Macular Degeneration 101

BrightFocus Foundation
“Macular Degeneration 101”

Transcript of Teleconference
December 17, 2014
1:00 – 2:00 p.m. EDT

Please note: BrightFocus Chats may be edited for clarity and brevity.

GUY EAKIN: Hello, everyone, and welcome to our monthly BrightFocus Chat presented by the BrightFocus Foundation. My name is Guy Eakin. I’m the Vice President of Scientific Affairs at BrightFocus.

Today we have a returning guest, Dr. Milam Brantley from Vanderbilt University. Milam is a clinician scientist, and I have to say that on the science side, some of his work has been supported through the BrightFocus Foundation. So, let’s welcome back Milam, who’s going to talk to us on the title of our conversation today, which is “Macular Degeneration 101.”

So, we’re going to be talking about what macular degeneration is and how do we treat it?

If you’d like to submit a question at any time during today’s call, please press *3 to submit your question to an operator. And if for some reason you’re disconnected from the call, I want to give you a number to call back in. That number is 877-229-8493. You’ll then be asked to punch in an ID code, which is 112435.

So, let’s just get started right off the bat. Milam, thank you so much for joining us today. And I’m going to start things off with a question that most of us have heard—that there are two forms of macular degeneration: a dry and a wet form. Within these categories we hear lots of other words. And so, if we’re talking to a clinician, we’re going to hear words like geographic atrophy or drusen. In fact, one of our listeners has already written in and asked, you know, for an explanation of what subfoveal choroidal neovascularization means. This is a huge alphabet soup.

So, could you walk us through the progression of a healthy eye toward advanced macular degeneration and maybe stop along the way to give us a definition of some of these more complicated words. And so, if we could start with the dry form … what’s happening to the patient’s eyes in that early dry form?

MILAM BRANTLEY: Sure. This is a really great question and actually I think the words “dry” and “wet,” while very useful, create a lot of confusion. I’d like to back up even just a little bit more and say I really like to think of and I like to talk to patients about AMD, age-related macular degeneration, as having early, intermediate, and advanced forms.

In the advanced forms, that’s where the vision loss can occur.

In the early form the patient probably doesn’t know they have it, and in the intermediate form, that’s when the patient may begin to have symptoms and the doctor definitely notices the changes are there and that there’s a risk for progression to the advanced form.

So, let’s talk about dry and wet for a second. First of all, let me say that the words have nothing to do with how the eye feels: My eye feels dry, my eye feels wet, it’s running water. Those things don’t have anything to do with AMD.

The term “wet” has to do with whether or not the vessels underneath the retina are leaking blood or fluid. Either one—either one makes it wet. And another term that is used for “wet” is neovascularization, and that simply means “new blood vessels.” So, the foundation of the “wet” expression of macular degeneration is that there are some abnormal blood vessels leaking blood or fluid.

So, now let’s back up. Early AMD—and this is, by definition, “dry” because you don’t have any of those abnormal vessels yet, or at least they’re not leaking fluid—early AMD shows, when we look in the back of the eye, we see the hallmark of AMD, which are called “drusen.” And drusen are one of those key words that maybe people have heard about before. And maybe you’ve seen pictures of the back of the eye, and these are little yellow spots; I call them waste deposits. So, the retina is very metabolically active and it makes lots and lots of waste products, and normally that’s just cleared out as a normal part of your everyday life and the layer underneath the retina, the retinal pigment epithelium, clears out those waste products. As we get older (and if we have certain risk factors that we can talk about later), we may be more susceptible to having those waste products not cleared out quite as well, and sometimes they end up as little deposits underneath the retina, between the retina and that layer underneath the retinal pigment epithelium.

We see those as these little yellow spots, and these are called “drusen.” They can be small, they could be medium, they could be large. Small drusen is what you find in early AMD. So, you can call it macular degeneration, but the risk of progressing—at least at that point over the next few years—is really small, and studies have shown that. If you have a few small drusen or even a lot of small drusen, you’re not very likely to progress to the advanced form in the next few years—5 to 7 to 10 years—and develop bad advanced AMD.

Now, let’s go to the intermediate stage. The intermediate stage is also dry, but now the drusen are bigger and perhaps there are more of them. If you’ve got a lot of middle-sized drusen or even a few large drusen, at that point it’s termed intermediate AMD. And now, really, you are at risk for progressing to the advanced form.

Now, the advanced form can be either dry or wet. Let’s talk about the dry form first. The dry form is called “geographic atrophy,” and that’s one of the key words that you mentioned. Why is it called that? Atrophy in a region: It means that there’s a region where the cells have died out. Atrophy just means without form or without shape. So, the retinal cells that used to be there doing all the work and seeing things for you have simply died away due to damage from AMD.

Why geographic? Because sometimes when you look in the back of the eye it looks a bit like a map. If you look at a picture of the retina, it may have a certain shape to it and you can easily draw or identify those areas of dead— where the cells have died, and we call that “geographic atrophy.”

In places where there is true atrophy we lose our ability in that spot. So if you have a small area of atrophy, you might have a small blank spot in your vision. If you have a large area of atrophy in the center, you may no longer be able to see people’s faces, to see the TV clearly, and that may be something that classifies you as legally blind if that is in both eyes. And again, all that is the dry form.

Now, the wet form. The wet is always advanced, and that’s again neovascular AMD for new blood vessels. That can simply be the leakage of these abnormal blood vessels leaking fluid, and usually that does not cause a blank spot but causes a distortion in the vision. So, you can think of that sort of like—Remember when we used to use cameras with film in them? So, say you’ve damaged the film by crinkling it up and it’s no long nice and flat and you took a picture. Well, that picture would be kind of wavy and distorted because the retina with fluid in it is wavy and distorted. Sometimes the fluid’s in the retina, sometimes it’s underneath it. Now, if those blood vessels bleed blood onto or into the retina, that also might be a spot that blocks your vision.

With wet macular degeneration, people usually notice a relatively sudden change in vision. Things were going along however, they were going along pretty well, and over the last week or two I don’t think I’m seeing as good in my right eye. That means that those vessels probably leaked blood or fluid some time recently. And that’s why we have patients look at their Amsler Grid or try to note if its straight lines remain straight.

So going back to kind of sum it all up, it’s a little bit tricky because wet is always advanced, whereas dry can be advanced and cause vision loss or it can be very mild forms of AMD. So it’s not simple to say, “Hurray, I’ve got the dry form!” Because that could be bad, but that could be not bad at all. And having the wet form is typically never a good sign.

I hope that helps to kind of sum things up, and I’ll be happy to expand on any of that.

GUY EAKIN: You know, you’ve laid this out for us in sort of a textbook format of, “Here’s the different stages of the disease and their definitions.” Maybe we could play a bit of a game and I’ll give you something that the patient sees and you can remind me of what’s causing it.

So you know, if I come in to you and I say I have a haziness to my vision, referring back to what you just said, what’s going to be the underlying—what’s the cause of that haziness?

MILAM BRANTLEY: Sure. And that can be a simple question, or it can be a very complicated question. But what I’m going to do first is I’m going to ask you a couple of questions. I’m going to say, “Well, how long has that haziness been going on? And is that haziness in one eye or both eyes? And is it there all the time or does it sometimes come and go?” And what I’m trying to do there is figure out if it’s a relatively new symptom that you’re having—something that happened suddenly—or something that’s happened gradually over a long period of time.

And I would encourage patients to pay particular attention if they think their vision is a little bit off…hmm…maybe even right down to when they notice the vision first being different and try to figure out if it’s just in my left eye or just my right eye by covering up one eye or the other and then the other. And also, making sure: Is this something that’s there all the time, or is it just there part of the time?

Because when I hear that story of haziness I’m trying to figure out if that’s something in the front part of the eye, like the cornea, that happened because of dry eye or if it’s something that’s in the lens because you have a cataract and that’s gotten worse over the last year since we saw you last, or if it’s something that came on very suddenly. Haziness to me usually points more toward the front of the eye in terms of dry eye or sudden—or cataract if over a long period of time; that certain word “haziness.”

GUY EAKIN: So if I—certainly many of our listeners will be familiar with black spots or holes, you know, in their vision which is a characteristic of AMD. You know, referring back to what you were saying earlier, what’s going on anatomically there that’s going to cause that black spot or that hole?

MILAM BRANTLEY: Sure.  This is something that can happen relatively suddenly, or it can be there for a long period of time. If you have a permanent black spot or a hole in your vision, that’s most likely—and if it’s related to AMD—that’s most likely due to what we talked about, the geographic atrophy. The cells have just died out in that small spot and your eye can’t see anything in that area anymore.

On the other hand, if last week everything was fine and then over the weekend you suddenly develop a spot in your vision, that could be from a bleed, and that could be the wet macular degeneration and that’s why it’s really important to try to get a handle on whether you suddenly notice something or if something changed… if something just kind of seems like it’s been that way for quite a while. That’s very helpful for the doctor to try to figure out what’s going on.

GUY EAKIN: Did I hear you correctly, that the new blood vessel or that wet form—if there are black spots or holes that are caused by that, that’s also what’s causing any smearing or distortion that somebody may be seeing?

MILAM BRANTLEY: Exactly. When I think of smearing or distortion—and what I mean by that is when I look at a straight line, when I look at a telephone pole, it’s wavy in the middle. Or if I look at lines on a book and print, the words are wavy. And certainly, if somebody has an Amsler Grid that they look at, those little squares are wavy. That really sounds to me like wet macular degeneration being caused by fluid leaking and making the retina uneven. Remember, I used the analogy of the film in the camera. The film is no longer nice and flat and straight to give you a good picture; it gives you a distorted picture.

GUY EAKIN: Well, I want to remind people that I don’t need to be the only one asking questions. So if you’d like to ask a question of our speaker today, you can do so by pressing *3 and that’ll take you over to an operator who will take down your question.

So we know that our ophthalmologist and optometrist will often prescribe a number of injections that might stop blood vessel growth or provide a recommendation for vitamins that might, in the dry form of the disease, prevent progression to the more advanced form. But if you ask a geneticist about the disease, they say—and we’ll read on the Internet or in literature that’s around the doctor’s office—that the genes that are involved in macular degeneration relate to our immune system. So, can you tell us what’s going on there? Is AMD an immune disorder?

MILAM BRANTLEY: Well, that’s a really good question. The answer is: kind of.

The first gene that was discovered to have an influence on AMD is something called “complement factor H.” Since then, several other complement genes have been found to be—little changes in these genes—have been found to be associated with AMD. And you notice I use the word “associated,” and I don’t use the word “cause” or “responsible for.” These are little changes in people’s genes that are very common. You might have it. I might have it. Maybe 30 or 40 or 50 percent of people have that specific change in complement factor H gene, but that doesn’t mean they necessarily will have AMD.

What we found is that it increases somebody’s risk for having AMD. Now, complement is actually—It’s a pathway that goes on throughout the body that helps protect us against foreign things like viruses and bacteria. So complement is, in fact, a part of our immune system and that’s involved with things like inflammation.

If you get a cold or if you have an infection on your finger, you’re going to recruit a bunch of white blood cells—part of your immune system—to fight that off and that’s a little area of inflammation, you know, it looks red on your skin.

Well, in the eye there are also inflammatory molecules and particles and some—the complement genes can be affected in a way that maybe increases the amount of inflammation in the eye or makes somebody’s eye a little bit more likely to succumb to toxins that are in the blood or in the atmosphere, such as smoking and that sort of thing. So, it’s not a straight-up immune disease like we think of if we think of rheumatoid arthritis or multiple sclerosis or something like that. What we’ve learned over the last 10–12 years is there is definitely an inflammatory component to it, so that looking at those layers of inflammation and part of the immune system has helped us figure out how, maybe, we can try to slow things down or stop them.

GUY EAKIN: I heard you mention smoking in there, and we see smoking comes up as a risk factor for macular degeneration all the time. Anything you read says, you know, smoking—

MILAM BRANTLEY: Absolutely.

GUY EAKIN: …may contribute to macular degeneration. So you know, it plays into the immune systems, you’re saying. So, is that is how it’s working? And is there anything known about how we might help people who have been smokers in the past, in terms of their risk for macular degeneration?

MILAM BRANTLEY: Sure. The word that we think of when we think of smoking is—well, we can call it “oxidation” or “reactive oxygen species.” Those are kind of fancy terms. But what that means is there are abnormal oxygen molecules that are found in cigarette smoke and in other things and they can cause damage to a number of different kinds of cells in the body.

So, a lot of the words that we do hear about are called “antioxidants.” This food or this vitamin may have antioxidant properties and, you know, in the AREDS formula, that’s the vitamin C and the vitamin E. Those are antioxidants and that helps clean up some of those damaging oxygen molecules.

Now, this is particularly important in the retina, because the retina is the most metabolically active tissue in the body. So just in its normal everyday work of seeing, it’s going to naturally produce a certain amount of oxygen molecules, and then when things come in on the top of that like smoking, the eye has to try to process all of that. And that’s why some of the AREDS vitamins and other eye vitamins that you may have heard about talk about antioxidants and how that can help. But really, when we’re thinking about smoking, we’re talking mostly about that kind of oxidation that we’re trying to prevent.

GUY EAKIN: And we hear antioxidants as being important in the context of aging, too, and aging is, of course, another risk factor for macular degeneration. It isn’t called age-related macular degeneration for nothing.

MILAM BRANTLEY: Right.

GUY EAKIN: So, am I correct in making that association, that these same antioxidant strategies or these same reactive oxygen species are kind of tied together? Smoking as a risk factor and age? Is that conclusive?

MILAM BRANTLEY: I think that’s really true. As all of us on the line know, the older we get a lot of things become a little bit more challenging and that happens to our cells, as well. When we’re 20 they have all sorts of abilities to fight off a cold or fight off these reactive oxygen species; to fight off any sort of thing that’s coming at us. And as we get older, that becomes a little bit more challenging. The machinery just doesn’t work as well as it used to.

So, that is a contributing factor. Now, not everybody who’s 85 gets macular degeneration—no way—but that aging process kind of makes us more susceptible to any sort of thing that would help cause damage to the retina, and smoking is a very specific thing that can cause damage to the retina. So, those things together start to add up and make it hard for us to fight it off.

GUY EAKIN: Well, I want to move the conversation a little bit. We’re talking about what macular degeneration is, but let’s talk about what we do, either in the clinic or in our own homes. And one of the things you’ve mentioned a couple of times is the role of an Amsler Grid in home monitoring of this disease.

Our organization gives out Amsler Grids; you can get them through our website or by asking on the phone. But if I go and collect a pile of them, I’m going to find that there’s lots of different flavors of Amsler Grids. There are some that are white with black lines; there are some that are black with white lines. You can find all different sizes of them, and I have found it very hard to find any studies out there that compare the different options. I was curious: From your standpoint as a clinician, what makes a good Amsler Grid and what makes a good user of an Amsler Grid?

MILAM BRANTLEY: That’s a great question. I don’t think, as least for general use, I don’t think there’s a huge difference in the black-on-white versus the white-on-black, and what makes a good Amsler Grid is one that’s being used. So, I’m appreciative that you guys have it on your website and have it available for people. I like for people to use their Amsler Grid. We give them away and we try to make sure that people look at them. It doesn’t do a lot of good if it sits in a drawer and never gets looked at.

You mentioned: what makes a good Amsler Grid user? And that’s somebody who looks regularly. Now, I’ll often tell somebody and kind of give them an estimation of how often I’d like for them to look. You know, some people have the Amsler Grids. I’m looking at one right now in my office that was on a—it’s a like a refrigerator magnet, and I’ve got it on a file cabinet here, but that’s a good way to put it on your fridge and look at it every day.

Now, if you’ve got a dark kitchen and you’re just kind of standing there, that’s not the best way to use it. The important thing about the Amsler Grid—the important things are these: Number one, that you’ve got your reading glasses on when you look at it. If you use those, that you’re looking at it at about 12 to 14 inches away; that you have plenty of light when you’re looking at it, and I prefer like a good light coming from behind your shoulder onto the grid so you can see it very clearly. And the most important thing is to cover one eye at a time, look with the right eye, look with the left eye, and see what you see.

And if you see wavy lines—that’s what we talked about, the smearing—that could be wet macular degeneration. If you see some of the areas of the grid are missing, if that’s something new, that needs to be reported to your doctor. But it’s just like any other kind of self-exam that doctors encourage patients to do. If you know you have macular degeneration, and you’ve looked at your Amsler Grid, and you know you have a spot in the upper-left corner where things are missing, and you know you have a tiny spot to the right of center, then that’s your baseline. And what you’re looking for are changes from your baseline to something new that needs to be reported to your doctor.

I like to tell people to look at it at least once a week. If somebody is at higher risk I might encourage them to look at it even more, but once a week and—you know—make it be part of your Monday morning routine, you know? Friday night’s not a good time to find out something’s wrong. Monday morning’s a good one because you call the doctor’s office and you can hopefully get an appointment soon. But the important thing is to know what your grid looks like on a normal basis so you can look and recognize a change.

GUY EAKIN: We have a number of questions coming in that relate to the injection.

MILAM BRANTLEY: Sure.

GUY EAKIN: There are questions about treatment for macular degeneration, but what are these drugs? How do they work? And then maybe we can address a couple of the callers’ questions. We’ll go through what drugs are available?

MILAM BRANTLEY: Sure. There basically are three drugs that are primarily used to treat wet AMD right now, and they are all variations of the same. They all have the same essential mechanism, and they are molecules that are against something called “vascular endothelial growth factor.” That’s a mouthful, and we call it VEGF, and VEGF is a normal part of the human body and it’s important to help us as we’re developing to grow appropriate blood vessels; it helps in blood vessel growth.

However, sometimes you can have a little bit too much VEGF, or a little bit too much VEGF in a certain place, like in the retina or near the retina and it can lead to—it can contribute to those new blood vessels that we talked about—that neovascularization.

The way that we’ve found that we can treat wet AMD is to inject with a tiny needle into the eye—and I’m sure many people on the line have had these injections—a small amount of this drug or one of these drugs and it can reduce the amount of VEGF in the eye and make those blood vessels shrivel up a little bit and maybe not leak anymore; that’s another important part of it.

Now, the three main things that are used,  just like most drugs, they have their trade name and they have a generic name.

So, some people may get the the first of the common three, which  was  approved by the FDA, and that is Lucentis.® And Lucentis® is also called ranibizumab.*

The other FDA-approved one that’s commonly used is Eylea® and that’s also known as aflibercept.

And the final one, which is probably used even the most, is called Avastin®, and that is also called bevacizumab.

Now, Avastin® is made by the same company as Lucentis® but it’s originally a colon cancer drug, and many people know that several years ago it was begun to be used off-label because it’s a cheaper version than the ranibizumab. And there have been many, many studies trying to compare the two.

There was a very large study sponsored by the National Eye Institute called the CATT trial—C-A-T-T—that essentially said: used in the same manner, whether that is monthly or on an injection as-needed basis, they functioned essentially similarly. So, there may be patients who respond better to one than the other, but one of those three drugs is typically what’s used these days.

A lot of patients get injections every month, some patients get injections every two months, some people get a series of injections to start out with, and then they’re brought back and they get injections when they need them. All of these things are routinely used in care of patients with wet AMD.

GUY EAKIN: So, we have one question that is, if I’m receiving a drug that isn’t on the list, what questions should I be asking my doctor if you’re receiving a treatment that wasn’t one of the ones that you described?

MILAM BRANTLEY: First of all, I’d be very surprised if you were and then I would—I think it’s just a very reasonable question: I’ve heard a lot about these anti-VEGF drugs—and you could even name those three that I talked about and say—why am I getting what you’re doing, instead of one of those drugs?

I think that will a rare thing but there may be a reason. There’s not a whole lot of reasons. You know, every once in a while you go…there’s a patient who just will not…will say, “I don’t want a needle. I don’t want an injection in my eye.” And then we try to do some other things. There was the cold laser, the PDP therapy; not as effective as these anti-VEGFs, but still used occasionally. So, I think it would be rare to not be getting one of those treatments. I think some steroid injections are used, but often in combination with one of these anti-VEGF molecules.

GUY EAKIN: So, we have three people—Francis from New York, Mary from Illinois and Geraldine from Pennsylvania—who are all asking similar questions. And, you know, they’re questions about how long do these injections last and do they last forever? So, you know, there’s sort of a couple of different ways of asking the question. You know, one is: how many times can you receive an injection? Is there a set number of times that you can…that you can actually have an injection into your eye?

MILAM BRANTLEY: That’s a great question. A lot of people ask that and the answer is that there’s no set number. The original trials—and the original trials were done with Lucentis®—the ANCHOR and MARINA trials looked at monthly injections for 2 years—24 months—and came to the conclusion that it was very effective. And then there have been some extension studies of that, which have gone out to 3 years. And then, other people have reported, “Well, gee, I’ve been injecting these people for 5 or 6 years and, look, they’re still doing well.”

There is a concern or…not because there’s been a whole lot of evidence but because if you’re injecting someone every month or 6 times a year, even, every 2 months, over a long period of time, you know, you wonder if that’s ever going to cause any damage to the retina. There hasn’t been a lot of evidence to say that it does, but it’s something that people are actively following to make sure that that doesn’t happen.

There’s always concern that once you start injecting someone, they might start being resistant to it. That hasn’t been a big issue, either, although there have been very small studies. And sometimes what you will see is patients who are started on one drug feel like they’ve kind of gotten to the best that they’re going to do with that drug. They might be switched to one of the other drugs because, as I said, sometimes one will work better than another for a specific person. We don’t exactly know why that is for an individual, but a lot of people are trying to study that as well. So, there’s no limits. I’ve had, you know, several people that have been getting monthly injections for several years.

GUY EAKIN: So, Dorothy from Maryland has a family member—her husband—who has dry macular degeneration and had been given samples of the vitamins from his retinal doctor and was told to check with the primary care doctor and ophthalmologist, and actually neither of those people was familiar with these vitamins. So when we hear about vitamins and dry macular degeneration, I think our thoughts kind of turn to the ARED, A-R-E-D, and ARED2 Trial. What are those and, you know, what should we be looking for on the label, and is that a bona fide therapy for dry macular degeneration?

MILAM BRANTLEY: Right. That’s a good question and it can also be very confusing for folks. When we talk about—you know, there’s certainly a treatment for wet macular degeneration, right? You have new blood vessels, you have vision loss, you get injections, and the hope is that that gets better; that’s treatment.

When you talk about treatment for dry AMD, you have to think of treatment in a different way. You think of treatment to prevent progression and the idea is that giving these antioxidants, along with the zinc, along with macular pigments—now lutein and the zeaxanthin—may help prevent the progression from that intermediate stage that we talked about early on to the advanced vision-threatening stage.

It’s tricky, because I know you and I have both been in the vitamin aisle at the grocery store or at WalMart—we’ve seen scores and scores of different eye vitamins. That makes it kind of complicated. It is not regulated in the same way as our prescription drugs are by the FDA, so people who think they have a good combination of vitamins can make a good vitamin and sell it, and that’s reasonable. The ones that—I mean, I will typically talk about the AREDS formulation because AREDS, the original study, looked at 5,000 people in a very well-designed study by the National Eye Institute. AREDS2 was a second complete from-scratch study with another several thousand people. And so, there’s large amounts of data that showed that these formulations will help reduce the risk of progressing to the advanced AMD.

Other people may say, well—you know, people come to me all the time and say, “Well, so-and-so my doctor said to try these.” They may be as good, but there’s not a large amount of evidence like there is for the AREDS. Now, the original AREDS formulation—it had vitamin C, vitamin E, it had zinc and copper to go along with the zinc, and it also had beta carotene. And that originally showed about a 25-percent reduction in progression at 5 years from the intermediate to the advanced AMD. It was also found along the way that there was a slight increase in lung cancer among smokers taking beta carotene. That came out in another study during AREDS. So, immediately they then began to offer a smokers’ formula, removing the beta carotene. And so, when the results were done several years later it was thought well, now there’s all this information about lutein and zeaxanthin and there are now commercially available macular pigments—pigments found in the macula of normal people—that seem to have a good reason to be helpful. And AREDS2 went about testing those instead of beta carotene, and so AREDS2 had a different formulation. It changed the amount of zinc and it replaced or it tested out lutein and zeaxanthin, instead of beta carotene or compared to, and it also tested out fish oil.

And the bottom line to the whole thing is that it looks like the best formula is one that still has the vitamin C and vitamin E, still has the zinc, replaces the beta carotene with lutein and zeaxanthin—and the fish oil didn’t seem to help much. So, they don’t have that in what they’re selling as the AREDS2 formula. It’s a little bit tricky. What was done for AREDS2 in the study is not the final formula that’s recommended by the study personnel at the National Eye Institute, but what I tell people to look for is the AREDS2 formula.

GUY EAKIN: There’s been an update in the AREDS2 news and it looks like sometimes items are going to the supermarket aisles that may not have exactly what AREDS2 specified as the formulation. And so, we put a write-up of that on our website just, I believe, yesterday. And anybody can go to our website or go to our Facebook page—you just use Facebook, you just put BrightFocus in the search bar—and you’ll find us or call us up. We’d be happy to send you a write-up of that if you’re curious about what you should actually be looking for in the formulation. But in general, you know, we just heard Dr. Brantley tell us to be looking for AREDS2, so the AREDS2 trial.

We’ve had a bunch of questions coming in about: what’s coming up in clinical trials, you know, including questions like the cell therapies, like these RPE transplants that are in clinical trials. We’re actually going to go and have a whole chat next month about what’s on the horizon in terms of research for macular degeneration; but in the meantime, is there anything, Dr. Brantley, that you think is particularly—that you have your eye on as something that you’re excited to see the data from?

MILAM BRANTLEY: Well, I think the important thing for patients to remember is that all of this stuff is a little bit down the road. Some of it has some certainly excellent potential. There are different formulations and different ways of delivering drugs. Wouldn’t it be nice to have a drop for wet macular degeneration, or a pill, so that you don’t have to get the injection? That’s a long way down the road, but people are working on that.

I think stem cells are an exciting thing and have the potential to work well for several different eye diseases, but also that’s down the road. I think, people—and rightfully so—these things get a lot of good press, and I think these are excellent research projects people are working on, but I think patients will see that and will tend to, you know, come to the office hoping to get stem cells that day. And we just have to remember that it’s a long process and it has to be done very carefully. It has to be done right.

So, companies are taking a cautious approach and an approach where they make sure that, when therapies are done, it doesn’t cause any damage and that it actually improves things for the patient, at a reasonable cost to everyone. So patience, as in most cases, patience is a virtue here and waiting for new things to come down the road. And in the meantime, you know, I’m thankful every day I’m in the clinic that we have the anti-VEGF medications, because just about the time I started in ophthalmology and in retina, you know, when someone came in with new wet macular degeneration, our response was often, “Gee, I’m really sorry about that. Let’s see how the scar heals up and I’ll see you back in a couple of months.” And it’s been wonderful to be able to offer improved vision for people, and I think that that will only continue in the future through these new efforts.

GUY EAKIN: Well, I certainly appreciate that sentiment. I do have to say on the subject of patience and longer horizons, I said we are going to have this talk about what’s on the horizon for clinical trials next month. That’s actually going to be in February. Next month we’ll be talking about driving safety and how we consider the subject of driving in the context of macular degeneration.

We probably have time for one more question. Judith from Arizona has written that she has a macular condition which her ophthalmologist is watching, and the ophthalmologist is putting off taking off cataracts as well as addressing the macular condition, and there’s sort of a process question. So, Judith says she doesn’t understand how the ophthalmologist can tell which condition is the more pressing one affecting her vision.

As a clinician, how do you address that question? When someone comes in with multiple conditions, how do you make the call of which one to treat first or do you ever go after them both at the same time?

MILAM BRANTLEY: That’s a very good question: it depends on what the macular condition is. Is it something that would require a surgery or is it like macular degeneration?

GUY EAKIN: Well, this is a macular.

MILAM BRANTLEY: Yeah, so…it’s a macular wet? I’m sorry?

GUY EAKIN: This is a macular pucker.

MILAM BRANTLEY: Oh, okay. So, perfect. So, a macular pucker: That’s a different thing from AMD and the treatment for macular pucker is, if it needs to be treated, is surgical. There’s now an injection that can kind of help sometimes with that; but a true macular pucker often involves a vitrectomy surgery.

There are ways to try to figure out how much someone’s cataract is affecting their vision in the office. They’re not fool-proof, but you may have been in the office and have seen somebody kind of shining a bright light at you or a RET on you and you’re still trying to read, trying to figure out how much that blurriness in your lens is causing your vision problem.

So having said that, there are some—there are limits—it’s a good question. A lot of times we don’t know exactly how much, on a percentage basis, a person’s decreased vision is due to the problem in the front of the eye, the cataract, versus the problem in the back of the eye. We can get, in this case, a macular pucker. We can do OCTs—and many of you have had those before—the optical coherence tomograph, that little thickness measurement of the retina, and that can give us an idea of what the architecture looks like for the macular pucker.

So if the pucker is mild and the cataract is mild, it’s reasonable to watch both, remembering of course that cataract surgery is a very routine thing. Most people end up having cataract surgery; it’s one of the most common surgeries done.

A macular pucker surgery, while routine for the surgeon, is a little bit more infrequently done and is a little bit bigger deal. So, when I’m faced with a patient that has a little bit of both of these issues, I’ll try to sort out the best I can how much is due to the cataract. If I can’t see to the back of the eye because the cataract is causing blurry vision both looking in and looking out, then the cataract is the—it’s easy to start with the cataract and then see what things look like with the pucker.

But if the view is crystal-clear for me or if it’s in a patient, you know, who hasn’t had cataracts or who hasn’t had cataract surgery and the view is clear, then that distortion is more likely to be because of the pucker.

And finally, in terms of symptoms, cataracts generally cause dimmed vision, blurred vision, dark haziness—those are words that people use—“yellow”…“things just aren’t as clear as they used to be.” And a macular pucker is more likely to cause distortion in vision. So, we talked about blurriness versus distorted. Things are clear, except they’re just kind of off to the side or wavy or something like that. So, that can help us figure out those things.

GUY EAKIN: Well, I certainly appreciate you for clearing that up and taking the time in general to talk to us today.

That’s about as much time as we have, and I wanted to just sort of recap. We went over a lot of things today on the call. We went over some of the anatomy and what’s going on in macular degeneration. We talked about risk factors that are associated with the disease but may not actually be causing the disease. Dr. Brantley clarified some very complicated words. We talked about treatments. We talked about these Amsler Grids.

And I guess what we’d like to know is: Is it helpful to everyone? So, we have the capability to actually do a poll on this call. If you—if you could press the numbers 1, 2, or 3, I’d appreciate it if you’d press the 1 if you found this topic very helpful today; 2 if you found the topic somewhat helpful; and 3 if you didn’t find the topic helpful at all and we have some work to do.

I do, again, want to thank Dr. Brantley for taking the time to speak with us today, and thank you to everyone who joined the call and asked us questions. Within about a week or so we’ll be posting a recording and a transcript of the call on our website. You can also listen to and download the past chats, as well as this one, on iTunes and SoundCloud.

Our next chat will be on driving safety and transportation alternatives, and that will be Wednesday, January 28, at 1 p.m. Eastern and 10 a.m. Pacific.

We certainly encourage you to register and submit questions in advance. And for anyone who’s registered on the call today, we’ll be sending you a reminder email about that chat topic. So in fact, you could actually register for the January call right now and request free materials from BrightFocus, like our Amsler Grid or our Macular Degeneration Essential Facts. And that’s by calling BrightFocus at 1-800-437-2423 or visiting our website at brightfocus.org.

Thank you to everyone, again, for joining us today and to Dr. Brantley for providing your expertise. And if you’d like to leave a comment after the call, just stay on the line. So, thank you from all of us at BrightFocus and have a great day and a very Happy New Year.

• BrightFocus Foundation website, www.brightfocus.org, or call us at 1-800-437-2423.
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