Efficacy and safety of trabeculectomy with mitomycin C for childhood glaucoma: a study of results with long-term follow-up

OBJECTIVE: To evaluate the safety and effectiveness of trabeculectomy with mitomycin C in the management of childhood glaucoma. INTRODUCTION: The use of antifibrotic agents enhances the success of trabeculectomy performed in both adults and children. METHODS: A retrospective chart review (1991-2001) of 114 patients (114 eyes) from 0-14 years of age with congenital or developmental glaucoma. These patients underwent trabeculectomy with mitomycin but had not been previously treated with any antifibrotic agent. RESULTS: The mean patient age was 57.36 51.14 months (range: 0.5-168 months). Treatment was considered successful in 63 eyes (55.26%), with a mean intraocular pressure of 12.11 3.98 mmHg. For patients categorized as successfully treated, the mean follow-up time was 61.16 26.13 months (range 12-113 months). A post-surgical intraocular pressure of < 16 was observed in 47 eyes. The life-table success rates for intraocular pressure control at 24, 36, 48, and 60 months were 90.2%, 78.7%, 60.7% and 50.8%, respectively. The cumulative probability of failure was 40.8% at 12 months. Following surgery, endophthalmitis appeared in eight eyes (4.88%) after an average 36.96 months (range: 1.7-106 months). Other complications included expulsive hemorrhage, flat anterior chamber and bleb leak. DISCUSSION: It has been reported in pediatric patients that trabeculectomy without adjunctive antimetabolites achieves a successful outcome in 30% to 50% of cases. In our study, treatment was considered successful in 63 eyes (55.26%) within 61.16 26.13 months of follow-up. CONCLUSIONS: Trabeculectomy with mitomycin is safe and effective for short-term or long-term treatment of congenital or developmental glaucoma. The frequency of bleb-related endophthalmitis was no higher in these patients than that described in adults

The vast complexity of primary open angle glaucoma:Disease genes, risks, molecular mechanisms and pathobiology

<p>Primary open angle glaucoma (POAG) is a complex progressive optic nerve neuropathy triggered by both environmental and genetic risk factors. Several ocular tissues, including the ciliary body, trabecular meshwork and optic nerve head, and perhaps even brain tissues, are involved in a chain of pathological events leading to POAG.</p><p>Genetic risk evidence for POAG came from family linkage-studies implicating a small number of disease genes (MYOC, OPEN, WDR36). Recent Genome Wide Association Studies (GWAS) identified a large number of new POAG loci and disease genes, such as CAV1, CDKN2B and GAS7. In the current study, we reviewed over 120 family and GWA studies. We selected in total 65 (candidate) POAG disease genes and proceeded to assess their function, mRNA expression in POAG relevant eye tissues and possible changes in disease state. We found that the proteins corresponding to these 65 (candidate) POAG disease genes take part in as few as four common functional molecular networks. Functions attributed to these 4 networks were developmental (dys)function, lipid metabolism, and inflammatory processes. For the 65 POAG disease genes, we reviewed the available (transgenic) mouse models of POAG, which may be useful for future functional studies. Finally, we showed that the 65 (candidate) POAG genes substantially increased the specificity and sensitivity of a discriminative POAG risk test. This suggests that personal risk assessment and personalized medicine for POAG are on the horizon. Taken together, the data presented are essential to comprehend the role of genetic variation in POAG, and may provide leads to understand the pathophysiology of POAG as well as other neurodegenerative disorders, such as Alzheimer's disease. (C) 2013 Elsevier Ltd. All rights reserved.</p>