Intervention Review

Medical interventions for primary open angle glaucoma and ocular hypertension

  1. Clemens Vass1,*,
  2. Cornelia Hirn1,
  3. Thomas Sycha2,
  4. Oliver Findl1,
  5. Stefan Sacu1,
  6. Peter Bauer3,
  7. Leopold Schmetterer4

Editorial Group: Cochrane Eyes and Vision Group

Published Online: 17 OCT 2007

Assessed as up-to-date: 28 MAY 2007

DOI: 10.1002/14651858.CD003167.pub3

How to Cite

Vass C, Hirn C, Sycha T, Findl O, Sacu S, Bauer P, Schmetterer L. Medical interventions for primary open angle glaucoma and ocular hypertension. Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD003167. DOI: 10.1002/14651858.CD003167.pub3.

Author Information

  1. 1

    Medical University of Vienna, Department of Ophthalmology, Vienna, Austria

  2. 2

    Medical University of Vienna, Department of Neurology, Vienna, Austria

  3. 3

    Medical University of Vienna, Institute of Medical Statistics, Vienna, Austria

  4. 4

    Medical University of Vienna, Institute of Medical Physics, Department of Clinical Pharmacology, Vienna, Austria

*Clemens Vass, Department of Ophthalmology, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, A-1090, Austria. clemens.vass@meduniwien.ac.at.

Publication History

  1. Publication Status: Edited (no change to conclusions)
  2. Published Online: 17 OCT 2007

SEARCH

 

Abstract

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

Background

Primary open angle glaucoma (POAG) is a progressive optic neuropathy with an elevated intraocular pressure (IOP), where the optic nerve head becomes pathologically excavated and the visual field (VF) is characteristically altered. Ocular hypertension (OHT) is a condition with elevated IOP but without discernible pathology of the optic nerve head or the VF. It is a major risk factor for development of POAG.

Objectives

To assess and compare the effectiveness of topical pharmacological treatment for POAG or OHT to prevent progression or onset of glaucomatous optic neuropathy.

Search methods

We searched CENTRAL, MEDLINE and EMBASE in May 2007. We searched the bibliographies of identified articles and contacted experts, investigators and pharmaceutical companies for additional published and unpublished studies.

Selection criteria

Randomised controlled trials comparing topical pharmacological treatment to placebo, no treatment or other treatment for specified endpoints which included people with POAG or OHT, and with duration of treatment of at least one year.

Data collection and analysis

Two authors independently extracted data and assessed trial quality. Where appropriate, we summarised data using Peto odds ratio and mean difference after testing for heterogeneity between studies.

Main results

We included 26 trials, which randomised 4979 participants, in this review. Meta-analysis of 10 trials clearly demonstrated reduction of onset of VF defects in treated OHT (OR 0.62, 95% CI 0.47 to 0.81). No single drug showed a significant VF protection compared to placebo or untreated controls. We did identify some border line evidence for a positive influence of treatment on VF prognosis (OR 0.67, 95% CI 0.45 to 1.00) for the beta-blockers .

Authors' conclusions

The results of this review support the current practice of IOP lowering treatment of OHT. A visual field protective effect has been clearly demonstrated for medical IOP lowering treatment. Positive but weak evidence for a beneficial effect of the class of beta-blockers has been shown.

Direct comparisons of prostaglandins or brimonidine to placebo are not available and the comparison of dorzolamide to placebo failed to demonstrate a protective effect. However, absence of data or failure to prove effectiveness should not be interpreted as proof of absence of any effect. The decision to treat a patient or not, as well as the decision regarding the drug with which to start treatment, should remain individualised, taking in to account the amount of damage, the level of IOP, age and other patient characteristics.

 

Plain language summary

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

Medical interventions for primary open angle glaucoma and ocular hypertension

Ocular hypertension (OHT) is a condition with raised intraocular pressure (IOP) without visual field changes or discernible pathology of the optic nerve head. Ocular hypertension with IOP above 21 mmHg untreated is a major risk factor for development of primary open angle glaucoma, which is progressive nerve fibre loss and damage to the optic disc so that the visual field develops characteristic defects. Topical medications are given to reduce the IOP as a way of preventing the onset or progression of damage and associated visual field loss. These medications may have local and systemic side effects that may be severe enough for the treatment to be stopped and include local irritation, drowsiness, shortage of breath and cardiovascular side effects, particularly in the elderly. The results of this review support the current practice of topical medication to lower IOP and clearly demonstrate a visual field protective effect. The review authors identified a total of 26 controlled trials that randomised 4979 people with OHT or open angle glaucoma to receive topical medication or a placebo, another topical medication or no treatment for at least a year. Meta-analysis of 10 trials testing different topical medications against placebo or untreated controls showed reduced incidence of glaucomatous visual field defects with treatment for people with OHT. The odds ratio (OR) was 0.62 (range 0.5 to 0.8). The class of beta-blockers (including timolol) had positive but weak evidence for a beneficial effect in protecting against visual field defects (OR 0.7, range 0.5 to 1.0). No single drug showed significant visual field protection in OHT with the evidence available. Medications included beta-blockers, dorzolamide, brimonidine, pilocarpine and epinephrine. From the reports, the majority of trials were of low methodological quality. Local and systemic side effects leading to treatment being stopped were often poorly reported and did not appear to differ between treatment groups. Drop-outs due to side effects occurred with similar frequency in people treated with beta-blocker or placebo and appeared to be less with timolol compared to brimonidine, in three trials.

 

摘要

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

背景

原發性廣角性青光眼及眼高壓的內科治療

原發性廣角性青光眼是一進行性視神經病變併有眼壓高,致視神經頭變成病理性凹陷且視野有典型的影響.眼高壓是一種眼壓升高但沒有視神經或視野獨特的病變. 它是原發性廣角性青光眼發生的主要危險因素.

目標

評估和比較對原發性廣角性青光眼或眼高壓局部治療的效果來預防青光眼視神經病變的發生或進行.

搜尋策略

我們在2007年5月搜尋CENTRAL, MEDLINE 及 EMBASE. 我們搜尋這些文獻的參考書目並與專家,研究者及藥廠聯絡來取得另外以刊登或未刊登的研究.

選擇標準

Randomised controlled trials 比較局部藥物治療與安慰劑, 無治療或其他為特別終點的治療,包括有原發性廣角性青光眼或眼高壓的患者,及治療時間持續至少一年者.

資料收集與分析

兩位作者獨立擷取資料及評估試驗品質. 在適當情況下, 我們在測試過研究間的差異性後用Peto odds ratio 及 mean differencewe 來總結資料.

主要結論

我們在此回顧包含26個研究,它們隨機分配 4979 參與者.綜論10個研究的Metaanalysis清楚的顯示眼高壓在治療後減少了視野缺陷的發作 (OR 0.62, 95% CI 0.47 to 0.81). 沒有單獨藥物顯現較安慰劑或無治療控制組有明顯的視野保護效果. 我們確實發現了betablockers在治療視野預後方面有正面影響的大致證據 (OR 0.67, 95% CI 0.45 to 1.00).

作者結論

此回顧的結果支持目前在眼高壓減低眼壓治療的行為.藥物降低眼壓的治療清楚的顯現有視野保護效果. 正向但微弱的證據顯示betablockers 有益的效果.沒有安慰劑與prostaglandins 或 brimonidine直接比較的研究,且比較dorzolamide與安慰劑無法顯現保護效果. 然而, 缺少數據或無法證實效果不可被解讀為沒有任何效果. 決定要不要治療病人,如同決定要使用何種藥物開始治療,仍需考量傷害的大小,眼壓的數值,年齡及其他病人的特性因人而異.

翻譯人

本摘要由高雄榮民總醫院王曉萍翻譯。

此翻譯計畫由臺灣國家衛生研究院(National Health Research Institutes, Taiwan)統籌。

總結

原發性廣角性青光眼及眼高壓的內科治療.眼高壓是一種眼壓升高但沒有視野變化或視神經頭獨特的病變. 眼高壓是眼壓高於 21 mmHg, 若不治療,是發生原發性廣角性青光眼的一個主要危險因子, 會有進行式神經纖維損失和傷害視神經盤,進而造成視野上獨特的缺陷. 使用局部藥物來降低眼壓是一種用來預防傷害及相關視野缺陷產生或進行的方式. 這些藥物可能有局部或全身性的副作用,那可能嚴重到足以使治療被停止,包括局部刺激,困倦,呼吸急促和心血管的副作用,特別是在老年人.此回顧的結果支持目前局部治療來降低眼壓的行為且清楚顯現視野的保護效果. 此回顧的作者確認總共26個controlled trials那共隨機分配 4979 有眼高壓或原發性廣角性青光眼的患者來接受局部治療或安慰劑, 另醫局部治療或無治療持續至少一年. Metaanalysis 10個研究來檢驗不同的局部治療相較安慰劑或無治療控制組,顯示治療眼高壓的患者可降低青光眼視野缺陷的發生率. odds ratio (OR)是 0.62 (從 0.5 到 0.8). betablockers類 (包括 timolol) 在保護減低視野缺陷上有正向但微弱的效果(OR 0.7, 從 0.5 到 1.0). 沒有單一藥物有證據顯示在眼高壓病人有明顯的視野保護. 藥物包括 betablockers, dorzolamide, brimonidine, pilocarpine and epinephrine. 從報告, 大部分研究的方法研究品質是低的.局部及全身性的副作用造成治療被停止,通常很少被報告且在治療組中並無不同的顯現. 因副作用而而退出實驗者在用 betablocker治療或安慰組出現的頻率相同, 而在三個研究中timolol 較少於brimonidine.