While glaucoma management at times seems hopelessly complex, I like to remind myself that we currently have but one target for the treatment of glaucoma: intraocular pressure (IOP). While we have a variety of other risk factors that are associated with glaucoma progression, only the modification of IOP has been shown experimentally to slow or stop glaucoma.

Other potentially modifiable risk factors for glaucoma include ocular perfusion pressure (blood pressure minus IOP), cerebrospinal  fluid pressure, corneal thickness, and corneal hysteresis. But we don’t have data to show that if we modify those factors, independent of IOP,  glaucoma progression will slow.  Personally, when managing glaucoma I currently target IOP only. While I pay attention to other risk factors, I do not change my treatment in an attempt to affect them.

Neuroprotection in glaucoma is defined as a treatment that protects the optic nerve without going through the primary mechanism of lowering IOP.

We currently have no proven neuroprotective agents for glaucoma. A few contenders have been identified. Memantine, the NMDA antagonist, was studied in a phase 3 clinical trial  but did not meet its primary endpoint. Brimonidine has been suggested to have neuroprotective qualities, but the medication additionally lowers intraocular pressure, making the study of this topic complex. One proposed neuroprotective approach has been the HMG Co-A reductase medication class, also known as the statins.  While it is not entirely clear why this class of medications would be neuroprotective, supporting evidence has come from several observational studies.

David C. Musch, PhD, MPH, and Joshua D. Stein, MD, MS have designed a prospective randomized trial investigating the role of statins in reducing  the progression of glaucoma.  Recently, along with co-author Nidhi Talwar, MA, they interrogated a Medicare database that contained claims information on more than 500 000 patients with hypercholesterolemia. The authors reported that the odds of a primary open-angle glaucoma diagnosis decreased by about 1% for every 3 months of statin consumption.  After 2 years of continuous statin consumption, the risk of glaucoma was reduced by 8%.   In a second study the authors sought to understand if the type of statin used or the magnitude of the statin dose impacted glaucoma risk.  A 40-mg dose of atorvastatin (the most commonly prescribed  statin) was as effective  as a high 80-mg dose.

The good news is that moderate doses of commonly used, generic, and inexpensive statins seem to be protective against glaucoma. We cannot be sure the association is explained by confounders but look forward to a randomized trial on patients who do not have hypercholesterolemia. Additionally, we don’t yet know if statins protect against the development of glaucoma or its progression, although most risk factors work the same for both.  I am hopeful that the prospective randomized trial proposed by Drs Stein and Musch investigating the role of statins in slowing glaucoma will be funded, and that we may learn the results in due time.






















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