Bimatoprost Monotherapy in CACG Patients with Extensive PAS

Bimatoprost Monotherapy in CACG Patients with Extensive PAS Intraocular Pressure-Lowering Efficacy of Bimatoprost in Chronic Angle-Closure Glaucoma Patients with Extensive Peripheral Anterior Synechiae: A Preliminary Study Introduction Glaucoma is the leading cause of irreversible blindness worldwide, affecting an estimated 64.3 million people aged 40–80 years, and this figure is expected to increase to 70 million in 2020.1 Open-angle glaucoma (OAG) is the more common form of glaucoma, but because angle-closure glaucoma (ACG) is more prevalent 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.3 ACG is defined by a partially occludable angle and elevated intra-ocular pressure (IOP) of more than 21 mmHg, with no or mild symptoms until very late in the disease and vision loss becomes evident. Detection by gonioscopy reveals very narrow angle with appositional contact between the iris and trabecular meshwork.4,5 This area of contact increases gradually and asymptomatically, with peripheral anterior synechiae (PAS) forming and spreading circumferentially, usually involving at least 180 degree-angle, which then increases IOP.3,6,7 The exact 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 Schwalbe’s 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 extent exceeds one clock hour on indentation gonioscopy. (Yoo et al. 2007) The level of IOP is directly related to the extent of the angle closure.4,7 The goal of treatment therefore is directed towards reopening of the angle and preventing and/or stopping nerve damage, and reduction of IOP.3 High IOP is a clinically important risk factor associated with progressive optic-disc changes and visual field loss.10 Aside from obstruction 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 barrier and corticosteroid-induced elevation. (Bodh SA, Kumar V, Raina UK, Ghosh B, Thakar M. Inflammatory glaucoma. Oman Journal of Ophthalmology. 2011;4(1):3-9. doi:10.4103/0974-620X.77655.) The Early Manifest Glaucoma Progression Trial, which evaluated the impact of reducing IOP in patients with OAG with normal or elevated IOP, showed the benefit of treatment (using laser trabeculoplasty plus topical betaxolol hydrochloride) on delaying the glaucoma progression in terms of visual field loss and optic disc changes by an average 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 progression and occurred significantly later in treated patients. (Heijl A, et al. 2002) Laser iridotomy is the standard initial approach to ACG.9,10 Treatment of acute ACG (AACG) can be satisfactorily treated with laser iridotomy alone, which is associated with good prognosis.8 However, chronic cases, after iridotomy with significant amount of PAS and suboptimal IOP control, require the use ÃŽ ²-adrenoreceptor antagonists (ÃŽ ²-blockers), topical carbonic anhydrase inhibitors, or selective ÃŽ ±2-adrenoreceptor agonists.10 A review of randomised controlled trials showed evidence that prostaglandin analogs and ÃŽ ²-blockers are recommended as monotherapy for the treatment of CACG when iridotomy has failed.9 Prostaglandin analogs have proven efficiency in lowering IOP in OAG with less side effects than ÃŽ ²-blockers.11 In addition, several trials have shown prostanoids to be more effective in reducing IOP than ÃŽ ²-blockers, topical carbonic anhydrase inhibitors, or selective ÃŽ ±2-adrenoreceptor agonists also patients with OAG.12However, recent studies have demonstrated 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 efficacy of anti-glaucoma drugs in patients with open-angle glaucoma, tension glaucoma or ocular hypertension showed bimatoprost to provide the greatest reduction in IOP.13 Bimatoprost 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 being blocked by PAS in CACG.14 This prospective, interventional case series was conducted to determine the efficacy of bimatoprost monotherapy in CACG patients with extensive PAS. References: 1. Tham YC, Li X, Wong TY, Quigley H a., Aung T, Cheng CY. Global Prevalence of Glaucoma and Projections of Glaucoma Burden through 2040. A Systematic Review and Meta-Analysis. Ophthalmology. 2014;121(11):2081-2090. doi:10.1016/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. 2006;90:262-267. doi:10.1136/bjo.2005.081224. 3. Rafael CastanÃÅ'Æ’eda-DiÃÅ' ez, Mariana MayorquiÃÅ' n-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. doi:10.5772/18123. 4. Yuji Kondo TY. Epidemiology of angle closure glaucoma. In: Chul Hong, Yamamoto T, eds. Angle Closure Glaucoma. Kugler Publications; 2007:278. 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; 2011:877. https://books.google.com/books?id=5jynsUAXg-ECpgis=1. Accessed February 22, 2015. 6. Mittal S. Classification of glaucomas. In: Garg A, ed. Mastering the Tech. of Glaucoma Diag. Management. Jaypee Brothers Publishers; 2006:556. 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. 2006;20(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; 2009:668. https://books.google.com/books?id=-1wtvjCY6dcCpgis=1. 9. Saw SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma CRD summary Authors ’ objectives. Database Abstr Rev Eff Qual Rev. 2003:2-5. 10. See JLS, Aquino MCD, Aduan J, Chew PTK. Management of angle closure glaucoma. Indian J Ophthalmol. 2011;59 Suppl:S82-S87. doi:10.4103/0301-4738.73690. 11. Yu A W-LU. [Mechanisms , clinical profile and role of prostaglandin and prostamide analogues in antiglaucomatous therapy ] Article in German. Kin Monbl Augenheilkd. 2013;230(2):127-132. doi:10.1055/s-0032-1327946. 12. Ishida N, Odani-Kawabata N, Shimazaki A, Hara H. Prostanoids in the therapy of glaucoma. Cardiovasc Drug Rev. 2006;24(1):1-10. doi:10.1111/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 commonly used glaucoma drugs: a meta-analysis of randomized clinical trials. Database Abstr Rev Eff Qual Rev. 2005. doi:10.1016/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 Off J Assoc Ocul Pharmacol Ther. 2007;23(4):351-358. doi:10.1089/jop.2006.0107.