Elsevier

The Lancet

Volume 350, Issue 9083, 4 October 1997, Pages 979-982
The Lancet

Articles
Risk of ocular hypertension or open-angle glaucoma in elderly patients on oral glucocorticoids

https://doi.org/10.1016/S0140-6736(97)03392-8Get rights and content

Summary

Background

Ocular hypertension and open-angle glaucoma are well-known side-effects of treatment with topical ophthalmic glucocorticoids. There is uncertainty about the risk of these disorders with oral glucocorticoid therapy.

Methods

Data from the Quebec universal health insurance programme for the elderly were used to identify 9793 patients with a new diagnosis of ocular hypertension or open-angle glaucoma, or on newly prescribed treatment for these disorders (cases). 38 325 controls were randomly selected from ophthalmology patients seen in the same month and year as the case (index date). Current use of oral glucocorticoids was defined as that within 14 days of the index date. All glucocorticoid doses were converted to the equivalent amount of hydrocortisone. The case-control analysis was done by conditional logistic regression and adjusted for age, sex, systemic hypertension, diabetes mellitus, ophthalmic glucocorticoids, glucocorticoid injections, and variables related to general health.

Findings

The mean ages of cases and controls were similar (74·9 [SD 6·3] vs 74·7 [6·4]). The adjusted odds ratio of ocular hypertension or open-angle glaucoma for current users of oral glucocorticoids compared with non-users was 1·41 (95% Cl 1·22–1·63). There was a dose-related increase in the adjusted odds ratios for current users: 1·26 (1·01–1·56) for less than 40 mg per day of hydrocortisone, 1·37 (1·06–1·76) for patients on 40–79 mg per day, and 1·88 (1·40–2·53) for patients on 80 mg or more per day. The odds ratios also increased with the duration of treatment over the first 11 months of exposure.

Interpretation

The use of oral glucocorticoids increases the risk of ocular hypertension or open-angle glaucoma in elderly patients. In patients in this age-group who need long-term treatment with high doses of oral glucocorticoids, monitoring of intraocular pressure may be justified.

Introduction

Ocular hypertension is a well-known side-effect of topical ophthalmic glucocorticoids.1 The lack of symptoms with raised intraocular pressure has prompted ophthalmologists to recommend routine monitoring of intraocular pressure in patients on long-term ophthalmic steroids.1, 2

Several case reports have suggested that oral glucocorticoid therapy can also result in ocular hypertension and open-angle glaucoma.3, 4, 5 However, investigations into the effects of oral corticosteroids on ocular pressure are scarce. There have been a few retrospective studies with small numbers of patients on glucocorticoids for variable periods of time.6, 7, 8, 9, 10 In some of these studies the mean intraocular pressure was higher in the steroid-treated group than in the control group.6, 7

Most ophthalmologists believe that the risk of ocular hypertension or open-angle glaucoma is lower with oral glucocorticoids than with topical ophthalmic glucocorticoids, although the risk has not yet been quantified.11, 12 Some investigators have hypothesised that months or years of treatment with oral glucocorticoids are needed to cause ocular hypertension. By contrast, most clinicians recognise an increased risk with topical ophthalmic steroids after weeks of treatment.11, 13

The most important factor in corticosteroid-induced ocular hypertension seems to be an increase in the resistance to aqueous-humour outflow.12, 14 There is a high concentration of steroid-specific receptors in trabecular-meshwork cells.15 These receptors probably have a role in the increased intraocular pressure induced by steroids. Morphological changes in the trabecular meshwork have been seen in this disorder. Other possible mechanisms for the increase in intraocular pressure with corticosteroids include accumulation of polymerised glycosaminoglycans in the trabecular meshwork and an increase in the expression of collagen, elastin, or fibronectin in the extracellular matrix.12 Oral glucocorticoids have a high systemic bioavailability; betamethasone (70%), dexamethasone or methylprednisolone (80%), and prednisone (98%),16 and therefore a high concentration of steroids will reach the eye with a subsequent risk of ocular side-effects.

We investigated the risk of ocular hypertension or open-angle glaucoma associated with oral glucocorticoids in a case-control study. In particular, we examined whether the risk of these disorders varies with the dose and duration of exposure to oral glucocorticoids, and whether a residual risk remains after the medication is stopped.

Section snippets

Methods

The methods have been described in detail elsewhere.17 Briefly, data from the Quebec health-insurance-plan database, which contains information about medical services and drugs dispensed for all individuals 65 years of age or older, were used for a case-control study. Information is available about the patient's age, sex, all filled prescriptions, medical procedures, diagnoses, and the specialty of their physician. Prescription-claims data such as drug name, dispensing date, dosage form, dose,

Results

We identified 9793 cases and 38 325 controls. Baseline characteristics of cases and controls are shown in table 1. Only two patients, both in the control group, were on more than one type of oral glucocorticoid.

The odds ratio of ocular hypertension or open-angle glaucoma was significantly increased in current users of oral glucocorticoids (1·41 [95% CI 1·22–1·63]) but not in former users (table 2). There was a graded relation between the current glucocorticoid dose and the odds ratio of ocular

Discussion

Our results show that the risk of ocular hypertension or open-angle glaucoma is increased in patients who have taken oral glucocorticoids in the past 14 days. Patients whose exposure to glucocorticoids ended 15-45 days previously did not have a significantly increased risk. This finding suggests that raised intraocular pressure from oral steroids is usually reversible within 2 weeks of stopping steroid treatment and confirms clinical observations.3, 4, 5. The 2-week interval for the return of

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