Non-prescription cold and flu medication-induced transient myopia with uveal effusion: case report.

BACKGROUND: To report a case of non-prescription cold and flu medication-induced transient myopia with uveal effusion. CASE PRESENTATION: Bilateral high intraocular pressure, shallow anterior chambers, uveal effusion, and a myopic shift were encountered in a 39-year-old Chinese male 1 night after taking a non-prescription flu medicine three times than the recommended dose. Ultrasound biomicroscopy (UBM) showed bilateral ciliochoroidal effusions, disappearance of the ciliary sulcus, closure of the angle of the anterior chamber, and anterior displacement of the lens-iris diaphragm. Treatment with aqueous suppressants was given. Within a week, the uncorrected vision restored, and the myopia had disappeared. UBM revealed major resolution of the ciliochoroidal effusions in both eyes, deepening of the anterior chamber, return of the lens-iris diaphragm to a more posterior position. CONCLUSIONS: Overdose of non-prescription cold and flu medication may cause bilateral uveal effusions inducing acute angle-closure glaucoma and acute myopia.

Multiple evanescent white dot syndrome following rabies vaccination: a case report.

BACKGROUND: To report a case of multiple evanescent white dot syndrome (MEWDS) following simultaneous rabies vaccination. CASE PRESENTATION: Review of the clinical, laboratory, photographic, optical coherence tomographic (OCT), fundus autofluorescent, angiographic, electrophysiologic, and perimetric records of a patient suffering from MEWDS. RESULTS: A healthy 33-year-old Chinese female suffering from rapidly progressive visual loss of her left eye associated with photopsia and a para-central scotoma, seven days after receiving simultaneous rabies vaccination. Both anterior segments and fundus examination were unremarkable. The findings on OCT, electrophysiology, and perimetry were pathognomonic for MEWDS. CONCLUSIONS: The clinical presentation and the benign course were consistent with the diagnosis of MEWDS. No other events could be identified as a cause, other than the rabies vaccination. This case may suggest an autoimmune basis for MEWDS in predisposed patients.

A case report of Werner's syndrome with bilateral juvenile cataracts.

BACKGROUND: To report a case of Werner's syndrome with bilateral juvenile cataracts. CASE PRESENTATION: Review of the clinical, laboratory, photographic, genetic testing of the patient. A 26-year-old Chinese man presented with impaired vision in both eyes for more than a year. Anterior segment examination of both eyes revealed cataract. According to the ocular symptoms and systemic signs, including low body weight, a short stature, a bird-like face, atrophic and scleroderma-like skin, in addition to the juvenile cataracts, the clinical diagnosis of Werner's syndrome was made. Next-generation sequencing identified a homozygous WRN mutation in this patient. CONCLUSIONS: The ocular and systemic findings in this patient in combination with the homozygous WRN mutation indicated the definitive Werner's syndrome diagnosis.

Different approaches for treating myopic choroidal neovascularization: a network Meta-analysis.

AIM: To evaluate the efficacy of intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF), photodynamic therapy (PDT), and laser treatment (LT) for anatomical and functional improvement in myopic choroidal neovascularization (mCNV) patients. METHODS: Two researchers independently searched PubMed, Cochrane Library, Web of Science, and other databases to screen studies comparing best-corrected vision acuity (BCVA) and foveal center thickness (FCT) changes after mCNV treatment. Post-treatment chorioretinal atrophy (CRA) is a secondary outcome indicator. The retrieval time limit is from the database construction to January 30, 2023. RESULTS: A total of 1072 eyes in 16 articles were included. In the RCTs, intravitreal bevacizumab (IVB) and intravitreal ranibizumab (IVR) were superior to PDT (MD=0.18, 95%CI: 0.02, 0.40, MD=0.18, 95%CI: 0.01, 0.42) in improving BCVA of mCNV patients (P<0.05). The relative effectiveness in improving BCVA, from high to low, appeared to be IVR, intravitreal aflibercept (IVA), IVB, LT, PDT, and sham first followed by IVA (Sham/IVA). While improving the FCT from high to low was IVA, IVR, IVB, PDT. In retrospective studies, the results of BCVA after long-term treatment showed that all the therapeutic effects from high to low was IVA, intravitreal conbercept (IVC), IVR, IVB, IVB/IVR, PDT with IVB/IVR, PDT. The effect of improving FCT was IVA, IVR, IVC, PDT, and IVB from high to low. And in the effects of improving CRA, the IVB appeared to be higher than IVR, while the PDT was the smallest, but none of the differences in the results were statistically significant. CONCLUSION: Anti-VEGF has the best effect on long-term vision improvement in mCNV patients, using IVB or IVR alone to treat mCNV may be better than IVB or IVR combined with PDT. There is no significant difference in the improvement of visual acuity, macular edema, and CRA in mCNV patients treated with any different anti-VEGF drugs.

PI3K-mediated glioprotective effect of epidermal growth factor under oxidative stress conditions.

AIM: To determine the effects of epidermal growth factor (EGF) on the proliferation and migration of Müller cell line Moorfields/Institute of Ophthalmology-Müller 1 (MIO-M1), and its related molecular mechanisms under normal and oxidative stress conditions. METHODS: Müller cells were cultured with different concentrations of EGF in the presence or absence of varied amounts of H2O2 and glucose oxidase (GO) which induced oxidative stress. The proliferation and migration of Müller cells were examined by 5-Bromo-2-deoxyUridine (BrdU), MTT assay, Transwell assay and scratch wound healing assays. The cell viability was determined with the MTT assay. The secretion of EGF by Müller cells was evaluated by ELISA. Western blot was performed to detect the activation of extracellular regulated protein kinases (ERK)1/2 and Akt signal pathways. RESULTS: EGF stimulated the proliferation and migration of Müller cells in a concentration-dependent manner in vitro. Under oxidative damage condition, 2h of pretreatment with 10-100 ng/mL EGF can mostly inhibit 50% lethal dose of 0.08 mmol/L H2O2-induced cell damage. The Western blot results showed that after Müller cells were exposed to varying EGF for 24h, Akt and ERK1/2 were phosphorylated in a dose-dependent manner. In the presence of the LY294002, the potent PI3K inhibitor, the p-Akt was significantly attenuated. CONCLUSION: EGF may induce the proliferation and migration of human Müller cells through the Akt and the ERK1/2 signal pathways, and induce PI3K-mediated glioprotective effect under oxidative stress.