Background Ahmed Glaucoma Valve implantation （AGVI） is blood-aqueous barrier （BAB） has been noted after some surgica BAB disruption afterAGVl. used to treat refractory glaucoma. Breakdown of the techniques. The current study was designed to assess Methods Anterior chamber protein content was measured by the laser flare cell photometry in 22 eyes of 22 patients with refractory glaucoma before AGVI and at each postoperative visit up to 1 month. Results Before AGVI the mean aqueous flare values in all eyes were （15.17＋9.84） photon counts/ms. After AGVI, the values significantly increased at day 1, day 3, and week I compared to those before AGVI （all P 〈0.05） with a peak at day 3. They returned to pre-operative levels at week 2, and were lower than preoperative level at month 1. Eyes with previous intraocular surgery history had greater aqueous flare values than those without previous intraocular surgery history, but there were no significant differences at all time points postoperatively （all P 〉0.05）. Furthermore, eyes with shallow anterior chambers had greater aqueous flare values at day 3 and week 1 （all P 〈0.05）. When comparing eyes with other refractory glaucoma conditions, neovascular glaucoma combined with intravitreal bevacizumab injection resulted in lower aqueous flare values after AGVI, but no significant differences were observed at all time points, postoperatively （all P 〉0.05）. Conclusions The BAB was impaired and inflammation was present in the anterior chamber in refractory glaucomatous eyes following AGVI. However, such conditions were resolved within 1 month postoperatively. Intravitreal bevacizumab treatment in neovascular glaucoma eyes before AGVI may prevent BAB breakdown.
Objective To review the updated research on neuroprotection in glaucoma, and summarize the potential agents investigated so far. Data sources The data in this review were collected from PubMed and Google Scholar databases published in English up to September 2012, with keywords including glaucoma, neuroprotection, and retinal ganglion cells, both alone and in combination. Publications from the past ten years were selected, but important older articles were not excluded. Study selection Articles about neuroprotection in glaucoma were selected and reviewed, and those that are cited in articles identified by this search strategy and judged relevant to this review were also included. Results Although lowering the intraocular pressure is the only therapy approved as being effective in the treatment of glaucoma, increasing numbers of studies have discovered various mechanisms of retinal ganglion cells death in the glaucoma and relevant neuroprotective strategies. These strategies target neurotrophic factor deprivation, excitotoxic damage, oxidative stress, mitochondrial dysfunction, inflammation, activation of intrinsic and extrinsic apoptotic signals, ischemia, and protein misfolding. Exploring the mechanism of axonal transport failure, synaptic dysfunction, the glial system in glaucoma, and stem cell used in glaucoma constitute promising research areas of the future. Conclusions Neuroprotective strategies continue to be refined, and future deep investment in researching the pathogenesis of glaucoma may provide novel and practical neuroprotection tactics. Establishing a system to assess the effects of neuroprotection treatments may further facilitate this research.
Glaucoma is one of the leading causes of visual impairment and blindness worldwide. Of known risk factors for glaucoma, an increased in intraocular pressure is most highly correlated with glaucomatous damage. Irrespective of the cause, apoptosis of the retinal ganglion cells is the eventual outcome. It is widely accepted that glaucoma is a neurodegenerative disease that is strongly correlated with central nervous system disorders, such as Alzheimer's disease. These two disorders also share some similarities in pathogenic mechanisms. Recent studies suggest that the transient receptor potential canonical 6 channel could work together with brain-derived neurotrophic factor to promote neuron survival in brain and retina. In this study, we propose that transient receptor potential canonical 6 may contribute to the pathogenesis of human glaucoma and become a potential therapeutic target.
Glaucoma is one of the leading causes of visual impairment and blindness. Improved knowledge of the pathogenesis of this disease has allowed the exploration of new therapeutic methods. In general, elevated intraocular pressure (IOP), oxidative stress, and vascular insufficiency are accepted as the major risk factors for the progression of glaucoma. Many natural compounds have been found beneficial for glaucoma. Nutritional therapies are now emerging as potentially effective in glaucomatous therapy. One nutritional supplement with potential therapeutic value is cod liver oil, a dietary supplement that contains vitamin A and omega-3 polyunsaturated fatty acids (PUFAs). Vitamin A is important for preserving normal vision and it is a well-known antioxidant that prevents the oxidative damage that contributes to the etiology and progression of glaucoma. Vitamin A is also a crucial factor for maintaining the integrity of conjunctival and corneal ocular surfaces, and preventing the impairment of ocular epithelium caused by topical antiglaucomatous drugs. Omega-3 fatty acids are beneficial for glaucoma patients as they decrease IOP, increase ocular blood flow, and improve optic neuroprotective function. In this article, we propose that cod liver oil, as a combination of vitamin A and omega-3 fatty acids, should be beneficial for the treatment of glaucoma. However, further studies are needed to explore the relationship between cod liver oil and glaucoma.
