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Dorzolamide

A Review of its Pharmacology and Therapeutic Potential in the Management of Glaucoma and Ocular Hypertension

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Summary

Dorzolamide (dorzolamide hydrochloride), the first topical carbonic anhydrase (CA) inhibitor to become available for clinical use, lowers intraocular pressure (IOP) by reducing aqueous humour formation. It is formulated as a 2% eyedrop for use in the management of glaucoma and ocular hypertension.

When administered 3 times daily, dorzolamide is effective in lowering IOP in patients with open-angle glaucoma or ocular hypertension. Mean IOP was reduced by approximately 4 to 6mm Hg at peak (2 hours postdose) and 3 to 4.5mm Hg at trough (8 hours postdose) in clinical trials. A 1-year comparative study showed that the ocular hypotensive efficacy of dorzolamide 2% 3 times daily was similar to that of betaxolol 0.5% twice daily, but slightly inferior to that of timolol 0.5% twice daily. Dorzolamide has additive ocular hypotensive effects when used in conjunction with topical α-adrenergic antagonists and was as effective as pilocarpine 2% 4 times daily as adjunctive therapy in patients receiving timolol.

Dorzolamide does not appear to produce the acid-base or electrolyte disturbances and severe systemic adverse events associated with oral CA inhibitors, and unlike α-adrenergic antagonists, it is not contraindicated in patients with asthma, reactive airways disease or heart disease. Furthermore, as CA inhibitors do not cause miosis, they may cause less interference with vision than pilocarpine or epinephrine (adrenaline). The most common adverse effects associated with dorzolamide are bitter taste and transient local burning or stinging. Conjunctivitis was the most common reason for discontinuation of dorzolamide in one large study.

Thus, available data suggest that dorzolamide has potential as an alternative therapy option in patients with glaucoma or ocular hypertension who are intolerant of, or unable to receive, ophthalmic α-adrenergic antagonists and as adjunctive therapy in patients already receiving these agents. Further efficacy and tolerability data are needed to determine the place of dorzolamide in therapy.

Pharmacodynamic Properties

Dorzolamide (dorzolamide hydrochloride), a nonbacteriostatic sulphonamide derivative, is the first topical carbonic anhydrase (CA) inhibitor to become clinically available. It is a highly selective inhibitor of CA-II [the isoenzyme which plays a key role in the regulation of aqueous humour production and intraocular pressure (IOP)], with a 4000-fold greater affinity for CA-II than CA-I. Inhibition of CA in the ocular ciliary processes reduces bicarbonate production and consequently reduces aqueous humour production and IOP. After treatment with dorzolamide 2% eyedrops for 12 months, mean CA-II activity in peripheral red blood cells of patients with open-angle glaucoma or ocular hypertension decreased to approximately 12% of baseline. However, as <1% enzyme activity is sufficient to maintain physiological function, dorzolamide is likely to have a low propensity to induce adverse effects resulting from systemic CA inhibition.

Dorzolamide was more potent than the oral CA inhibitors acetazolamide and methazolamide in inhibiting CA-II isolated from human erythrocytes (>20-fold) and CA activity in a homogenate of rabbit iris and ciliary body (4- to 8-fold). It produced 100% inhibition at a concentration of 0.1% in the latter system.

Dorzolamide has demonstrated topical ocular hypotensive effects in animals, healthy volunteers and patients with glaucoma; the peak effect occurs at about 2 hours postdose in humans. A dose-response effect was seen with single doses of dorzolamide ≤2%, but was less evident after repeated doses. In healthy volunteers, the effects of dorzolamide 1% on aqueous protein concentration and IOP were similar to those of oral acetazolamide 250mg.

Pharmacokinetic Properties

Studies in rabbits suggest that dorzolamide penetrates well into ocular tissues and fluids, with concentrations of >5 mg/kg or mg/L being found in the cornea, iris/ciliary body, retina and aqueous humour after instillation of dorzolamide 2%. As with other drugs applied topically to the eye, dorzolamide can enter the systemic circulation by drainage through the nasolacrimal duct and absorption from the nasopharyngeal mucosa.

Dorzolamide and its active metabolite, N-desethyldorzolamide, accumulate in erythrocytes after ocular administration, as a result of binding to CA. Concentrations of dorzolamide in erythrocytes reached steady-state after approximately 8 days of administering dorzolamide 2% 3 times daily to both eyes of a healthy volunteer. Mean red blood cell concentrations of dorzolamide and its metabolite in 56 patients with glaucoma or ocular hypertension were 20.5 and 7.7 µmol/L, respectively, after 12 months’ treatment with dorzolamide 2% eyedrops 3 times daily. Concentrations of the drug in plasma were 11µg/L after administration of dorzolamide 2% 3 times daily for 6 months in patients with glaucoma or ocular hypertension. Dorzolamide is approximately 33% bound to plasma proteins.

In vitro studies using rat liver microsomes suggest that the drug is de-ethylated in the liver by the cytochrome P450 system. Dorzolamide has a terminal elimination half-life ≥ 120 days in red blood cells and is mainly excreted unchanged in the urine. No data regarding the effects of age and renal or hepatic impairment on the disposition of dorzolamide are available.

Therapeutic Potential

In clinical trials in patients with open-angle glaucoma or ocular hypertension, dorzolamide 2% 3 times daily lowered mean IOP by approximately 4 to 6mm Hg at peak (2 hours postdose) and 3 to 4.5mm Hg at trough (8 hours postdose) and was significantly more effective than placebo. Efficacy was maintained during extended treatment periods of up to 1 year.

In a 1-year comparative study with two topical α-adrenergic antagonists, the ocular hypotensive efficacy of dorzolamide 2% 3 times daily was similar to that of betaxolol 0.5% twice daily but slightly inferior to that of timolol 0.5% twice daily: IOP was reduced by 22.9 vs 20.8 vs 25.3% at peak.

Addition of dorzolamide 2% twice daily to existing timolol therapy (0.5% twice daily) in 2 randomised double-masked studies resulted in further reductions in IOP in patients with open-angle glaucoma or ocular hypertension. Dorzolamide 0.7 or 2% twice daily and pilocarpine 2% 4 times daily produced similar additional IOP reductions (14.3 vs 12.6 vs 16.9% at peak).

Dorzolamide has also been successfully substituted for various oral CA inhibitors. In patients with more severe glaucoma associated with pseudoexfoliation syndrome, dorzolamide 2% 3 times daily effectively lowered IOP and showed similar efficacy to timolol 0.5% twice daily, with mean peak IOP reductions of 24 vs 29% after 6 months’ treatment.

Tolerability

The most common adverse effects associated with dorzolamide are bitter taste and transient local burning or stinging. Few long term tolerability data have been published. In a comparative 1-year study in patients with open-angle glaucoma or ocular hypertension, the most common adverse events in dorzolamide recipients (2% 3 times daily; n = 313) were bitter taste (27% of patients), digestive disturbances (7%), headache (5%), cardiovascular events (angina, hypertension, tachycardia; 3%) and local ocular effects such as burning (12%), blurred vision, itching, tearing, foreign body sensation, stinging, eyelid discomfort (6 to 9%) and conjunctivitis (4%).

In this study, dorzolamide tended to cause more bitter taste, stinging, burning and conjunctival irritation than timolol or betaxolol (both 0.5% twice daily), but a similar incidence of other local symptoms (blurred vision, tearing, itching, eyelid discomfort and foreign body sensation). Conjunctivitis (which appeared to be an allergic reaction) was the most common reason for discontinuation of dorzolamide. Dorzolamide was associated with a significantly lower incidence of cardiovascular system adverse events than timolol or betaxolol (3 vs 8 and 8%), but a significantly higher incidence of gastrointestinal disturbance than timolol (7 vs 1%).

A comparative study evaluating interference of adverse effects of ophthalmic medications with quality of life in patients already receiving timolol showed that dorzolamide 2% twice daily caused less visual disturbance and brow ache than pilocarpine 2% 4 times daily and was preferred to the latter agent as adjunctive therapy.

Dorzolamide caused irreversible corneal decompensation in 4 patients with borderline endothelial function and therefore appears to be contraindicated in this patient group.

Dorzolamide does not appear to produce the acid-base or electrolyte disturbances and associated severe systemic symptoms characteristic of oral CA inhibitors. Indeed, disappearance of these symptoms was noted after patients were switched from oral CA inhibitors to dorzolamide. However, as with oral CA inhibitors, dorzolamide is a sulphonamide derivative, and it enters the systemic circulation after ocular administration. Thus, it is possible that sulphonamide hypersensitivity or serious sulphonamide-type reactions could develop during therapy with the drug. However, no such reactions appear to have been reported to date.

Dosage and Administration

The recommended dosage of dorzolamide 2% ophthalmic solution for the treatment of glaucoma or ocular hypertension is one drop into the conjunctival sac of the affected eye(s), 3 times daily (when used as monotherapy) or twice daily (when used as an adjunct to ophthalmic α-adrenergic antagonists). When more than one ophthalmic agent is being used, they should be administered at least 10 minutes apart.

Use of dorzolamide should be discontinued if signs of sulphonamide hypersensitivity or serious sulphonamide-type reactions develop. It would appear advisable to avoid use of dorzolamide in patients with previous hypersensitivity reactions to sulphonamides. Dorzolamide is contraindicated in patients with severe renal impairment (creatinine clearance <1.8 L/h) and should be used with caution in those with hepatic impairment. It should not be used while wearing soft contact lenses.

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    Julia A. Balfour & Michelle I. Wilde

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Correspondence to Julia A. Balfour.

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Various sections of the manuscript reviewed by: J. Biollaz, Division de Pharmacologie Clinique, Département de Médecine, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; L. Collum, Department of Ophthalmology, Royal Victoria Eye and Ear Hospital, Dublin, Ireland; R.P. Crick, International Glaucoma Association, King’s College Hospital, London, England; F.T. Fraunfelder, Oregon Health Sciences University, School of Medicine, Casey Eye Institute, Portland, Oregon, USA; I. Goldberg, Eye Associates Pty Ltd, Sydney, New South Wales, Australia; L.M. Hurvitz, Gulf Coast Glaucoma Clinic, Sarasota, Florida, USA; Y. Kitazawa, Department of Ophthalmology, School of Medicine, Gifu University, Gifu, Japan; J.D.C. Macdiarmid, Hamilton Eye Clinic, Hamilton, New Zealand; T.H. Maren, Department of Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, Florida, USA.

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Balfour, J.A., Wilde, M.I. Dorzolamide. Drugs & Aging 10, 384–403 (1997). https://doi.org/10.2165/00002512-199710050-00006

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