Reports

This report is based on medical evidence presented at sanctioned medical congress, from peer reviewed literature or opinion provided by a qualified healthcare practitioner. The consumption of the information contained within this report is intended for qualified Canadian healthcare practitioners only.

World Ophthalmology Congress 2006

São Paulo, Brazil / February 19-24, 2006

According to Dr. Harry Quigley, Director, Glaucoma Service, Wilmer Institute, Johns Hopkins University, Baltimore, Maryland, “For many years, open-angle glaucoma [OAG] was defined as a disease of elevated eye pressure, but now we believe that it is defined by optic neuropathy.” Leading specialists now define glaucoma as damage to the optic disc, observed in two ways. The first signal is an abnormal cup:disc ratio that is only present in 2.5% of the population. “If you combine it with a visual field defect criterion, which is also quantitative, it means that we finally have a way to say to each other that there is damage if there is a certain size cup and a certain visual field defect,” he told delegates.

Since intraocular pressure (IOP) has long stood as glaucoma’s defining characteristic, including for treatment, Dr. Quigley asked the rhetorical question, “Why have we removed IOP from the definition of glaucoma damage for OAG?” Studies that show that “many persons who have typical OAG have a normal level of eye pressure always,” he added, “so we should stop using this magic number of 21 [mm Hg] as a way of defining glaucoma.”

An Individual Target IOP for Each Patient

IOP is no longer part of the definition, but it remains an important factor, noted Dr. Quigley. “IOP does not define who has glaucoma, but it determines the severity of the disease and the progression rate,” he explained. “We now know from clinical trials that lowering the IOP works—that it slows the progression of the disease.”

Physicians need to analyze the appropriate IOP for each individual patient, noted Dr. Quigley. “The risk factor for OAG is not elevated eye pressure, it is the level of the eye pressure in the individual person,” he stated. “We must determine the baseline eye pressure at which the disease is occurring in each person and set a target pressure lower than that.” In this context, there is “no basis for the term ‘low-tension glaucoma’”—just different relevant IOPs for different patients. “The message today is that low-tension glaucoma is a dead issue,” he said. “We should be talking [only] about OAG.”

Dr. Paul F. Palmberg, Professor of Ophthalmology, University of Miami School of Medicine, Florida, went into greater depth about individualized IOPs. “When I made up this term ‘target pressure’ in 1989—not the concept, which goes way back, but the particular term—it meant your best guess of what pressure would be low enough to prevent pressure-dependent damage,” he said. Dr. Palmberg analyzed several studies related to target pressures. “After $100 million and six clinical trials, we now know that Dr. Paul Chandler was right in 1960,” he noted. Dr. Chandler had said that eyes with advanced glaucoma require a pressure below the normal average to be stable and that eyes with limited cupping confined to one pole of the disc could better withstand pressure. “Maybe 15 to 17 mm Hg is okay, as long as it is down about 30%. In eyes with high ocular hypertension, you could probably follow them up to a pressure of 30 mm Hg and do very well. Look at the disc and know how aggressive to be. How aggressive was the disease? You decide what you are going to do to match it,” Dr. Palmberg told delegates.

Determining Target Pressure

In determining an individualized target pressure, physicians should consider risk factors such as the amount of initial damage, age, family history of blindness and rate of progression. “If somebody developed five decibels of loss since you saw them last year, you might be more aggressive than you would in the case of somebody whose history you do not know,” suggested Dr. Palmberg, adding that physicians should take gradual steps to reach the patient’s individual target IOP. “I would encourage you to try to get the target pressure first by adding simple, safe measures,” he offered. “You may have to go on to surgery, but that is a complex decision of management and not just a case of simply choosing a target pressure.”

Studies on Blood Flow and Lowering IOP

Dr. Alon Harris, Director, Glaucoma Research and Diagnostic Center, Indiana University School of Medicine, Indianapolis, and colleagues are about to publish a paper in a major journal that demonstrates for the first time in humans the relationship between changes in blood flow created in different physiological setups and actual oxygen saturation. This helps make the case that “oximetry, the actual end product of blood flow changes, could have some clinical importance in the near future,” Dr. Harris explained.

He stressed that long-term studies are needed to prove the relationship of blood flow to visual function in glaucoma. However, he pointed to a promising seven-year post-diagnosis study in Europe that found that “patients with a stable visual field have higher diastolic velocities [and] lower resistance indices than patients with deteriorating fields. More important, the odds of visual field deterioration with a large resistance index of 0.78 or higher was about six times greater than that of patients with low resistance indices” (Galassi et al. Arch Ophthalmol 2003;121(12):1711-5).

During another presentation here during the scientific sessions, Dr. Colm O’Brien, Professor of Ophthalmology, consultant ophthalmic surgeon and investigator, University College Dublin and Mater Misericordiae Hospital, Dublin, Ireland, discussed a review of studies carried out over the last 15 years. “We now know that there is a significant association that tends to correlation between the blood flow and glaucoma damage,” he stated. “The problem with these studies is that they are cross-sectional and they did not address what comes first: is reduced ocular blood flow secondary to the damage, to the loss of nerve tissue or is it a primary event causing some of the nerve damage? That is the question we need to address.”

Dr. Harris reported that some treatments have been found to both lower IOP and independently enhance circulation. “One class that is clearly consistent is the carbonic anhydrase inhibitors [CAIs],” he noted. “That is not so curious because we have seen these results in the brain as well. The new data that we have is that the combination of CAIs with other products, such as beta blockers, lowered pressure as indicated and also maintained its blood flow effect.”

Dr. Cengaver Tamer, Mustafa Kemal University, Medical Faculty, Ophthalmology, Antakya, Turkey, and colleagues compared IOP readings over a 24-hour period after dorzolamide or timolol maleate were added to a treatment regimen for patients with primary OAG whose IOPs had not been lowered adequately under latanoprost monotherapy. Combinations of latanoprost/dorzolamide and latanoprost/timolol both appeared effective in lowering IOP, with a higher amount of reduction attributed to the former, “especially at night time, which is a very critical period for glaucoma patients,” concluded the investigators.