Bimatoprost Monotherapy in CACG Patients with Extensive PAS

Bimatoprost Monotherapy in CACG Patients with great PASIntraocular Pressure-Lowering Efficacy of Bimatoprost in Chronic Angle- layover Glaucoma Patients with Extensive Peripheral Anterior Synechiae A Preliminary StudyIntroductionGlaucoma is the ahead(p) take a leak of irreversible blindness worldwide, affecting an estimated 64.3 gazillion people sr. 4080 years, and this figure is expected to enlarge to 70 million in 2020.1 Open-angle glaucoma (OAG) is the more common form of glaucoma, but because angle- law of liquidation glaucoma (ACG) is more predominate in Asia, the continent that accounts for 60% of the world population, ACG causes a disproportionate burden of morbidity.1,2 ACG is also more critical due to its greater likelihood to cause blindness than OAG.3ACG is defined by a partially occludable angle and imposing intra-ocular pressure (IOP) of more than 21 mmHg, with no or mild symptoms until truly late in the disease and vision loss becomes evident. Detection by go nioscopy reveals very narrow angle with appositional contact between the flagstone and trabecular meshwork.4,5 This area of contact increases gradually and asymptomatically, with peripheral anterior synechiae (PAS) forming and dissemination circumferentially, usually involving at least 180 degree-angle, which then increases IOP.3,6,7The exact chemical mechanism of PAS formation is not clearly understood, but it is known that the formation of PAS starts as the peripheral part of the iris adheres to the Schwalbes line and extends towards the angle recess. PAS is considered to be present when the adhesion of the iris reaches the mid-trabecular meshwork and its consequence exceeds one measure hour on indentation gonioscopy. (Yoo et al. 2007) The level of IOP is directly related to the extent of the angle closure.4,7The goal of discussion therefore is directed towards reopening of the angle and preventing and/or stopping nerve damage, and reduction of IOP.3 High IOP is a clinicall y important risk factor associated with progressive optic-disc changes and visual field loss.10 Aside from obstructor of the trabecular meshwork, Bodh et al. reported that the elevation of IOP may be caused by prostaglandin E1 and prostaglandin E2-mediated increase in secretion or the breakdown of blood aqueous bar and corticosteroid-induced elevation. (Bodh SA, Kumar V, Raina UK, Ghosh B, Thakar M. Inflammatory glaucoma. Oman Journal of Ophthalmology. 20114(1)3-9. inside10.4103/0974-620X.77655.)The Early Manifest Glaucoma Progression Trial, which evaluated the tint of reducing IOP in patients with OAG with normal or elevated IOP, showed the benefit of treatment (using laser trabeculoplasty plus local betaxolol hydrochloride) on delaying the glaucoma progression in monetary value of visual field loss and optic disc changes by an mean(a) of 18 months longer than patients who did not receive treatment. An average reduction of IOP by about 5.1 mmHg resulted in less frequent prog ression and occurred significantly afterward in treated patients. (Heijl A, et al. 2002)Laser iridotomy is the standard initial approach to ACG.9,10 interference of acute ACG (AACG) can be satisfactorily treated with laser iridotomy alone, which is associated with right prognosis.8 However, chronic cases, after iridotomy with significant amount of PAS and suboptimal IOP control, require the use -adrenoreceptor antagonists (-blockers), topical carbonic anhydrase inhibitors, or selective 2-adrenoreceptor agonists.10 A review of randomised controlled trials showed prove that prostaglandin analogs and -blockers are recommended as monotherapy for the treatment of CACG when iridotomy has failed.9Prostaglandin analogs have proven efficiency in lowering IOP in OAG with less side effects than -blockers.11 In addition, some(prenominal) trials have shown prostanoids to be more effective in reducing IOP than -blockers, topical carbonic anhydrase inhibitors, or selective 2-adrenoreceptor ag onists also patients with OAG.12However, recent studies have present that prostaglandin analogs such as latanoprost, bimatoprost and travopost to be effective in lowering IOP in chronic ACG (CACG), even in the presence of 360-degree PAS.10A meta-analysis on the cleverness of anti-glaucoma drugs in patients with open-angle glaucoma, tension glaucoma or ocular hypertension showed bimatoprost to provide the greatest reduction in IOP.13Bimatoprost monotherapy has been demonstrated to decrease IOP in CACG patients with at least 9 clock hours of PAS on gonioscopy. However, the IOP-lowering efficacy of bimatoprost in eyes with extensive PAS is not fully understood. It has been suggested that that bimatoprost increases the aqueous outflow through the uveoscleral or the trabecular pathways world blocked by PAS in CACG.14This prospective, interventional case series was conducted to determine the efficacy of bimatoprost monotherapy in CACG patients with extensive PAS.References1. Tham YC, L i X, Wong TY, Quigley H a., Aung T, Cheng CY. Global Prevalence of Glaucoma and Projections of Glaucoma nucleus through 2040. A Systematic Review and Meta-Analysis. Ophthalmology. 2014121(11)2081-2090. doi10.1016/j.ophtha.2014.05.013.2. Quigley H a, Broman a T. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 200690262-267. doi10.1136/bjo.2005.081224.3. Rafael Castaneda-Diez, Mariana Mayorquin-Ruiz CE-L and OA-D. Current Diagnosis and Management of Angle-closure glaucoma. In Dr. Pinakin Gunvant, ed. Glaucoma Current clinical and Research Aspects. InTech 2011. doi10.5772/18123.4. Yuji Kondo TY. Epidemiology of angle closure glaucoma. In Chul Hong, Yamamoto T, eds. Angle Closure Glaucoma. Kugler Publications 2007278. https//books.google.com/books?id=PV6ehhSdis0Cpgis=1. Accessed February 22, 2015.5. Harmohina Bagga G Chandra Sekhar. Chapter 9. Primary Angle-Closure Glaucoma. In Saxena S, ed. Clinical Ophthalmology Medical and Surgical Approach. Jaypee Brothers Publishers 2011877. https//books.google.com/books?id=5jynsUAXg-ECpgis=1. Accessed February 22, 2015.6. Mittal S. categorization of glaucomas. In Garg A, ed. Mastering the Tech. of Glaucoma Diag. Management. Jaypee Brothers Publishers 2006556. https//books.google.com/books?id=CA6kwpx9A9YCpgis=1.7. Lee JY, Kim YY, Jung HR. Distribution and characteristics of peripheral anterior synechiae in primary angle-closure glaucoma. Korean J Ophthalmol. 200620(2)104-108. http//www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2908823tool=pmcentrezrendertype=abstract. Accessed February 22, 2015.8. Salmon J. Chapter 13 Gonioscopy. Section 3 Diagnosis of Glaucoma. In Sharaway T, ed. Glaucoma Medical Diagnosis and Therapy. Elsevier Health Sciences 2009668. https//books.google.com/books?id=-1wtvjCY6dcCpgis=1.9. Saw SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma CRD drumhead Authors objectives. Database Abstr Rev Eff Qual Rev. 20032-5.10. See JLS, Aquino MCD, Aduan J, Chew PTK. Management of angle closure glaucoma. Indian J Ophthalmol. 201159 SupplS82-S87. doi10.4103/0301-4738.73690.11. Yu A W-LU. Mechanisms , clinical visibleness and role of prostaglandin and prostamide analogues in antiglaucomatous therapy Article in German. Kin Monbl Augenheilkd. 2013230(2)127-132. doi10.1055/s-0032-1327946.12. Ishida N, Odani-Kawabata N, Shimazaki A, Hara H. Prostanoids in the therapy of glaucoma. Cardiovasc Drug Rev. 200624(1)1-10. doi10.1111/j.1527-3466.2006.00001.x.13. Valk R Van Der, Webers CA, Schouten JS, Zeegers MP, Hendrikse F, Prins MH. Intraocular pressure-lowering effects of all ordinarily used glaucoma drugs a meta-analysis of randomized clinical trials. Database Abstr Rev Eff Qual Rev. 2005. doi10.1016/j.ophtha.2005.01.042.14. Gupta V, Srinivasan G, Sharma A, Kapoor KS, Sihota R. Comparative evaluation of bimatoprost monotherapy in primary chronic angle closure and primary open angle glaucoma eyes a three-year study. J Ocul Pharmacol Ther forward J Assoc Ocul Pharmacol Ther. 200723(4)351-358. doi10.1089/jop.2006.0107.