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Steroid-induced glaucoma: causes, symptoms, diagnosis, treatment
Last reviewed: 08.07.2025

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Epidemiology of steroid-induced glaucoma
The incidence of steroid-induced glaucoma in the general population is unknown. Significant increases in intraocular pressure with topical glucocorticoids have been reported in 50% to 90% of patients with glaucoma and in 5% to 10% of patients with normal intraocular pressure. The incidence of such reactions to glucocorticoids varies with the type, dose, and route of administration. Increases in intraocular pressure have been reported with topical, nitro-ocular, periocular, inhalation, oral, intravenous, and transdermal administration, as well as with endogenous increases in glucocorticoid levels in Cushing's syndrome.
Pathophysiology of steroid-induced glaucoma
In response to glucocorticoid administration, the amount of glycosaminoglycans in the trabecular meshwork increases, which prevents normal outflow of intraocular fluid and leads to an increase in intraocular pressure. Glucocorticoids also reduce the permeability of the trabecular meshwork membranes, phagocytic activity of cells, and cause the breakdown of extracellular and intercellular structural proteins, which leads to a further decrease in the permeability of the trabecular meshwork. It has been shown that in response to glucocorticoid administration, the myocillin/TIGR gene (trabecular meshwork steroid-induced response) is activated in the endothelial cells of the trabecular meshwork. The connection between the gene and glaucoma and steroid-induced increase in intraocular pressure has not yet been identified.
Symptoms of steroid-induced glaucoma
The main fact in the anamnesis is the use of glucocorticoids in any form. The use of glucocorticoids in the distant past with subsequent normalization of intraocular pressure can lead to the development of typical normal-tension glaucoma. The presence of asthma, skin diseases, allergies, autoimmune diseases and similar conditions in the anamnesis indicates the possible use of glucocorticoids. Sometimes patients note a change in the quality of vision associated with a pronounced narrowing of the visual fields.
Diagnosis of steroid-induced glaucoma
Biomicroscopy
Usually nothing is detected. Even in the case of very high intraocular pressure due to a chronic process, corneal edema does not occur.
Gonioscopy
Usually nothing is found.
Posterior pole
In the case of a significant and prolonged increase in intraocular pressure, changes in the optic nerve characteristic of glaucoma are detected.
Special studies
Withdrawal of glucocorticoids, if possible, results in a sustained reduction in intraocular pressure. The time required to reduce intraocular pressure varies and may be very long in cases of prolonged glucocorticoid use. If local glucocorticoid use cannot be withdrawn (e.g., if there is a risk of corneal transplant rejection), steroid damage to the second eye may manifest as an increase in intraocular pressure, confirming the diagnosis.
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Treatment of steroid-induced glaucoma
Withdrawal of glucocorticoids may result in complete recovery. When using topical drugs, switching to weaker glucocorticoids that increase intraocular pressure to a lesser extent (e.g., loteprednol, rimexolone, fluorometholone) may be useful. Patients with severe uveitis require special attention, as treatment may require glucocorticoids. In addition, uveitis may lead to the development of various forms of glaucoma or mask glaucoma with decreased secretion of intraocular fluid.
Treatment of steroid-induced glaucoma
The day after the operation |
Intraocular pressure (mmHg) |
Treatment regimen |
Operation #1. Vitrectomy/membranectomy, subconjunctival administration of glucocorticoid depot |
||
1 |
25 |
Prednisolone, scopolamine, erythromycin |
6 |
45 |
Timolol, iopidin, acetazolamide added |
16 |
20 |
Acetazolamide has been discontinued. |
30 |
29 |
Dorzolamide added, prednisolone tapering started |
48 |
19 |
Prednisolone withdrawal |
72 |
27 |
Continue to prescribe timolol, apraclonidine, dorzolamide |
118 |
44 |
Latanoprost added; glaucoma consultation scheduled |
154 |
31 |
Purpose of removal of glucocorticoid depots |
Operation #2. Removal of glucocorticoid depot |
||
1 |
32 |
Timolol, dorzolamide added |
4 |
28 |
The same thing continues |
23 |
24 |
The same thing continues |
38 |
14 |
Discontinuation of dorzolamide |
Note: The patient subsequently discontinued timolol; since discontinuation of the drug, intraocular pressure has remained at 10-14 mmHg.
In general, topical antiglaucoma drugs of all types are effective in patients with steroid-induced intraocular pressure elevation. In general, laser trabeculoplasty is less effective in these patients than in patients with other types of glaucoma. The results of operations aimed at increasing filtration are the same as in primary open-angle glaucoma.