Systemic Medications and Glaucoma

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Article initiated by:
Fabliha A. Mukit, M.D.
All contributors:
Brian T. Fowler, MD, Emily Y. Kim, Fabliha A. Mukit, M.D., Muhammad Elahi, Hamza Jalal, Jodi Southerland, Jonathan Glaze, Daniel B. Moore, MD, Fabliha A. Mukit, M.D., Shivani Kamat, MD
Assigned editor:
Shivani Kamat, MD
Review:
Assigned status Up to Date
 by Shivani Kamat, MD on April 20, 2024.


Introduction

Glaucoma is an ongoing health concern as its prevalence continues to rise. There are two main types of glaucoma: open angle and closed angle, or angle closure, glaucoma. In the United States, more than 80% of people with glaucoma have an open angle, however angle closure glaucoma contributes to a more severe and aggressive vision loss. Both types of glaucoma can be further classified into primary or secondary glaucoma. Secondary causes of glaucoma include medications, systemic inflammation, intraocular and systemic tumors, and other contributing systemic conditions such as diabetes[1] and hypertension.[2] Glaucoma presents with irreversible vision loss typically affecting peripheral vision first due to optic nerve damage from elevated intraocular pressure. This is most often due to impaired drainage of aqueous humor through the trabecular meshwork.[3] Due to the presence of other chronic comorbidities in patients with glaucoma, it is necessary to assess the effect of systemic medications on glaucoma and intraocular pressure.[2]

Healthcare Burden of Glaucoma

There is a significant cost associated with caring for patients with glaucoma, mainly due to the high prevalence of POAG in the United States. Studies have estimated the cost per patient ranges between $623 to $3,000 per year. This depends on disease progression and the functional burden on patients with glaucoma.[4] [5] Severe and advanced glaucoma have a congruent rise in healthcare burden. Patients with glaucoma are at greater risk for falls and loss of productivity, requiring a more significant overall cost and burden on the healthcare system.[5][6]The total economic burden of glaucoma in the US is estimated at $2.9 billion.[6] Due to this, preventative measures in glaucoma patients can have a significant impact on healthcare costs.

Epidemiology

Globally, it is estimated that by 2040, more than 110 million people will suffer from glaucoma around the world, and the prevalence of POAG is around 2.4%.[7][5][8] It is estimated that 69 million people worldwide are diagnosed with POAG and 17 million people worldwide have primary angle-closure glaucoma (PACG).[2][9] [10]There is an extensive list of known potential risk factors for glaucoma. Cardiovascular conditions are reported to be associated with glaucoma. Studies have shown there is an additional 5% increased risk of developing glaucoma per year after a diagnosis of diabetes.[11] This indicates the significant risk and co-occurrence of type 2 diabetes, obesity, and cigarette smoking with POAG.[12][13] [14][15][16] Association between hyper- or hypo- tension and glaucoma has also been reported. Certain classes of medications, such as cholinergic, anti-depressants, sulfa-based drugs, steroids, and sympathomimetics, which are used to treat systemic conditions, are known to cause acute angle closure glaucoma.[2] Common risk factors of glaucoma are listed below.

Risk Factors
  • Age (more than 60)
  • African American
  • Family history of Glaucoma
  • Diabetes
  • Hypertension
  • High myopia
  • Elevated intraocular pressure (ocular hypertension)

[8][17][18][19]

Pathophysiology of Glaucoma

Primary Open Angle Glaucoma (POAG) causes damage to the retinal ganglion cell (RGC) axons due to poorly controlled intraocular pressure from reduced aqueous humor outflow. The threshold for retinal ganglion cell damage from IOP is individual-dependent; however, injury to RGCs causes an impediment to axoplasmic transport (resulting in poor cell nutrition and removal of toxins), reduced ocular hypoperfusion, and a resultant cupped optic nerve head. This presents clinically as peripheral to central visual field loss.[20]

Medications that Increase the Risk of Glaucoma

Corticosteroids

Ocular Impact

Corticosteroids affect the trabecular meshwork by increasing the resistance of aqueous humor outflow.[21][22] Corticosteroids are known to reduce the expression of matrix metalloproteinases (MMP) 2 and 9 in the trabecular meshwork. MMPs are enzymes that degrade extracellular matrix proteins. This causes increased resistance in the structures of the TM, preventing aqueous humor outflow and conversely, leading to increased IOP. This can lead to steroid-induced glaucoma or secondary open-angle glaucoma. Interestingly, increased MMP-9 activity can also use can cause mechanical changes in the microstructure of the TM via the formation of cross-linked actin networks, enhanced myocilin and fibronectin expressions, and extracellular matrix deposition in the trabecular meshwork. Together, this can further increase resistance of aqueous humor outflow.[23]

Effect on IOP

Corticosteroid use is known to increase IOP and increase the risk of glaucoma, especially in patients with a family history of OAG.[21] IOP tends to show signs of elevation within 3-6 weeks following initiation of corticosteroids, and studies have shown that IOP tends to normalize within a month's time after discontinuation of corticosteroids. Chronic steroid use is more concerning, as long-term usage could result in permanent IOP elevation.

Sulfonamides

Ocular Impact

Sulfonamide-containing drugs are known to induce acute angle closure glaucoma (AACG). The proposed mechanism of action entails thickening and displacement of the lens-iris diaphragm, or anterior ciliary body rotation due to ciliary body edema.[21] There is a broad category of sulfonamide-containing drugs, including antibiotics, diuretics, anti-inflammatory drugs, and anti-epileptics.

Effect on IOP

Some medications within this category known to acutely elevate IOP include Topiramate, with IOP normalizing following medication cessation.[21][24] Some diuretic medications, such as acetazolamide and methazolamide, are used to decrease IOP, however, for patients with sulfonamide induced AACG, these medications are typically avoided.

Anticholinergics

Ocular Impact

Anticholinergics are implicated in causing an increased risk of AACG.[25][26] The mechanism involves inhibition of muscarinic receptors in the iris, which leads to closure of the iridocorneal angle.[27] Topical anticholinergics are more commonly implicated, with intravenous and oral medications carrying a much lower risk.[21]

Effect on IOP

Compared to other medications that increase the risk of glaucoma, anticholinergics seem to have a more blunted effect on IOP.[27][28] Mydriasis can cause pupillary block with anterior displacement of the iris and obstruction of the trabecular meshwork, resulting in acute elevation of IOP.

Anticoagulants

Ocular Impact

Patients taking anticoagulants are at increased risk of developing a spontaneous suprachoroidal hemorrhage leading to an acute angle closure crisis. A spontaneous suprachoroidal hemorrhage can detach choroid and retina, which can mechanically displace the lens-iris diaphragm forward, closing access to the trabecular meshwork.[21]

Effect on IOP

Suprachoroidal hemorrhage with resultant angle closure can increase IOP. IOP can be lowered by either taking topical aqueous suppressants and oral carbonic anhydrase inhibitors. In elderly patients with multiple risk factors, discontinuation of the anticoagulant may be necessary.

Medications that Decrease the Risk of Glaucoma

Beta blockers

Ocular impact

Beta blockers are primarily used for their antihypertensive and anti-arrhythmic properties. These medications can be non-selective (targets beta 1 and beta 2 receptors) or selective (target beta 1 or beta 2).[21] Beta-blockers inhibit sympathetic receptors in the ciliary epithelium, causing reduction in aqueous humor production.[29]

Effect on IOP

The synergistic effects of beta blockers on IOP control have been cited since 1967. A study from the Manchester Royal Eye Hospital in 1967 reported that systemic beta blocker usage led to decreases in IOP in multiple patient cases.[30] A large population study from the UK found that glaucoma patients on oral beta blockers were found to have IOP around 1 mmHg lower than other patients.[31] This study and similar studies led to the development of topical beta blocker eye drops for the treatment of glaucoma. Furthermore, it was found that nonselective beta blockers were more efficacious in lowering IOP than cardioselective beta blockers.[32][33]

Metformin

Ocular impact

Metformin is the first-line medication for Type 2 Diabetes. It works in a systemically synergistic mechanism by increasing insulin sensitivity (increased ability to use available glucose in the blood for glycolysis and the Kreb’s cycle) thereby decreasing glucose production in the liver, and decreasing glucose absorption in the intestines.[34][35] In the eye, it has been found to protect against mitochondrial dysfunction, prevent fibrosis, reduce angiogenesis and inflammation.[36][37][38]

Effect on IOP

Metformin has been shown to have positive clinical outcomes in glaucoma patients.[39] One study found that patients on metformin for diabetes mellitus showed a 25% reduction in the risk of OAG compared to those without metformin.[40] This protective effect could be from improved vascular health from better glycemic control, however other hypoglycemic medications (sulfonylureas, thiazolidinediones, meglitinides, and insulin) did not show any role against OAG.[41] Additionally, there is also a report that metformin use does not reduce the risk of OAG progression. Therefore, additional studies may be warranted to further establish the role of Metformin in OAG management.[42] [21]

Statins

Ocular Impact

Statins are first-line therapy for treating hyperlipidemia. They lower lipid levels by inhibiting HMG-CoA reductase, which plays a key role in cholesterol production. Due to this cholesterol-lowering property, statins are frequently used to decrease the risk of cerebrovascular and cardiovascular disease. Similarly, statins were shown to have neuroprotective effects by protecting retinal ganglion cells from optic nerve injury and reducing apoptosis in the retina.[43][44]

Statins have been associated with a lowered risk of developing OAG and normal tension glaucoma.[45][46][47][48][49] One theory postulates that statins upregulate endothelial nitric oxide synthase (eNOS), which leads to an increase in nitric oxide. Consequent vasodilation and enhanced perfusion to the retina were found to protect the optic nerve and retinal nerve fiber layer.[50] Another study showed that the risk of OAG was 8% lower in subjects after 2 years of therapy compared to subjects not on statin therapy.[46]

Effect on IOP

Statins may reduce the IOP by increasing aqueous outflow.[51] However, two studies reported no significant association between statin use and IOP. Other studies demonstrated that statin could potentially cause increased IOP.[52][53] Further investigation on the effects of statin on IOP is warranted.

Hormone replacement

Ocular Impact

Hormone replacement therapy (HRT) is commonly used in postmenopausal women to counter the vasomotor and genitourinary symptoms of menopause by increasing estrogen levels.[54] However, the use of HRT, especially estrogen-only, was found to increase the risk of dry eye syndrome.[55]

Because of the presence of estrogen receptors on retinal ganglion cells, estrogen has been found to play a protective role in glaucoma pathogenesis. Multiple studies report that decreased lifetime estrogen exposure could potentially increase the risk of glaucoma. The Rotterdam Study found that women with early menopause (before 45 years of age) had a higher risk of developing OAG.[56] The Blue Mountains Eye Study found that menarche after the age of 13 resulted in significant increases in the risk of developing OAG.[57]

Effect on IOP

A number of studies have found that HRT, particularly estrogen, in post-menopausal women may have an effect on lowering IOP. One study reported that post-menopausal women on estrogen-only therapy showed a small but significant IOP reduction of 0.5 mmHg.[58] Estrogen’s effect on nitric oxide production can induce vasodilation, which is important for IOP regulation. Another theory is that estrogen activates collagen fiber production at the lamina cribrosa, a structure in the optic nerve head, and improves the compliance of the structure. This can enhance the flexibility of the eye, thus decreasing IOP.[59] However, the mechanism of estrogen’s effect on IOP continues to evolve and additional investigation is necessary.

Cannabinoids

Ocular Impact

Cannabinoid drugs are psychoactive compounds that have medical uses in the treatment of nausea, chemotherapy, neuropathy, and spasticity. They act on the CB-1 and CB-2 receptors in the central nervous system. CB-1 receptors are also found in ciliary epithelium, trabecular meshwork, and Schlemm’s canal.[60] Cannabinoids have a potential vasodilatory effect on the blood vessels of the anterior uvea. Furthermore, many studies reported the neuroprotective action of cannabinoids on the optic nerve in animal studies.[61]

Effect on IOP

Immunofluorescence studies have repeatedly demonstrated that cannabinoids can lower IOP by increasing aqueous humor outflow or decreasing aqueous humor production when they bind to the CB-1 receptors in the ciliary and trabecular receptors.[62]Additionally, its vasodilatory effect on the blood vessels of the anterior uvea has been hypothesized to increase uveoscleral outflow.[61] However, this effect has a short duration of action and may come with neurological and cardiovascular side effects as well as potential ophthalmic side effects. Hence, the American Glaucoma Society cautioned against the use of cannabinoids for glaucoma management.[63]

Medications with Conflicted Reports on Glaucoma

Calcium channel blockers

Ocular Impact

Calcium channel blockers (CCBs) target calcium receptors on myocardium, vascular smooth muscle, and adrenal cortex, and also provide anti-arrhythmic and antihypertensive effects. Some studies have suggested that CCBs may have acute ocular hypotensive effect [64][65] and vasodilation effect, increasing perfusion to organs including the optic nerve head and choroid.[66][67][68] CCBs may also cause relaxation of trabecular meshwork.[69]

Effect on IOP

Studies have found contradictory effects of CCBs on IOP. In vitro analysis has shown that the blockade of calcium channels reduces extracellular matrix proliferation in lamina cribrosa cells.[70] This causes a relaxing effect on trabecular meshwork formation which leads to an increase in outflow of aqueous humor and lower IOP.[69] However, other studies have found that CCBs have led to increased IOP. One study by Zheng et al found that glaucoma patients on CCBs, particularly amlodipine, were 26% more likely to require filtration surgery compared to other patients when controlling for other factors.[71]Another study found that patients who had exposure to CCBs were 1.8 times more likely to develop OAG.[72]

Antidepressants

Ocular Impact

Antidepressants increase the availability of neurotransmitters such as serotonin, norepinephrine, and dopamine in the synaptic cleft by preventing their re-uptake. Selective serotonin reuptake inhibitors (SSRIs), particularly, were shown to have potential vascular side effects by inducing vasospasm in the optic nerve, suggesting that increased serotonin levels may be a factor in the development of ocular and/or optic nerve perfusion disorders.[73] Furthermore, the susceptibility to perfusion/ischemic disorders of the retina and optic nerve head increases in atherosclerotic individuals due to enhanced serotonin release during platelet aggregation on an atherosclerotic plaque.[74][75]

Effect on IOP

There are conflicting reports on the effect of antidepressants on IOP. SSRIs and Bupropion (dopamine and norepinephrine reuptake inhibitors) have been found to be beneficial for IOP management. Zheng et al. found that POAG patients on SSRIs were 30% less likely to require filtration surgery.[71] Another study reported that patients on bupropion therapy for over a year had a 90% decreased chance of being diagnosed with glaucoma.[76]

Contrary to the studies above, antidepressants and serotonergic medications are also reported to increase the risk of AACG through pupillary block. They can also cause mydriasis and IOP elevation from increased production of aqueous humor.[27] Some studies have shown a more than five-fold increased risk of AACG in patients taking SSRIs daily, with elderly female patients at the greatest risk.[77] There is inconclusive evidence regarding the decreased risk of OAG for patients taking serotonergic medications, with some studies indicating a benefit while others suggesting no association between SSRI and OAG.[71][78]Therefore, SSRIs and other antidepressant medications should generally be cautioned for use in patients at risk of developing AACG.

Adrenergic

Ocular Impact

Adrenergic medications are known to increase the risk of AACG.[21] The mechanism of action depends on whether they are acting on alpha or beta receptors; however, it generally involves a combination of ciliary muscle relaxation, increased aqueous humor production, and mydriasis.

Effect on IOP

Increased aqueous production coupled with mydriasis can cause elevated IOP. However, some studies indicate that certain beta-adrenergic agonists, such as salbutamol, may result in a net decrease in IOP due to its secondary effects on increased uveoscleral outflow.[27] Contrary to this finding, nebulized albuterol, a beta-2 adrenergic agonist, can cause pupil dilation and subsequently exacerbate AACG. Nebulized albuterol can act on the beta-2 adrenergic receptors in ciliary bodies, which promotes aqueous humor production, thus increasing IOP. Wearing protective goggles during albuterol nebulizer treatment has been showed to mitigate the increase in IOP.[79]

The evidence remains inconclusive, so physicians should take caution when prescribing adrenergic medications to patients with other pre-existing risk factors for AACG.

Cholinergic

Ocular Impact

Cholinergic receptors are found in multiple structures of the eye. Cholinergic agonists predominantly bind directly to the muscarinic M3 cholinoceptors in the eye. This causes contraction of the iris sphincter muscles, the ciliary muscles, and trabecular meshwork. When they act on the muscarinic receptors in the conjunctiva, they stimulate goblet cell secretion contributing to the protective tear film. Similarly, when they bind to those receptors in the retina, the neuronal firing in retinal ganglion cells is altered.[80]

Effect on IOP

Due to the mechanisms of action previously discussed (see “Cholinergic Ocular Impact section”) cholinergic agonists (acetylcholine, carbachol, echothiopate Iodide, and pilocarpine), are widely used in glaucoma management. However, there are reports of cases in which these cholinergic agents may worsen AACG. Miotic agents such as pilocarpine can worsen pupillary block by intensifying the contact between the iris and lens.[27] Careful medication management is warranted in patients with risk factors for AACG or OAG.

Advantages of Systemic Medications in Glaucoma Management

Given the frequent co-occurrence of glaucoma with other systemic diseases, it is critical to understand how other medications can positively or negatively affect glaucoma management. This will help to better serve patients and manage their IOP more efficaciously. It will also help in educating patients about eye disease and proactively screening for glaucoma.

Disadvantages of Systemic Medications in Glaucoma Management

There are no significant disadvantages with researching how systemic medications can affect IOP. Eye care providers and primary care providers need to know and educate their patients on the side effects of systemic therapies.

Limitations

Most of the studies cited in this review are epidemiological, which can be subject to bias, limitations, and generalizations. More clinical studies and randomized control trials are needed to provide precise and bias-free data.

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  2. ↑ 2.0 2.1 2.2 2.3 Hsu E, Desai M. Glaucoma and Systemic Disease. Life (Basel). 2023 Apr 15;13(4):1018. doi: 10.3390/life13041018. PMID: 37109547; PMCID: PMC10143901.
  3. ↑ Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363(9422):1711-1720. doi:10.1016/S0140-6736(04)16257-0. Accessed [04/06/2024].
  4. ↑ Varma R, Lee PP, Goldberg I, Kotak S. An assessment of the health and economic burdens of glaucoma. Am J Ophthalmol. 2011;152(4):515-522. doi:10.1016/j.ajo.2011.06.004. Accessed [04/06/2024].
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  20. ↑ Hurley DJ, Irnaten M, O’Brien C. Metformin and Glaucoma—Review of Anti-Fibrotic Processes and Bioenergetics. Cells. 2021; 10(8):2131. https://doi.org/10.3390/cells10082131. Accessed [04/06/2024].
  21. ↑ 21.0 21.1 21.2 21.3 21.4 21.5 21.6 21.7 21.8 Wu A, Khawaja AP, Pasquale LR, Stein JD. A review of systemic medications that may modulate the risk of glaucoma. Eye (Lond). 2020;34(1):12-28. doi:10.1038/s41433-019-0603-z. Accessed [04/06/2024].
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  32. ↑ van der Valk, R., Webers, C. A., Schouten, J. S., Zeegers, M. P., Hendrikse, F., & Prins, M. H. (2005). Intraocular pressure-lowering effects of all commonly used glaucoma drugs: a meta-analysis of randomized clinical trials. Ophthalmology, 112(7), 1177–1185. https://doi.org/10.1016/j.ophtha.2005.01.042. Accessed [04/06/2024].
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  35. ↑ Food and Drug Administration. Glumetza TM, 500 mg (metformin hydrochloride extended release tablets) tablet, film coated, extended release. Access Data, Food and Drug Administration. https://www.accessdata.fda.gov/drugsatfda_docs/label/2006/021748s002lbl.pdf. Accessed [04/06/2024].  
  36. ↑ Hurley DJ, Irnaten M, O’Brien C. Metformin and Glaucoma—Review of Anti-Fibrotic Processes and Bioenergetics. Cells. 2021; 10(8):2131. https://doi.org/10.3390/cells10082131. Accessed [04/06/2024].
  37. ↑ Scott RA, Langenberg C, et al. The link between family history and risk of type 2 diabetes is not explained by anthropometric, lifestyle or genetic risk factors: the EPIC-InterAct study. Diabetologia. 2013;56(1):60-69. doi:10.1007/s00125-012-2715-x Accessed [04/06/2024].
  38. ↑ Li X, Leng Y, Jiang Q, et al. Eye Drops of Metformin Prevents Fibrosis After Glaucoma Filtration Surgery in Rats via Activating AMPK/Nrf2 Signaling Pathway. Front Pharmacol. 2020;11:1038. Published 2020 Jul 31. doi:10.3389/fphar.2020.01038. Accessed [04/06/2024].
  39. ↑ Maleškić S, Kusturica J, Gušić E, et al. Metformin use associated with protective effects for ocular complications in patients with type 2 diabetes - observational study. Acta Med Acad. 2017;46(2):116-123. doi:10.5644/ama2006-124.196. Accessed [04/06/2024].
  40. ↑ Lin HC, Stein JD, Nan B, et al. Association of Geroprotective Effects of Metformin and Risk of Open-Angle Glaucoma in Persons With Diabetes Mellitus. JAMA Ophthalmol. 2015;133(8):915-923. doi:10.1001/jamaophthalmol.2015.1440. Accessed [04/06/2024].
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  57. ↑ Lee AJ, Mitchell P, Rochtchina E, Healey PR. Female reproductive factors and open angle glaucoma: the Blue Mountains Eye Study. Br J Ophthalmol. 2003;87:1324–8.
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