Benefit of hyperbaric oxygen therapy treatment in direct traumatic optic neuropathy: case report.

Direct traumatic optic neuropathy (TON) is a devastating condition and clinical challenge. Its adequate treatment remains controversial. Hyperbaric oxygen (HBO2) therapy has been proposed as an adjunctive treatment for eye disease but has rarely been used in optic neuropathy. The patient was a 57-year-old woman who had direct TON and brain injury after contusion injury. After receiving delayed HBO2 therapy her visual acuity got better - from hand motion to 6/60 - along with improvement of visual field and color vision. She was treated at 2.5 atmospheres absolute for 100 minutes, five times a week, for a total of 61 sessions. Our case highlights that HBO2 may be beneficial as an alternative treatment for direct TON, particularly when combined with brain injury. Although this entity is promising, further randomized controlled trials will be needed to clarify the efficacy of HBO2 in the treatment of direct TON.

Glucosamine-Induced Autophagy through AMPK⁻mTOR Pathway Attenuates Lipofuscin-Like Autofluorescence in Human Retinal Pigment Epithelial Cells In Vitro.

Age-related macular degeneration (AMD) is a vision-threatening age-associated disease. The retinal pigment epithelial (RPE) cells phagocytose and digest photoreceptor outer segment (POS). Incomplete digestion of POS leads to lipofuscin accumulation, which contributes to the pathology of the AMD. Autophagy could help reduce the amount of lipofuscin accumulation. In the present study, we evaluated the effects of glucosamine (GlcN), a natural supplement, on the induction of autophagy and POS-derived lipofuscin-like autofluorescence (LLAF) in ARPE-19 cells in vitro, and investigated the potential molecular pathway involved. Our results revealed that GlcN had no effect on phagocytosis of POS at the lower doses. GlcN treatment induced autophagy in cells. GlcN decreased the LLAF in native POS-treated cells, whereas malondialdehyde or 4-hydroxynonenal-modified POS attenuated this effect. 3-Methyladenine inhibited GlcN-induced autophagy and attenuated the effect of GlcN on the decrease of the native POS-derived LLAF. Furthermore, GlcN induced the phosphorylation of AMP-activated protein kinase (AMPK) and inhibited the phosphorylation of mammalian target of rapamycin (mTOR), whereas Compound C inhibited these effects of GlcN. Altogether, these results suggest that GlcN decreased the native POS-derived LLAF through induction of autophagy, at least in part, by the AMPK⁻mTOR pathway. This mechanism has potential for the preventive treatment of lipofuscin-related retinal degeneration such as AMD.

Epidemiology and Mortality-Related Prognostic Factors in Endophthalmitis.

Purpose: Endophthalmitis describes any intraocular inflammation that involves both the posterior and anterior segments and is divided into endogenous and exogenous types according to its pathogenesis. The incidence of endophthalmitis and its risk factors have been extensively evaluated. However, few studies have explored the mortality rate in patients diagnosed with endophthalmitis. Methods: We obtained data entered into the National Health Insurance Research Database (NHIRD) from 2000 to 2013. The data collected included all discharge diagnoses of endophthalmitis in inpatients. Baseline characteristics, comorbidities, and prognostic factors were evaluated. Results: This study identified 7764 patients who were diagnosed with endophthalmitis in Taiwan from 2000 to 2013. The mortality rate was 0.97% (75/7764), and the mean age was 63.57 ± 15.72 years. Epidemiological characteristics were compared as "with or without" for different systemic comorbidities, and the results indicated that the adjusted odds ratio (AOR) was significantly higher in cases comorbid with renal disease (AOR 2.864, P = 0.001), septicemia (AOR 8.886, P < 0.001), pneumonia (AOR 2.072, P = 0.030), and tumors (AOR 7.437, P < 0.001). However, comorbidity with diabetes mellitus (DM) lowered the AOR by 0.500-fold (P = 0.026). There was no significant difference in ORs between patients comorbid with hypertension, depression, anxiety, hyperlipidemia, thyrotoxicosis, liver disease, or injury (all P > 0.05). Conclusions: Among inpatients with endophthalmitis, predictors of mortality include renal disease, septicemia, pneumonia, neoplasia, a greater burden of comorbidity (especially catastrophic illness), longer hospital stays (more than 11 days), and higher medical costs. Interestingly, DM decreased the OR for inpatient mortality.

Combined trabeculotomy-trabeculectomy using the modified Safer Surgery System augmented with MMC: its long-term outcomes of glaucoma treatment in Asian children.

BACKGROUND: This study aimed to study the long-term surgical outcomes of combined trabeculotomy-trabeculectomy (CTT) using the modified Safer Surgery System in treating childhood glaucoma at a tertiary medical center in Taiwan. METHODS: Retrospective, consecutive, noncomparative case series. We retrospectively reviewed medical records of 42 pediatric patients (age 0-18 years) who had CTT performed on their 65 eyes using the modified Safer Surgery System. The study period spanned 18 years (from January 1, 1997, to December 31, 2014). We evaluated the outcome in terms of postoperative intraocular pressure (IOP), axial length growth, disc cupping reversal, and use of antiglaucoma medications. The surgical success was rated using the Kaplan-Meier survival analysis and based on the incidence of complications. RESULTS: The mean follow-up period was 85.05 ± 32.17 months (range 14-200). After operation, IOP dropped significantly from 35.76 ± 9.44 mmHg (mean ± SD) to 16.18 ± 7.20 mmHg together with a significant reversal of optic disc cupping. Similarly, the use of antiglaucoma medications was also significantly reduced in number from 1.26 ± 0.50 to 0.43 ± 0.70. Most of the axial lengths of the eyes measured at the last follow-up visit showed growths within the average ± 2 SDs in comparison with the healthy, age-matched population. After surgery, the qualified success rate was 90.77% at the end of the first year, 90.77% at the second year, 87.64% at the fifth year, 84.51% at the 10th year, and 81.38% at the 15th year. No serious intraoperative or postoperative complications were found. CONCLUSIONS: For Taiwanese children, the combined trabeculotomy-trabeculectomy using the modified Safer Surgery System offered an efficient and safe surgical option for treating glaucoma with long-term satisfactory control of IOP.

Silibinin treatment prevents endotoxin-induced uveitis in rats in vivo and in vitro.

Uveitis, an intraocular inflammatory disease, occurs mostly in young people and can result in the loss of socioeconomic capabilities. Silibinin has been shown to exert anti-inflammatory effects in human retinal pigment epithelial (RPE) cells. The present study investigated the anti-inflammatory effect of silibinin pretreatment on endotoxin-induced uveitis (EIU) in rats and the mechanisms by which it exerts these effects. Uveitis was induced via injection of lipopolysaccharides (LPS) into Lewis rats. Twenty-four hours after the LPS injection, histological examination showed that silibinin decreased inflammatory cell infiltration in the anterior segment of the eyes of LPS-treated rats. Analyses of the aqueous humor showed that silibinin decreased cell infiltration, protein concentration, nitric oxide (NO), and prostaglandin (PG)-E2 production. Western blot analysis indicated that silibinin decreased the expression of inducible NO synthase (iNOS), cyclooxygenase (COX-2), and phosphorylated IkB in the iris-ciliary body (ICB). Immunohistochemistry showed that silibinin decreased intercellular adhesion molecule (ICAM-1) expression in the ICB. In addition, western blot analysis showed that silibinin attenuated the expression of iNOS, COX-2, ICAM-1, and nuclear p65 in LPS-treated RAW cells. In conclusion, silibinin pretreatment prevents EIU and the subsequent production of proinflammatory mediators and ICAM-1, at least in part, by blocking the NF-κB-dependent signaling pathway both in vivo and in vitro. These effects may contribute to the silibinin-mediated preventive effects on intraocular inflammatory diseases such as acute uveitis.

Hyperbaric oxygen therapy ameliorates the blood-retinal barrier breakdown in diabetic retinopathy.

BACKGROUND: To study the effect of hyperbaric oxygen (HBO) therapy on diabetic retinopathy in a streptozotocin-induced diabetic rat model. METHODS: Sprague-Dawley albino male rats were divided into three groups. The three groups were as follow: (i) non-diabetic control group (non-DM control); (ii) diabetic control group (DM control); and (iii) diabetic rats receiving hyperbaric oxygen therapy (DM HBO). Rats in DM HBO group were incubated in an oxygen monoplace chamber. The HBO condition was set at 2.5 atmospheres and 100% oxygen. The duration of a single HBO treatment was 90 min. Rats in DM HBO groups received HBO three times per week for 3 months. Retinal vascular permeability was assessed by measuring fluorescein isothiocyanate-labelled bovine albumin and retinal Evans blue leakage into the retina. RESULTS: We found that the retinal parenchyma showed prominent thickening but not statistically significant in rats with DM, corresponding to the retinal oedema, compared with the control and DM HBO groups. fluorescein isothiocyanate relative fluorescence intensity (Mean+/-SE) in normal control animals, diabetic animals, and HBO-treated diabetic animals was 356+/-47, 865+/-78, and 518+/-49, respectively, demonstrating significant difference between the means of diabetic and HBO-treated diabetic animals, and between means of control and diabetic animals (n=8, P<0.05). Retinal Evans blue leakage in control animals, diabetic animals, and HBO-treated diabetic animals was 7.6+/-2.9, 18.5+/-4.2 and 10.2+/-3.1 microL plasma/g retinal dry weight/h, respectively, demonstrating significant difference between the means of diabetic and HBO-treated diabetic animals, and between means of control and diabetic animals (n=8, P<0.05). CONCLUSION: HBO therapy may diminish the extent of the increased blood-retinal barrier breakdown in diabetic animals.