Frequency and Risk Factors for Neovascular Glaucoma After Vitrectomy in Eyes with Diabetic Retinopathy: An Observational Study.

INTRODUCTION: Vitrectomy is one of the main treatments for proliferative diabetic retinopathy (PDR). Postoperative neovascular glaucoma, in which it is difficult to obtain satisfactory results using conventional filtering surgery, is one of the most serious complications of vitrectomy. It often requires destructive surgery, such as ciliary body photocoagulation or freezing, and the outcome with regard to visual acuity (VA) is extremely poor. The purpose of this study was to evaluate the prevalence of neovascular glaucoma (NVG) after modern vitrectomy techniques and investigate how variables assessed before and after vitrectomy are associated with patients who develop NVG after PDR surgery. METHODS: This was an observational study including the medical records of patients who underwent vitrectomy for PDR at Tianjin Eye Hospital from June 2014 to July 2016, were followed for at least 24 months postoperatively, and NVG developed within 2 years after surgery was recorded. Each patient underwent complete preoperative ophthalmic examinations in both preoperative and follow-up appointments. Factors associated with survival were determined using the Kaplan-Meier (KM) survival analysis to calculate the incidence of NVG after vitrectomy for PDR. Multivariable analysis was performed with the Cox regression proportional hazards model to verify the results of the analysis and eliminate interference factors between variables. All statistical analyses were performed using R statistical software ( http://www.r-project.org ) for Windows. RESULTS: In all, 238 patients (238 eyes) fulfilled the study criteria. NVG occurred in 11 of 238 eyes (4.6%). The percentages of NVG development after vitrectomy at 6, 12, and 24 months were 0.42%, 3.3%, and 4.6%, respectively. After step analysis, multivariable regression identified preoperative high intraocular pressure (IOP) combined with retinal vein occlusion (RVO), severe PDR, no postoperative intravitreal injection of ranibizumab (IVR), and higher HbA1c levels as significant predictors of NVG. CONCLUSION: Preoperative high IOP combined with RVO, severe PDR, no postoperative intravitreal injection of ranibizumab (IVR), and higher HbA1c levels are significant predictors of NVG after vitrectomy.

Intravitreal ranibizumab injection at the end of vitrectomy for diabetic vitreous hemorrhage (Observational Study).

To evaluate the outcomes and complications of intravitreal injections of ranibizumab in patients during pars plana vitrectomy for treatment of diabetic vitreous hemorrhage. This retrospective, observational, comparative study included 103 patients (103 eyes) who underwent pars plana vitrectomy for treatment of diabetic vitreous hemorrhage. Sixty-six patients received an intravitreal injection of 0.05 mg (0.05 cc) of ranibizumab at the end of surgery. Main outcome measures were the occurrence of recurrent early vitreous hemorrhage, reoperation, intraocular pressure, best corrected visual acuity. Mean follow-up time was 6 months. The rate of rebleeding in the intravitreal ranibizumab (IVR) group was 6.1% (4 eyes), which is significantly lower than the control group (24.3%, 9 eyes, P < .01). The incidence of postoperative diabetic vitreous hemorrhage (PDVH) was significantly lower in the IVR group than the control group, OR=0.26, 95% CI= (0.06, 0.95). Visual acuity 6 months after operation was better in IVR group (P<.01) There was no difference in mean intraocular pressure between the 2 groups (P=.56). The present clinical study suggests that intravitreal injection of ranibizumab is effective in the prevention of postoperative diabetic vitreous hemorrhage in eyes undergoing pars plana vitrectomy for the treatment of diabetic vitreous hemorrhage.

Sanguinarine induces apoptosis of human lens epithelial cells by increasing reactive oxygen species via the MAPK signaling pathway.

Posterior capsular opacification (PCO) remains a major complication of cataract surgery and is the most common reason for loss of vision. PCO is primarily associated with uncontrolled proliferation of residual human lens epithelial cells (HLEs). Sanguinarine is a type of benzophenanthridine alkaloid extracted from the herbaceous plant Sanguinaria canadensis, which is widely used for its anti­microbial, anti­inflammatory, anti­oxidative and anti­proliferative properties. However, studies examining the effect of sanguinarine on HLEs and the underlying mechanism are scarce. The present study aimed to investigate the effects of sanguinarine on HLEs. An MTT assay was used to determine the effect of sanguinarine on cell viability. Flow cytometry was used to evaluate cell apoptosis, and the mitochondrial membrane potential and reactive oxygen species (ROS) levels. A caspase 3/7 activity assay was also used to evaluate cell apoptosis, while western blotting was performed to determine protein levels. The results demonstrated that sanguinarine exerted an anti­proliferative effect by inducing ROS, and caused cell apoptosis via mitochondrial and caspase­dependent pathways. Treatment with sanguinarine led to the loss of mitochondrial membrane potential. Sanguinarine also significantly increased the phosphorylation levels of c­Jun N­terminal kinase and p38, which indicated the involvement of the mitogen­activated protein kinase signaling pathway. These results suggested that sanguinarine may have a noteworthy pro­apoptotic effect on HLEs, and may be used as a potential drug for PCO or even cataract prevention.

Shikonin inhibits the proliferation of human lens epithelial cells by inducing apoptosis through ROS and caspase-dependent pathway.

Shikonin is a compound from the herbal plant Lithospermum erythrorhizon that has been proved to possess powerful anti-proliferative effect on many kinds of cancers and to be safe in in vivo study. Posterior capsular opacification (PCO), the most frequent complication of cataract surgery, is mainly caused by the uncontrolled proliferation of retained human lens epithelial cells (HLEs). In this study, we investigated the effect of shikonin on the proliferation of HLEs and explored its underlying mechanism of action. Shikonin significantly inhibited the proliferation of HLEs in a dose- and time-dependent manner. Its anti-proliferative effect was exerted through induction of apoptosis. Reactive oxygen species (ROS) generation played an essential role in this apoptotic process. Interestingly, scavenging of ROS completely blocked the apoptosis induced by shikonin. In addition, the treatment of shikonin in HLEs significantly increased the ratio of Bax/Bcl-2, disrupted mitochondria membrane potential (MMP) and activated caspases. The inhibition of caspase largely blocks the apoptosis. The changes of MAPK pathway were also demonstrated. Shikonin effectively inhibited the phosphorylation of ERK, while it activated the phosphorylation of JNK and p38. These results suggested that shikonin inhibited the proliferation of HLEs by inducing apoptosis through ROS generation and the caspase-dependent pathway and the MAPK pathway was also involved.

Clinical analysis of tear film after lamellar keratoplasty.

AIM: To study the tear film stability after lamellar keratoplasty. METHODS: Five female and eight male patients with lamellar keratoconus, aged from 18 to 32, were involved. After lamellar keratoplasty, Schirmer I test(S I t), tear break-up time(BUT) test, fluorescein staining test were used to judge the effect of the surgery at different time point. RESULTS: The S I t were greatly increased in 7 days post operation (11.86±2.28 -25.14±1.97, 19.86±1.61) (P<0.05), there is no significant difference between 2(nd) month, 3(rd) month post-operative and pre-operation (11.86±2.28 - 14.57±1.48, 8.14±0.86) (P>0.05). The mean break-up time decreased in 7 days post operation (5.00±1.31 - 2.71±0.18, 2.57±0.20, 2.71±0.36, 2.43±0.20) (P<0.05). The mean scores of fluorescence increased post-operatively (0.14±0.14 - 8.00±0.00, 8.00±0.00, 8.00±0.00, 7.57±0.20) (P<0.01). CONCLUSION: Lamellar keratoplaty influence the tear film stability, artificial tears and improving corneal epithelium cured medicine should be used after surgery.

SiRNA targeting EGFR effectively prevents posterior capsular opacification after cataract surgery.

PURPOSE: We investigated the effect of epidermal growth factor receptor (EGFR) siRNA on human lens epithelium (HLE) cells and the development of posterior capsular opacity (PCO). METHODS: We designed EGFR siRNA and used it to knockdown the expression of EGFR in HLE cells. Cell proliferation was examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell growth curve assay and cell cycle analysis. Next, we selected an adaptable concentration of recombinant epidermal growth factor (EGF) for stimulating the growth of HLE cells to further test the suppressive effect of siRNA. At last, we established the model of PCO in rats to further investigate whether knocking down EGFR would prevent the progression of PCO in vivo. RESULTS: The cell proliferation of EGFR siRNA group was apparently inhibited no matter in short or long term and cell cycle was arrested in G(1) phase. Over expression EGF cannot rescue the inhibition of EGFR siRNA on HLE cells and the proliferation activity in HLE cells greatly decreased when EGF-EGFR signal pathway blockaded. In vivo experiments, the extent of PCO of EGFR siRNA group is much lower than the control group. CONCLUSIONS: Our results demonstrate that EGFR siRNA can effectively inhibit the progression of PCO. Thus, siRNA targeting EGFR may provide a totally new way for preventing PCO or even cataract.