotein antibody associated disorders (MOGAD).Methods:Thirty-nine MOGAD patients, admitted to our hospital from January 2018 to April 2021, were chosen in our study. The clinical and imaging data and follow-up results of these patients at acute attack period (first-onset or relapse) were collected and their features were analyzed.Results:In these 39 patients with MOGAD, 20 patients (51.3%) had non-reversing course, and 19 patients (48.7%) had relapsing course. The clinical and imaging data of 55 episodes of these 39 patients were collected. In these 55 episodes, optic neuritis was noted in 27 episodes (49.1%), encephalitis was noted in 10 episodes (18.2%), brainstem encephalitis was noted in 8 episodes (14.5%), meningoencephalitis in 2 episodes (14.5%), myelitis in 3 episodes (5.5%), encephalomyelitis in 1 episode (1.8%), optic neuromyelitis in 1 episode(1.8%), optic neuritis+meningoencephalitis in 2 episodes (3.6%), and optic neuritis+encephalitis in 1 episode (1.8%). The positive rate of antinuclear antibody (ANA) was 11.1% (4/36); the cerebrospinal fluid results of 28 samples were collected from 22 patients, and CSF pleocytosis occurred in 67.9% of the samples with value of 54.89±67.70×10 6/L. Twenty-seven brain MRIs of 19 patients at the acute episode were collected; one completely normal MRI was recorded; among the remaining 26 MRIs, 6 were with one single lesion, 5 were with 2 lesions, and 15 were with 3 or more lesions; in terms of distribution, lesions involving brainstem and its adjacent structures were found in 9 MRIs, lesions involving diencephalon and deep gray matter were found in 7 MRIs, supratentorial white matter lesions were found in 13 MRIs, and cortical lesions were found in 13 MRIs. Meningeal enhancement were found in 4 contrast-enhanced brain MRIs (4/20). Long or short segmental myelitis in the spinal MRIs was noted in spinal lesions, involving cervical spinal cord, thoracic spinal cord and conus, and the "H" sign could be seen in the cross section. All patients received steroids therapy at the acute phase and the doses of steroids were tapered down gradually. Thirty-eight patients (97.4%) had good prognosis after 3 months of treatment. Conclusions:MOGAD is a disease entity widely involving the white matter, gray matter and meninges of the central nervous system with various clinical manifestations such as optic neuritis, encephalitis, brainstem encephalitis, meningoencephalitis and myelitis or a combination of the above. Immunotherapy is effective in most patients, but the recurrence rate is high, and some patients require long-term immunotherapy.
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Objective:To explore the protective effect of vitexin on retinal ganglion stem cells (RGCs) from oxidative stress caused by retinal ischemia-reperfusion (RIR) in rats and its possible mechanism.Methods:Sixty male SD rats were randomly divided into the model group, vitexin group and normal control group by random number table, with 20 rats in each group.The right eyes were taken as experimental eyes.Rats in the model group and the vitexin group were treated with anterior chamber perfusion to establish RIR models.Rats in the vitexin group were given intraperitoneal injection of vitexin at a dose of 25 mg/(kg·d) for 7 days.Rats in the model group were intraperitoneally injected with the same volume of normal saline.For the normal control group, the experimental eyes underwent anterior chamber puncture without increasing the intraocular pressure, and were intraperitoneally injected with the same volume of normal saline.On the 7th day following modeling, the rats were sacrificed by overdose anesthesia.Histopathology staining was used to detect the thickness of retina and the number of RGCs.Retrograde tracing with Fluoro-Gold was used to detect the density of RGCs.TUNEL staining was used to detect the apoptosis of RGCs.Colorimetric method was used to detected superoxidate dismutase (SOD) activity and concentration of malondialdehyde (MDA) and nitric oxide (NO). Western blot method was used to detect the relative expression levels of cytoplasmic Nrf2, HO-1, NQO1, nuclear Nrf2 proteins in rat retina.The use and care of animals followed the ARVO Statement.This study protocol was approved by the Experimental Animal Ethics Committee of Henan Eye Hospital (No.HNEECA-2019-04).Results:The retinal thickness was (90.21±3.55)μm in the model group, which was significantly lower than (128.20±5.31)μm in the normal control group and (119.65±6.14)μm in the vitexin group, and the differences were statistically significant (both at P<0.05). The average density of RGCs was (1 300.85±14.00)/mm 2 in the model group, which was significantly lower than(2 330.12±15.05)/mm 2 in the normal control group and (1 921.64±11.78)/mm 2 in the vitexin group, and the differences were statistically significant (both at P<0.05). The rate of TUNEL positive RGCs was (68.34±5.04)% in the model group, which was significantly higher than (3.01±0.18)% in the normal control group and (35.51±2.04)% in the vitexin group, and the differences were statistically significant (both at P<0.05). Compared with the normal control group and the vitexin group, the SOD activity in the retinal tissue of the rats was lower and the concentrations of MDA and NO were higher in the model group, and the differences were statistically significant (all at P<0.05). The expression level of cytoplasmic Nrf2 protein was the lowest in the vitexin group, then following the model group and the normal control group, and the relative expression levels of HO-1, NQO1 and nuclear Nrf2 protein were the highest in the vitexin group, then followed the model group and normal control group, and the differences were statistically significant (all at P<0.05). Conclusions:Vitexin can reduce the apoptosis of RGCs and alleviate oxidative stress damage of retina in RIR rat model.This protective effect may be achieved by activating Nrf2-related signaling pathway.