Subconjunctival trastuzumab injection effectively suppressed subconjunctival scarring after experimental glaucoma filtration surgery.

Damage to retinal ganglion cells due to elevation of intraocular pressure (IOP) is responsible for vision loss in glaucoma. Given that loss of these cells is irreversible, neuroprotection is crucial in the treatment of glaucoma. In this study, we investigated the possible antioxidant and neuroprotective effects of ghrelin on the retina in an experimental glaucoma model. Twenty-one Sprague–Dawley rats were randomly assigned to three groups comprising seven rats each. The rats in the control group were not operated on and did not receive any treatment. In all rats in the other groups, IOP was increased by cauterization of the limbal veins. After creation of the IOP increase, saline 1 mL/kg or ghrelin 40 μg/kg was administered intraperitoneally every day for 14 days in the vehicle control group and ghrelin groups, respectively. On day 14 of the study, the eyes were enucleated. Levels of malondialdehyde (MDA), nitric oxide (NO), and nitric oxide synthase-2 (NOS2) in anterior chamber fluid were measured. The retinas were subjected to immunohistochemistry staining for glial fibrillary acidic protein (GFAP), S-100, and vimentin expression. Mean levels of MDA, NO, and NOS2 in the aqueous humor were higher in the vehicle control group than in the control group (P<0.05). Mean levels of MDA, NO, and NOS2 in the ghrelin group did not show a significant increase compared with levels in the control group (P>0.05). Retinal TUNEL and immunohistochemistry staining in the vehicle control group showed an increase in apoptosis and expression of GFAP, S-100, and vimentin compared with the control group (P<0.05). In the ghrelin group, apoptosis and expression of GFAP, S-100, and vimentin was significantly lower than in the vehicle control group (P<0.05). This study suggests that ghrelin has antioxidant and neuroprotective effects on the retina in an experimental glaucoma model.

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Purpose To evaluate the concentration of serum cystatin C (CysC) in patients with Graves’ ophthalmopathy (GO) and the usability of the serum CysC concentrations in the follow-up of the disease. Methods Thirty patients with GO and 30 healthy age-matched volunteers were included in this cross-sectional study. GO was diagnosed based on the European Group on Graves’ Orbitopathy consensus. Serum thyroid-stimulating hormone, free triiodothyronine, free thyroxine, and CysC concentrations were measured in the participants. The serum CysC concentrations were compared between patients with GO and controls. Patients with GO were subdivided into hyperthyroid and euthyroid patients, and their serum CysC concentrations were compared. In addition, the CysC concentrations in hyperthyroid and euthyroid patients with GO were compared separately with those of healthy subjects. Kruskal-Wallis test and Student’s t -test were used for statistical evaluation. Results The mean serum CysC concentrations in GO patients and controls were 1.04 ± 0.36 and 0.74 ± 0.09 mg/L, respectively. There was a statistically significant difference in the serum CysC concentrations between patients with GO and control subjects ( p < 0.001). Fifteen patients had hyperthyroid status, and 15 patients had euthyroid status. The mean serum CysC concentrations in hyperthyroid and euthyroid patients with GO were 1.35 ± 0.22 and 0.72 ± 0.13 mg/L, respectively. Serum CysC concentrations were significantly higher in hyperthyroid patients than in euthyroid patients ( p = 0.001). In addition, hyperthyroid patients had significantly higher serum CysC concentrations than healthy subjects. Among patients with GO, 21 and nine had mild and moderate-to-severe GO, respectively. Active and inactive GO were observed in eight and 22 patients, respectively. Conclusions The serum CysC concentrations in hyperthyroid patients were higher than those in healthy subjects. Moreover, hyperthyroid patients had higher serum CysC concentrations than euthyroid patients. Further studies with a larger sample size are needed to confirm these results.

Aim: To evaluate the changes in central macular thickness after penetrating keratoplasty. Material and Methods: A total of 24 eyes of 24 patients who had undergone penetrating keratoplasty were included in the study. This study was performed retrospectively by reviewing the charts of the patients. Postoperative 1st week, 1st month, 3rd month, 6th month and 12th month mean total macular volume, central macular thickness, parafoveal area and perifoveal area thickness and retinal nevre fiber layer (RNFL) thickness results obtained with optic coherence tomography were compared. ANOVA test was used for statistical analysis. Results: The postoperative 1st week, 1st month, 3rd month, 6th month and 12th month mean total macular volume measurements were 7.03±0.2 mm³, 7.05±0.4 mm³, 7.0±0.6 mm³, 7.02±0.5 mm³ and 6.12±0.6 mm³, respectively. Mean central macular thickness measurements were 227.6±4.6 μm, 228.7±5.5 μm, 227.2±4.6 μm, 227.5±7.1 μm, 226.3±5.1μm respectively; mean parafoveal area thickness measurements were 290.2±3.7 μm, 289.9±7.8 μm, 288.7±6.3 μm, 288.8±4.7 μm, 288.6±8.3 μm respectively, mean perifoveal area thickness measurements were 261.1±4.2 μm, 261.4±1.9 μm, 260.4±3.6 μm, 259.8±2.7 μm, 259.3±4.7 μm respectively, and mean RNFL thickness measurements were 106.54±11.28 μm, 107.28±8.75 μm, 107.45±13.64 μm, 105.62±9.27 μm, 105.16±12.74 μm; respectively. Conclusion: No significant change was seen in macular thickness after penetrating keratoplasty. Although the macular thickness increases in the early postoperative stage, it decreases in time.

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