What is the role of medications in the treatment of primary open-angle glaucoma (POAG)?

Updated: Mar 16, 2020
  • Author: Kristin Schmid Biggerstaff, MD; Chief Editor: Inci Irak Dersu, MD, MPH  more...
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Answer

Current medical therapy is limited toward lowering IOP. A rational approach to choosing antiglaucoma medications should minimize the number of medications and the probability of significant adverse effects. The ideal drug for treatment of POAG should have the following characteristics: (1) effectively lower IOP, (2) no adverse effects or systemic exacerbation of disease, and (3) inexpensive with once-a-day dosing. However, because no medicine possesses all of the above, these qualities must be prioritized based on the patient's individual needs and risks; then, therapy should be chosen accordingly.

Once a medicine has been initiated, close follow-up care should be performed to assess its effect. Initial follow-up care should be performed 3-4 weeks after the beginning of therapy. IOP should be rechecked at the drug's peak and trough times to see if the target IOP has been reached and is maintained throughout the day. Look for signs of allergy (eg, hyperemia, skin rash, follicular reaction). Inform the patient of systemic adverse effects and symptoms that may occur. Treatment should be continued if a therapeutic trial has shown effective lowering of IOP without adverse effects. Reevaluation should be performed 2-4 months later depending on the clinical picture.

A monocular therapeutic trial should be considered when first initiating the medical therapy, as the other eye's IOP can be used as a baseline control to gauge effect of a medication (particularly useful in patients with a widely fluctuating diurnal curve). A difference of more than 4 mm Hg between the 2 eyes posttreatment is strongly suggestive of a clinical effect. However, some agents (especially beta-blockers) may have crossover effects on the other eye even with monocular treatment, so clinical correlation must be kept in mind. If monocular therapy is found to be effective, then initiation of binocular therapy may be considered.

Some medications (eg, latanoprost, brimonidine) may have an effect that plateaus at 6-8 weeks in certain patients; keep this effect in mind when scheduling further follow-up examinations. Other patients will be nonresponders to some therapies. If this occurs, the medication should be discontinued and a new drug initiated. While discontinuing or changing therapies, keep in mind that many drugs have a wash-out period of up to 2-4 weeks (especially beta-blockers), during which they may still have some IOP-lowering effect or residual systemic response.

If one medication is not adequate in reaching the target pressure, a second medication should be chosen that has a different mechanism of action, so that the 2 drug therapies will have an additive effect. (Usually, no additive effect is seen if 2 medications from the same drug class are used.)

The fixed-dose combination of a Rho-kinase inhibitor and a prostaglandin F2-alpha analogue (netarsudil/latanoprost) was approved by the FDA in 2019. Approval of netarsudil/latanoprost ophthalmic was based on two phase 3 trials, MERCURY 1 (n=718) and MERCURY 2 (n=750). The studies compared the mean IOP after 3 months of once-daily ophthalmic administration of netarsudil/latanoprost, netarsudil, or latanoprost. Patients who received the netarsudil/latanoprost combination achieved an average of 1-3 mm Hg lower mean IOP compared with netarsudil or latanoprost monotherapy. Nearly twice as many patients taking the combination achieved a diurnal IOP of 16 mm Hg or less, and nearly three times as many reached 14 mm Hg or lower compared with latanoprost. [23]

A specific plan of pharmacotherapy should be administered only after the possible effects of the systemic medications that a patient is taking (eg, beta-blockers, calcium channel blockers, ACE inhibitors) have been taken into consideration.

Before mention of particular medications currently used in most practices, note that as the mechanisms of axonal death by apoptosis are becoming better understood, therapies are being developed to protect nerve fibers from undergoing injury and death by several possible theoretical mechanisms. This halting of processes that is believed to contribute to ganglion cell death in glaucoma has been termed neuroprotection, and several new pharmaceuticals are being developed that hopefully will work in this manner. Agents currently under investigation as neuroprotective include glutamate receptor blockers, calcium channel blockers, inhibitors of nitric oxide synthase, free radical scavengers, and drugs to increase blood flow to the optic nerve.

See Ocular Hypertension and AAO monograph #13 for further in-depth descriptions of particular drugs.


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