Uveitic Glaucoma Medication

Common anti-inflammatory treatment entails use of nonsteroidal anti-inflammatory drugs (eg, topical, systemic); corticosteroids (eg, topical, subconjunctival, systemic); and, rarely, immunosuppressive agents. Mydriatic-cycloplegic agents may be used to prevent or break posterior synechiae and to relieve pain and discomfort of ciliary muscle spasm. Available agents include atropine 1%, homatropine 1-5%, scopolamine, phenylephrine 2.5-10%, and tropicamide 0.5-1%.

Topical corticosteroids are effective in the control of anterior uveitis but vary in strength, ocular penetration, and adverse effect profile. Systemic corticosteroids are widely used for the management of posterior segment inflammation, which requires treatment, particularly when it is associated with systemic disease or when bilateral ocular disease is present. However, when ocular inflammation is unilateral, or is active in one eye only, local therapy has considerable advantages, and periocular injections of corticosteroid is a useful alternative to systemic medication and is very effective in controlling mild or moderate intraocular inflammation.

Many agents are available for lowering of IOP, including topical beta-blockers, adrenergic agents, and topical and systemic carbonic anhydrase inhibitors.

Miotics are avoided in uveitic glaucoma because of the risk of formation of posterior synechiae or a pupillary membrane. They also may increase inflammation by enhancing breakdown of the blood-aqueous barrier.

The role of prostaglandin analogs (PGAs) in uveitic glaucoma is unknown; PGAs have been used to help lower IOP in these often difficult to manage eyes. However, controversy exists concerning their use in uveitic patients owing to the theoretically higher risk of anterior uveitis, development of cystoid macular edema, and reactivation of herpes simplex keratitis. Little evidence suggests that PGAs disrupt the blood-aqueous barrier and only anecdotal evidence suggests an increased risk of these rare findings. PGA may be used in uveitic glaucoma if other topical treatments have not lowered IOP to the patient's target range.^[6]

Markomichelakis et al, reported that latanoprost was safe and equally effective compared with a fixed combination of dorzolamide and timolol in the treatment of uveitic glaucoma.^[7]

Class Summary

Lower IOP by decreasing the production of aqueous humor.

Carteolol 1% (Ocupress, Cartrol)

Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic effects.

Levobunolol 0.25% or 0.5% (Betagan, AKBeta)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production.

Class Summary

Lower IOP by decreasing aqueous production. Oral and topical forms are available.

Acetazolamide (Diamox)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP.

Methazolamide (Neptazane, GlaucTabs)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Dorzolamide 2% (Trusopt); Brinzolamide 1% (Azopt)

Both act by inhibition of carbonic anhydrase in the ciliary processes that decreases aqueous humor formation.

Class Summary

Lower IOP by a combination of decreasing production of aqueous and increasing aqueous outflow.

Apraclonidine (Iopidine)

Reduces IOP whether or not accompanied by glaucoma. Selective alpha-adrenergic agonist (alpha2) without significant local anesthetic activity. Has minimal cardiovascular effect.

Brimonidine (Alphagan)

Selective alpha2-receptor that reduces aqueous humor formation and possibly increases uveoscleral outflow.

Class Summary

Lower IOP by increasing aqueous outflow.

Latanoprost 0.005% (Xalatan)

Decreases IOP by increasing outflow of aqueous humor.

Bimatoprost ophthalmic solution (Lumigan)

A prostamide analogue with ocular hypotensive activity. Mimics the IOP-lowering activity of prostamides via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension. Now with BAK-free formulation called travoprost-Z.

Class Summary

Have analgesic and anti-inflammatory activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms also may exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ketorolac tromethamine 0.5% (Acular)

The mechanism of action is believed to be due, in part, to its ability to inhibit prostaglandin biosynthesis.

Diclofenac ophthalmic (Voltaren)

Believed to inhibit cyclooxygenase, which is essential in the biosynthesis of prostaglandins.

Class Summary

Treatment of ocular inflammation.

Prednisolone acetate 1% (Pred Forte)

Inhibits the edema, fibrin deposition, capillary dilation, and phagocytic migration of the acute inflammatory response and capillary proliferation. Causes the induction of phospholipase A-2 inhibitory proteins.

Fluorometholone 0.1% (FML)

Believed to act by the induction of phospholipase A-2 inhibitory proteins. Shows a lower propensity to increase IOP than dexamethasone in clinical studies.

Nepafenac ophthalmic suspension (Nevanac)

Nonsteroidal anti-inflammatory prodrug for ophthalmic use. Following administration, converted by ocular tissue hydrolases to amfenac, an NSAID. Inhibits prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production. Indicated for treatment of pain and inflammation associated with cataract surgery.

Bromfenac ophthalmic solution (Xibrom)

Nonsteroidal anti-inflammatory drug for ophthalmic use. Blocks prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. Indicated to treat postoperative inflammation and reduce ocular pain after cataract extraction.

Difluprednate ophthalmic emulsion (Durezol)

Ophthalmic corticosteroid indicated for inflammation and pain associated with ocular surgery. Available as a 0.05% ophthalmic emulsion.

Brimonidine tartrate, timolol maleate ophthalmic solution (Combigan)

Selective alpha-2 adrenergic receptor agonist with a nonselective beta-adrenergic receptor inhibitor. Each of them decreases elevated IOP, whether or not associated with glaucoma.

Dorzolamide hydrochloride-timolol maleate (Cosopt)

Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.

Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility.

Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.