ObjectiveTo observe the short-term intraocular pressure changes of the affected eye after the implantation of dexamethasone vitreous implant (Ozurdex), and indirectly understand the tightness of the scleral perforation of the 22G implant device.MethodsThis is a prospective cohort design clinical observational study. From January 2018 to January 2020, 90 eyes (90 patients) who underwent vitreous Ozurdex implantation in the Department of Ophthalmology of Beijing Hospital were included in the study. There were 52 males (52 eyes), and 38 females (38 eyes); they were 14-79 years old. Forty-three eyes (43 patients) had retinal vein occlusion with macular edema, 29 eyes (29 patients) had uveitis with or without macular edema, 18 eyes (18 patients) had diabetic macular edema. All eyes underwent standard scleral tunnel vitreous cavity implantation Ozurdex treatment. The intraocular pressure was measured with a non-contact pneumatic tonometer 10 min before implantation (baseline) and 10, 30 min and 2, 24 h after implantation. The difference were compared between the intraocular pressure at different time points after implantation and the baseline. Wilcoxon signed rank test was used to compare intraocular pressure between baseline and different time points after implantation.ResultsThe average baseline intraocular pressure of the affected eye was 14.85 [interquartile range (IQR): 11.60, 17.63] mmHg (1 mmHg=0.133 kPa). The average intraocular pressure at 10, 30 and 2, 24 hours after implantation were 11.90 (IQR: 8.95, 16.30), 13.75 (IQR: 9.95, 16.80), 13.60 (IQR: 10.95, 17.20), and 14.65 (IQR: 12.20, 17.50) mmHg. Compared with the baseline intraocular pressure, the intraocular pressure decreased at 10 and 30 minutes after implantation, the difference was statistically significant (P＜0.001, P=0.002); the intraocular pressure difference was not statistically significant at 2, 24 h after implantation (P=0.140, 0.280).ConclusionsThere is a statistically significant difference in intraocular pressure reduction compared with the baseline in 10 and 30 minutes after vitreous implantation of Ozurdex, and there is no statistically significant difference between 2, 24 hours. This suggests that the 22G scleral puncture port of the preinstalled implant device cannot be completely closed immediately, and short-term intraocular pressure monitoring after implantation should be appropriately strengthened.
Objective The aim of present study was to investigate the protective effect of vitamin U on renal toxicity induced by sodium valproate (VPA) and provide laboratory data for clinical application of VPA. Methods In this study, 48 female rats were used. These animals were randomly divided into 4 groups: control group (group A), vitamin U group (group B), VPA group (group C), vitamin U+ VPA group (group D). Group A was given the same amount of normal saline, group B was given Vit U 50 mg/(kg·d), group C was given VPA 300 mg/(kg·d) and group D was given Vit U 50 mg/(kg·d) firstly, then VPA 300 mg/(kg·d) after 1 hours by gavage. After 2 or 4 weeks of continuous administration, the kidneys were collected from these rats after blood collection. Total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL), serum creatinine (Cr), urea (BUN) and uric acid (UA) were detected by automatic biochemical analyzer. Result ① Blood lipid. There were significant differences in TC and LDL between the group A and group C (P<0.05), and the level of TC and LDL in group C were significantly higher. ② Serum biochemical indexes of renal function. There was no significant difference in Cr, UA and BUN four groups at 2w (P>0.05). At 4w, compared with the other three groups, the Cr, BUN and UA level of VPA group were significantly higher (P<0.05). But there was no significant difference between the group A and the group D. ③ Pathological morphology of renal tissue. At 2w, there was no obvious abnormality in renal structures among the four groups. At 4w, inflammatory lesions were only seen in VPA group, and mild inflammatory cell infiltration were seen in other three groups. Conclusion VPA can lead to a higher level of blood lipid. The renal toxicity induced by VPA may have a certain relationship with the time of drug exposure, and vitamin U has a protective effect on the renal toxicity induced by VPA.