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New Developments in the Drug Treatment of Glaucoma

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Summary

This article reviews standard treatment modalities for patients with glaucoma and describes 3 classes of drugs which are undergoing development: apraclonidine (aplonidine, ALO 2145), an α2-adrenergic agonist which has been released for clinical use; topical carbonic anhydrase inhibitors, a modification of the systemic carbonic anhydrase inhibitors currently in use; and prostaglandins (PGs), a new class of drugs with topical ocular hypotensive activity.

Standard treatment modalities include parasympathomimetic agents such as pilocarpine, car-bachol, and phospholine iodide, which lower intraocular pressure (IOP) by increasing aqueous outflow through the trabecular meshwork. A newer form of pilocarpine as a gel produces a longer action. Adrenergic agonist medications, such as epinephrine (adrenaline) and its prodrug dipivefrine (dipivalyl epinephrine), function by increasing uveoscleral outflow and trabecular outflow facility.

A decrease in aqueous formation by the ciliary processes is thought to be the mechanism of action of β-adrenoceptor antagonists, but the physiological basis for this action has not been clearly demonstrated. A newer β-blocker, betaxolol, has relatively selective β2-blocking activity.

Carbonic anhydrase inhibitors are nonbacteriostatic sulphonamide derivatives which decrease aqueous formation by the ciliary body. Almost 50% of patients taking these medications are unable to tolerate them because of their adverse effects, and there is thus much interest in the development of a topical carbonic anhydrase inhibitor with the potential for fewer adverse effects. MK 507 is the most recent and most potent compound in the series of topically active carbonic anhydrase inhibitors.

Apraclonidine hydrochloride is a derivative of clonidine hydrochloride, an α2-adrenergic agonist. Clonidine has previously been shown to lower IOP significantly, but has the potential to produce marked lowering of both systolic and diastolic blood pressures. Its major ocular effect appears to be a decrease in aqueous production. The structural modification to apraclonidine decreases corneal absorption and the drug’s ability to cross the blood-brain barrier, minimising the risk of centrally mediated cardiovascular side effects.

Apraclonidine may also influence secondary avenues of aqueous outflow, such as uveoscleral outflow, and may also affect conjunctival and episcleral vascular flow. It produces a mean decrease in IOP of 25% for as long as 12 hours. Adverse effects include blanching of the conjunctiva, minimal mydriasis and eyelid retraction. This drug has been approved in the US for use in prevention of elevated IOP after argon laser trabeculoplasty and iridotomy, and has potential uses in preventing an IOP rise after YAG laser posterior capsulotomy and cataract surgery in patients already on other antiglaucomatous medications.

Lower doses of certain prostaglandins, especially PGF2α, have produced a dramatic IOP lowering effect. A 10 to 25% decrease in IOP can occur in humans at doses which are probably submaximal, with little or no evidence of intraocular inflammation. There is no effect on pupillary diameter or visual acuity; however, conjunctival hyperaemia, ocular irritation and a foreign body sensation have been noted. It is hoped that new drug analogues will eliminate these adverse effects. The primary mechanism of the ocular hypotensive action of prostaglandins is thought to be an increase in uveoscleral outflow.

Twice-daily doses of the isopropylester derivative of PGF2α (PGF2α-IE) for several days have the ability to consistently reduce IOP by 50 to 60%, to pressures of less than 10mm Hg in cynomolgus monkeys. Prostaglandins are thus the most powerful topical ocular hypotensive agents yet tested in subhuman primates. It remains to be seen whether maximal doses in humans will produce as dramatic an effect. If so, prostaglandin treatment could provide an alternative to surgery for very difficult patients in whom high-risk procedures are necessary in an attempt to achieve these very low IOPs.

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Authors and Affiliations

  1. University of South Florida, Tampa, Florida

    Lawrence M. Hurvitz

  2. Gulf Coast Glaucoma Clinic, Sarasota, Florida, USA

    Lawrence M. Hurvitz

  3. University of Wisconsin-Madison, Madison, Wisconsin, USA

    Paul L. Kaufman & Kathryn Crawford

  4. Johns Hopkins University, Baltimore, Maryland, USA

    Alan L. Robin

  5. University of California-San Diego, La Jolla, California, USA

    Robert N. Weinreb & Blake Shaw

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  1. Lawrence M. Hurvitz
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Hurvitz, L.M., Kaufman, P.L., Robin, A.L. et al. New Developments in the Drug Treatment of Glaucoma. Drugs 41, 514–532 (1991). https://doi.org/10.2165/00003495-199141040-00002

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