IMPORTANCE Infantile cataract surgery bears a significant risk for postoperative glaucoma, and no consensus exists on factors that may reduce this risk.OBJECTIVE To assess the effect of primary intraocular lens implantation and timing of surgery on the incidence of postoperative glaucoma.DATA SOURCES We searched multiple databases to July 14, 2013, to identify studies with eligible patients, including PubMed, MEDLINE, EMBASE, ISI Web of Science, Scopus, Central, Google Scholar, Intute, and Tripdata. We also searched abstracts of ophthalmology society meetings.STUDY SELECTION We included studies reporting on postoperative glaucoma in infants undergoing cataract surgery with regular follow-up for at least 1 year. Infants with concurrent ocular anomalies were excluded. DATA EXTRACTION AND SYNTHESISAuthors of eligible studies were invited to contribute individual patient data on infants who met the inclusion criteria. We also performed an aggregate data meta-analysis of published studies that did not contribute to the individual patient data. Data were pooled using a random-effects model. MAIN OUTCOMES AND MEASURESTime to glaucoma with the effect of primary implantation, additional postoperative intraocular procedures, and age at surgery. RESULTSSeven centers contributed individual patient data on 470 infants with a median age at surgery of 3.0 months and median follow-up of 6.0 years. Eighty patients (17.0%) developed glaucoma at a median follow-up of 4.3 years. Only 2 of these patients had a pseudophakic eye. The risk for postoperative glaucoma appeared to be lower after primary implantation (hazard ratio [HR], 0.10 [95% CI, 0.01-0.70]; P = .02; I 2 = 34%), higher after surgery at 4 weeks or younger (HR, 2.10 [95% CI, 1.14-3.84]; P = .02; I 2 = 0%), and higher after additional procedures (HR, 2.52 [95% CI, 1.11-5.72]; P = .03; I 2 = 32%). In multivariable analysis, additional procedures independently increased the risk for glaucoma (HR, 2.25 [95% CI,; P = .01), and primary implantation independently reduced it (HR, 0.10 [95% CI, 0.01-0.76]; P = .03). Results were similar in the aggregate data meta-analysis that included data from 10 published articles. CONCLUSIONS AND RELEVANCEAlthough confounding factors such as size of the eye and surgeon experience are not accounted for in this meta-analysis, the risk for postoperative glaucoma after infantile cataract surgery appears to be influenced by the timing of surgery, primary implantation, and additional intraocular surgery.

Purpose To investigate the role of vitrectomy without prone posturing in the anatomic and functional outcome of macular hole surgery (MHS). Methods Forty-one consecutive eyes of 41 patients with stage II-IV full-thickness macular holes underwent pars plana vitrectomy and 16% C3F8 tamponade. In 25 cases posturing group (P), subjects were instructed to assume prone positioning for 10 days postoperatively, whereas in 16 cases nonposturing group (NP) patients were advised to avoid lying supine but no other posturing instructions were given. Preoperative, intraoperative and postoperative clinical data were collected, with macular hole closure rate and change in LogMAR visual acuity, contrast sensitivity, metamorphopsia, and 25-Visual Function Questionnaire (VFQ-25) being the primary outcome measures. Results Over a mean follow-up of 4.271.2 months, anatomical hole closure was noted in 22/25 (88%) and 14/16 (87.5%) in groups P and NP respectively. Visual acuity improved by a mean of eight letters and there was no significant difference in the two groups (P ¼ 0.724). Similarly, postoperative prone posturing did not have an effect on the final contrast sensitivity, metamorphopsia, and VFQ-25 composite scores (P ¼ 0.238, P ¼ 0.472, and P ¼ 0.87, respectively). However, eyes in group NP developed significantly more severe cataract in the early postoperative period (P ¼ 0.02). Conclusions Prone posturing following MHS provides no functional or anatomic benefit but it is associated with slower progression of cataract. Combined phacovitrectomy without face down positioning may be considered for all phakic patients undergoing MHS.

Diabetic retinopathy is considered one of the vision-threatening diseases among working-age population. The pathogenesis of the disease is regarded multifactorial and complex: capillary basement membrane thickening, loss of pericytes, microaneuryms, loss of endothelial cells, blood retinal barrier breakdown and other anatomic lesions might contribute to macular edema and/or neovascularization the two major and sight threatening complications of diabetic retinopathy. A number of proangiogenic, angiogenic and antiangiogenic factors are involved in the pathogenesis and progression of diabetic retinal disease, Vascular Endothelial Growth Factor (VEGF) being one of the most important. Other growth factors, which are known to participate in the pathogenesis of the disease, are: Platelet Derived Growth Factor (PDGF), Fibroblast Growth Factor (FGF), Hepatocyte Growth Factor (HGF), Transforming Growth Factor (TGF), Placental Endothelial Cell Growth Factor (PlGF), Connective Tissue Growth Factor (CTGF). Other molecules that are involved in the disease mechanisms are: intergrins, angiopoietins, protein kinase C (PKC), ephrins, interleukins, leptin, angiotensin, monocyte chemotactic protein (MCP), vascular cell adhesion molecule (VCAM), tissue plasminogen activator (TPA), and extracellular matrix metalloproteinases (ECM-MMPs). However, the intraocular concentration of angiogenic factors is counterbalanced by the ocular synthesis of several antioangiogenic factors such as pigment epithelial derived factor (PEDF), angiostatin, endostatin, thrombospondin, steroids, atrial natriuretic peptide (ANP), inteferon, aptamer, monoclonal antibodies, VEGF receptor blocker, VEGF gene suppressors, intracellular signal transduction inhibitors, and extracellular matrix antagonists. Growth stimulation or inhibition by these factors depends on the state of development and differentiation of the target tissue. The mechanisms of angiogenesis factor action are very different and most factors are multipotential; they stimulate proliferation or differentiation of endothelial cells. This review attempts to briefly outline the knowledge about peptide growth factor involvement in diabetic retinopathy. Further ongoing research may provide better understanding of molecular mechanisms, disease pathogenesis and therapeutic interactions.

No abstract

ACCS was significantly greater after hydrophilic IOL implantation when compared with hydrophobic lenses, while there was no statistical significant difference between the two hydrophilic IOL models.