submit to the journals

Recent Advances in the Treatment of Glaucoma – The Need to Maintain Intraocular Pressure Over 24 Hours

European Ophthalmic Review, 2011,5(1):33-7 DOI: http://doi.org/10.17925/EOR.2011.05.01.33

Abstract:

In the treatment of glaucoma, maintenance of intraocular pressure (IOP) over a 24-hour period is of considerable importance. Some glaucoma medications do not sustain low IOP, allowing it to fluctuate with the potential to damage the optic nerve, leading to blindness. Several topically applied prostaglandins have become available, which have the advantage of maintaining 24-hour control. With these developments, it is timely to consider the relative merits of glaucoma surgery compared with medical treatments including eye drops and systemic medications, and which of the medications provides the most benefit to patients. Medications that control IOP over 24-hour periods require monitoring methods to assess their efficacy. Most determination procedures are carried out in a clinician or ophthalmologist’s office and provide only a single measure at one point in time. These require fixed equipment and cannot provide an overview of IOP variation over time or indicate whether treatments are providing continuous control. A development to address this monitoring need is the Sensimed Triggerfish®. This system uses a soft contact lens with an embedded pressure-sensing chip and associated monitoring equipment to provide multiple readings over a 24-hour period. The initial clinical experience with this device led to an immediate treatment change in two-thirds of patients. A clinical trial evaluating the efficacy of a new prostaglandin treatment, tafluprost, over 24 hours using the contact lens IOP monitoring system is currently underway. Based on the initial data, tafluprost effectively reduces IOP during the full 24-hour period, further supporting its use in the treatment of glaucoma.

Support: The publication of this article was funded by Santen Oy.
Keywords: Alpha-agonist, beta-adrenergic blocker, glaucoma, intraocular pressure, prostaglandin, tafluprost
Disclosure: The authors have no conflicts of interest to declare.
Received: February 25, 2011 Accepted: May 03, 2011
Correspondence: Tarek Shaarawy, Director, Glaucoma Sector, Department of Ophthalmology, University of Geneva, 22, Rue Alcide Jentzer, 1211 Genève, Switzerland. E: tarekshaarawy@hcuge.ch

Elevated intraocular pressure (IOP) is the most important and the only modifiable, known risk factor for glaucoma1–8 and consequently, most therapeutic interventions are directed at its modification.1–31 Both the peak levels2–4,18,21 and fluctuations15,19,23 have been known to impact disease development and progression, even in cases with statistically normal pressures.1,2,6,9,10,15,20,30 Most authors concur that IOP peaks tend to be associated with visual field (VF) decline,10,22,31 but whether or not IOP fluctuation is a risk factor for progression of glaucoma is still controversial.10,11,13–16,19,23,26 This article is an attempt to elucidate the role of 24-hour IOP control and its relevance to current glaucoma practice, as well as emerging therapeutic and diagnostic techniques.
The Efficacy of Intraocular Pressure Reduction
The efficacy of IOP reduction in retarding the progression of glaucoma over a wide spectrum of disease – from low to high IOPs and from early to advanced disease – has been conclusively demonstrated.2–4,18,21
In the Advanced glaucoma intervention study (AGIS), long-term IOP fluctuation was associated with VF progression in subjects with low mean IOP but not in patients with high mean IOP.15 Diurnal and long-term IOP fluctuations were not found to be significant risk factors for progression of early glaucoma or ocular hypertension (OHT) in the Early manifest glaucoma trial (EMGT),13 the Malmo ocular hypertension study,12 or the Ocular hypertension treatment study (OHTS).23
Lowering IOP by at least 18% (mean) from baseline has been shown to result in at least a 40% reduction in rates of worsening of glaucoma over five years.2,5,18,21,28
The mean IOPs of those who progress to blindness, however, have been reported to not differ from those who do not, with the severity of glaucoma at the time of diagnosis and the range of IOPs found during follow-up (long-term IOP fluctuation) being important predictive factors.17,27
References:
  1. Collaborative Normal-Tension Glaucoma Study Group, Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures, Am J Ophthalmol, 1998;126:487–97.
  2. Collaborative Normal-Tension Glaucoma Study Group, The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma, Am J Ophthalmol, 1998;126:498–505.
  3. The AGIS Investigators, The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration, Am J Ophthalmol, 2000;130:429–40.
  4. Kass MA, Heuer DK, Higginbotham EJ, et al., The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma, Arch Ophthalmol, 2002;120:701–13.
  5. Leske MC, Heijl A, Hussein M, et al., Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial, Arch Ophthalmol, 2003;121:48–56.
  6. Leske MC, Heijl A, Hyman L, et al., Predictors of long-term progression in the early manifest glaucoma trial, Ophthalmology, 2007;114:1965–72.
  7. Miglior S, Torri V, Zeyen T, et al., Intercurrent factors associated with the development of open-angle glaucoma in the European glaucoma prevention study, Am J Ophthalmol, 2007;144:266–75.
  8. Shirakashi M, Iwata K, Sawaguchi S, et al., Intraocular pressure-dependent progression of visual field loss in advanced primary open-angle glaucoma: a 15-year follow-up, Ophthalmologica, 1993;207:1–5.
  9. Anderson DR, Drance SM, Schulzer M, Factors that predict the benefit of lowering intraocular pressure in normal tension glaucoma, Am J Ophthalmol, 2003;136:820–9.
  10. Asrani S, Zeimer R, Wilensky J, et al., Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma, J Glaucoma, 2000;9:134–42.
  11. Bengtsson B, Heijl A, Diurnal IOP fluctuation: not an independent risk factor for glaucomatous visual field loss in high-risk ocular hypertension, Graefes Arch Clin Exp Ophthalmol, 2005;243:513–8.
  12. Bengtsson B, Heijl A, A long-term prospective study of risk factors for glaucomatous visual field loss in patients with ocular hypertension, J Glaucoma, 2005;14:135–8.
  13. Bengtsson B, Leske MC, Hyman L, et al., Fluctuation of intraocular pressure and glaucoma progression in the early manifest glaucoma trial, Ophthalmology, 2007;114:205–9.
  14. Bergea B, Bodin L, Svedbergh B, Impact of intraocular pressure regulation on visual fields in open-angle glaucoma, Ophthalmology, 1999;106:997–1004.
  15. Caprioli J, Coleman AL, Intraocular pressure fluctuation a risk factor for visual field progression at low intraocular pressures in the advanced glaucoma intervention study, Ophthalmology, 2008;115:1123–9.
  16. Collaer N, Zeyen T, Caprioli J, Sequential office pressure measurements in the management of glaucoma, J Glaucoma, 2005;14:196–200.
  17. Hattenhauer MG, Johnson DH, Ing HH, et al., The probability of blindness from open-angle glaucoma, Ophthalmology, 1998;105:2099–104.
  18. Heijl A, Leske MC, Bengtsson B, et al., Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial, Arch Ophthalmol, 2002;120:1268–79.
  19. Hong S, Seong GJ, Hong YJ, Long-term intraocular pressure fluctuation and progressive visual field deterioration in patients with glaucoma and low intraocular pressures after a triple procedure, Arch Ophthalmol, 2007;125:1010–3.
  20. Inatani M, Iwao K, Inoue T, et al., Long-term relationship between intraocular pressure and visual field loss in primary open-angle glaucoma, J Glaucoma, 2008;17:275–9.
  21. Lichter PR, Musch DC, Gillespie BW, et al., Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery, Ophthalmology, 2001;108:1943–53.
  22. Martinez-Bello C, Chauhan BC, Nicolela MT, et al., Intraocular pressure and progression of glaucomatous visual field loss, Am J Ophthalmol, 2000;129:302–8.
  23. Medeiros FA, Weinreb RN, Zangwill LM, et al., Long-term intraocular pressure fluctuations and risk of conversion from ocular hypertension to glaucoma, Ophthalmology, 2008;115:934–40.
  24. Miglior S, Pfeiffer N, Torri V, et al., Predictive factors for open-angle glaucoma among patients with ocular hypertension in the European Glaucoma Prevention Study, Ophthalmology, 2007;114:3–9.
  25. Musch DC, Gillespie BW, Lichter PR, et al., Visual field progression in the Collaborative Initial Glaucoma Treatment Study the impact of treatment and other baseline factors, Ophthalmology, 2009;116:200–7.
  26. Nouri-Mahdavi K, Hoffman D, Coleman AL, et al., Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study, Ophthalmology, 2004;111:1627–35.
  27. Oliver JE, Hattenhauer MG, Herman D, et al., Blindness and glaucoma: a comparison of patients progressing to blindness from glaucoma with patients maintaining vision, Am J Ophthalmol, 2002;133:764–72.
  28. Sultan MB, Mansberger SL, Lee PP, Understanding the importance of IOP variables in glaucoma: a systematic review, Surv Ophthalmol, 2009;54:643–62.
  29. Varma R, Hwang LJ, Grunden JW, et al., Using diurnal intraocular pressure fluctuation to assess the efficacy of fixed-combination latanoprost/timolol versus latanoprost or timolol monotherapy, Br J Ophthalmol, 2010;94:80–4.
  30. Weinreb RN, Khaw PT, Primary open-angle glaucoma, Lancet, 2004;363:1711–20.
  31. Zeimer RC, Wilensky JT, Gieser DK, et al., Association between intraocular pressure peaks and progression of visual field loss, Ophthalmology, 1991;98:64–9.
  32. Singh K, Shrivastava A, Intraocular pressure fluctuations: how much do they matter?, Curr Opin Ophthalmol, 2009;20:84–7.
  33. Bagga H, Liu JH, Weinreb RN, Intraocular pressure measurements throughout the 24 h, Curr Opin Ophthalmol, 2009;20:79–83.
  34. Stewart WC, Konstas AG, Kruft B, et al., Meta-analysis of 24-h intraocular pressure fluctuation studies and the efficacy of glaucoma medicines, J Ocul Pharmacol Ther, 2010;26:175–80.
  35. Konstas AG, Boboridis K, Tzetzi D, et al., Twenty-four-hour control with latanoprost-timolol-fixed combination therapy vs latanoprost therapy, Arch Ophthalmol, 2005;123:898–902.
  36. Higginbotham EJ, Feldman R, Stiles M, et al., Latanoprost and timolol combination therapy vs monotherapy: one-year randomized trial, Arch Ophthalmol, 2002;120:915–22.
  37. Pfeiffer N, A comparison of the fixed combination of latanoprost and timolol with its individual components, Graefes Arch Clin Exp Ophthalmol, 2002;240:893–9.
  38. Hughes E, Spry P, Diamond J, 24-hour monitoring of intraocular pressure in glaucoma management: a retrospective review, J Glaucoma, 2003;12:232–6.
  39. Konstas AG, Maltezos A, Bufidis T, et al., Twenty-four hour control of intraocular pressure with dorzolamide and timolol maleate in exfoliation and primary open-angle glaucoma, Eye (Lond), 2000;14 (Pt 1):73–7.
  40. Konstas AGP, Kozobolis VP, Leech J, Stewart WC, The efficacy and safety of the timolol/dorzolamide fixed combination vs latanoprost in exfoliation glaucoma, Eye (Lond), 2003;14:41–6.
  41. Michaud JE, Friren B, Comparison of topical brinzolamide 1% and dorzolamide 2% eye drops given twice daily in addition to timolol 0.5% in patients with primary open-angle glaucoma or ocular hypertension, Am J Ophthalmol, 2001;132:235–43.
  42. Stewart WC, Stewart JA, Day D, et al., Efficacy and safety of timolol maleate/latanoprost fixed combination versus timolol maleate and brimonidine given twice daily, Acta Ophthalmol Scand, 2003;81:242–6.
  43. Stewart WC, Konstas AG, Nelson LA, et al., Meta-analysis of 24-hour intraocular pressure studies evaluating the efficacy of glaucoma medicines, Ophthalmology, 2008;115:1117–22 e1.
  44. Konstas AG, Mylopoulos N, Karabatsas CH, et al., Diurnal intraocular pressure reduction with latanoprost 0.005% compared to timolol maleate 0.5% as monotherapy in subjects with exfoliation glaucoma, Eye (Lond), 2004;18:893–9.
  45. Larsson LI, Mishima HK, Takamatsu M, et al., The effect of latanoprost on circadian intraocular pressure, Surv Ophthalmol, 2002;47(Suppl. 1):S90–6.
  46. Liu JH, Kripke DF, Weinreb RN, Comparison of the nocturnal effects of once-daily timolol and latanoprost on intraocular pressure, Am J Ophthalmol, 2004;138:389–95.
  47. Orzalesi N, Rossetti L, Bottoli A, et al., Comparison of the effects of latanoprost, travoprost, and bimatoprost on circadian intraocular pressure in patients with glaucoma or ocular hypertension, Ophthalmology, 2006;113:239–46.
  48. Parrish RK, Palmberg P, Sheu WP, A comparison of latanoprost, bimatoprost, and travoprost in patients with elevated intraocular pressure: a 12-week, randomized, masked-evaluator multicenter study, Am J Ophthalmol, 2003;135:688–703.
  49. Walters TR, DuBiner HB, Carpenter SP, et al., 24-Hour IOP control with once-daily bimatoprost, timolol gel-forming solution, or latanoprost: a 1-month, randomized, comparative clinical trial, Surv Ophthalmol, 2004;49 (Suppl. 1):S26–35.
  50. Netland PA, Landry T, Sullivan EK, et al., Travoprost compared with latanoprost and timolol in patients with open-angle glaucoma or ocular hypertension, Am J Ophthalmol, 2001;132:472–84.
  51. Noecker RS, Dirks MS, Choplin NT, et al., A six-month randomized clinical trial comparing the intraocular pressure-lowering efficacy of bimatoprost and latanoprost in patients with ocular hypertension or glaucoma, Am J Ophthalmol, 2003;135:55–63.
  52. Susanna R Jr, Medeiros FA, Vessani RM, et al., Intraocular pressure fluctuations in response to the water-drinking provocative test in patients using latanoprost versus unoprostone, J Ocul Pharmacol Ther, 2004;20:401–10.
  53. Vetrugno M, Sisto D, Trabucco T, et al., Water-drinking test in patients with primary open-angle glaucoma while treated with different topical medications, J Ocul Pharmacol Ther, 2005;21:250–7.
  54. Watson PG, Latanoprost. Two years’ experience of its use in the United Kingdom. Latanoprost Study Group, Ophthalmology, 1998;105:82–7.
  55. DuBiner H, Cooke D, Dirks M, et al., Efficacy and safety of bimatoprost in patients with elevated intraocular pressure: a 30-day comparison with latanoprost, Surv Ophthalmol, 2001;45(Suppl. 4):S353–60.
  56. Konstas AG, Maltezos AC, Gandi S, et al., Comparison of 24-hour intraocular pressure reduction with two dosing regimens of latanoprost and timolol maleate in patients with primary open-angle glaucoma, Am J Ophthalmol, 1999;128:15–20.
  57. Noecker RJ, Earl ML, Mundorf T, et al., Bimatoprost 0.03% versus travoprost 0.004% in black Americans with glaucoma or ocular hypertension, Adv Ther, 2003;20:121–8.
  58. Konstas AG, Mantziris DA, Cate EA, et al., Effect of timolol on the diurnal intraocular pressure in exfoliation and primary open-angle glaucoma, Arch Ophthalmol, 1997;115:975–9.
  59. Konstas AG, Nakos E, Tersis I, et al., A comparison of once-daily morning vs evening dosing of concomitant latanoprost/timolol, Am J Ophthalmol, 2002;133:753–7.
  60. Mundorf T, Williams R, Whitcup S, et al., A 3-month comparison of efficacy and safety of brimonidine-purite 0.15% and brimonidine 0.2% in patients with glaucoma or ocular hypertension, J Ocul Pharmacol Ther, 2003;19:37–44.
  61. Schuman JS, Horwitz B, Choplin NT, et al., A 1-year study of brimonidine twice daily in glaucoma and ocular hypertension. A controlled, randomized, multicenter clinical trial. Chronic Brimonidine Study Group, Arch Ophthalmol, 1997;115:847–52.
  62. Orzalesi N, Rossetti L, Invernizzi T, et al., Effect of timolol, latanoprost, and dorzolamide on circadian IOP in glaucoma or ocular hypertension, Invest Ophthalmol Vis Sci, 2000;41:2566–73.
  63. Sit AJ, Weinreb RN, Crowston JG, et al., Sustained effect of travoprost on diurnal and nocturnal intraocular pressure, Am J Ophthalmol, 2006;141:1131–3.
  64. Shaarawy T, Flammer J, Haefliger IO, Reducing intraocular pressure: is surgery better than drugs?, Eye (Lond), 2004;18:1215–24.
  65. Sharaawy T, Bhartiya S, Surgical management of glaucoma: evolving paradigms, Indian J Ophthalmol, 2011;59(Suppl):S123–30.
  66. Agarwal HC, Sihota R, Das C, et al., Role of argon laser trabeculoplasty as primary and secondary therapy in open angle glaucoma in Indian patients, Br J Ophthalmol, 2002;86:733–6.
  67. Greenidge KC, Spaeth GL, Fiol-Silva Z, Effect of argon laser trabeculoplasty on the glaucomatous diurnal curve, Ophthalmology, 1983;90:800–4.
  68. Heijl A, Bengtsson B, The short-term effect of laser trabeculoplasty on the glaucomatous visual field. A prospective study using computerized perimetry, Acta Ophthalmol (Copenh), 1984;62:705–14.
  69. Kothy P, Toth M, Hollo G, Influence of selective laser trabeculoplasty on 24-hour diurnal intraocular pressure fluctuation in primary open-angle glaucoma: a pilot study, Ophthalmic Surg Lasers Imaging, 2010;41:342–7.
  70. Prasad N, Murthy S, Dagianis JJ, et al., A comparison of the intervisit intraocular pressure fluctuation after 180 and 360 degrees of selective laser trabeculoplasty (SLT) as a primary therapy in primary open angle glaucoma and ocular hypertension, J Glaucoma, 2009;18:157–60.
  71. Nagar M, Luhishi E, Shah N, Intraocular pressure control and fluctuation: the effect of treatment with selective laser trabeculoplasty, Br J Ophthalmol, 2009;93:497–501.
  72. Konstas AG, Topouzis F, Leliopoulou O, et al., 24-hour intraocular pressure control with maximum medical therapy compared with surgery in patients with advanced open-angle glaucoma, Ophthalmology, 2006;113:761–5 e1.
  73. Malerbi FK, Hatanaka M, Vessani RM, et al., Intraocular pressure variability in patients who reached target intraocular pressure, Br J Ophthalmol, 2005;89:540–2.
  74. Mansouri K, Orguel S, Mermoud A, et al., Quality of diurnal intraocular pressure control in primary open-angle patients treated with latanoprost compared with surgically treated glaucoma patients: a prospective trial, Br J Ophthalmol, 2008;92:332–6.
  75. Mansouri K, Shaarawy T, Continuous intraocular pressure monitoring with a wireless ocular telemetry sensor: initial clinical experience in patients with open angle glaucoma, Br J Ophthalmol, 2011;95(5):627–9.
  76. Medeiros FA, Pinheiro A, Moura FC, et al., Intraocular pressure fluctuations in medical versus surgically treated glaucomatous patients, J Ocul Pharmacol Ther, 2002;18:489–98.
  77. Barkana Y, Anis S, Liebmann J, et al., Clinical utility of intraocular pressure monitoring outside of normal office hours in patients with glaucoma, Arch Ophthalmol, 2006;124:793–7.
  78. Buguet A, Py P, Romanet JP, 24-hour (nyctohemeral) and sleep-related variations of intraocular pressure in healthy white individuals, Am J Ophthalmol, 1994;117:342–7.
  79. De Vivero C, O’Brien C, Lanigan L, et al., Diurnal intraocular pressure variation in low-tension glaucoma, Eye (Lond), 1994;8(Pt. 5):521–3.
  80. Liu JH, Kripke DF, Hoffman RE, et al., Nocturnal elevation of intraocular pressure in young adults, Invest Ophthalmol Vis Sci, 1998;39:2707–12.
  81. Liu JH, Kripke DF, Twa MD, et al., Twenty-four-hour pattern of intraocular pressure in the aging population, Invest Ophthalmol Vis Sci, 1999;40:2912–7.
  82. Liu JH, Zhang X, Kripke DF, et al., Twenty-four-hour intraocular pressure pattern associated with early glaucomatous changes, Invest Ophthalmol Vis Sci, 2003;44:1586–90.
  83. Rota-Bartelink AM, Pitt A, Story I, Influence of diurnal variation on the intraocular pressure measurement of treated primary open-angle glaucoma during office hours, J Glaucoma, 1996;5:410–5.
  84. Sensimed AG, Sensimed Trigger Fish. A breakthrough solution to continuously monitor fluctuations of intraocular pressure, 2010.
Keywords: Alpha-agonist, beta-adrenergic blocker, glaucoma, intraocular pressure, prostaglandin, tafluprost