January 8, 2025 • 22 mins
For decades now, we have been able to offer anti-VEGF treatments to patients with wet AMD. Yet for dry AMD, there have been few options we can recommend to our patients outside of AREDS formulations and lifestyle modifications. But with newer scientific advances, there are indeed new classes of injectable medications that are now being offered to some patients wtih dry AMD. Retinal specialist Dr. Ashkan Abbey joins the podcast to share the latest research.
This episode is sponsored by Thea Pharma Canada - https://www.theapharma.ca
Become a supporter of this podcast: https://www.spreaker.com/podcast/blind-spot-the-eye-doctor-s-podcast--5819306/support.
This episode is sponsored by Thea Pharma Canada - https://www.theapharma.ca
Become a supporter of this podcast: https://www.spreaker.com/podcast/blind-spot-the-eye-doctor-s-podcast--5819306/support.
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:11):
Hey everybody, I'm zaeo Mednik and welcome to another episode
of Blindspot. This episode is sponsored by THEA Pharma Canada.
THEA pharm of Canada is the Canadian subsidiary of THEA,
Europe's leading pioneering and innovative eye health brand. Founded in
nineteen ninety four by Henri Chibre. With five generations of history,
the Chibret family has been dedicated to I care for
(00:32):
more than one hundred and fifty years. Their commitment to
improving lives is born of their pioneering spirit. They continue
to lead the worldwide preservative free movement in eye care.
They've created innovative delivery systems. They've focused on making products
accessible and cost effective for patients. They live this mission
every day because everyone should have the same opportunities to
see the world through healthy eyes. So thank you THEO
(00:54):
Pharmer Canada for supporting Blindspot for the past twenty plus years.
Macular degenera treatment has been revolutionized by anti veget medications.
When a patient comes in with wet macular degeneration, there's
something we can truly offer them, not only to prevent
vision from getting worse, but to actually restore vision. As well.
But when a patient comes in with dry macular degeneration,
(01:16):
there's little we can offer outside of Aeror's formulation, diet changes,
and lifestyle changes. There isn't a medication we've typically been
able to offer patients to prevent progression or to even
provide some sort of hope that things might not get worse.
But perhaps that is all changing. I'm joined today by
doctor Ashcan Abbey to discuss some of the newer treatments
for dry macular degeneration. Doctor Abbey graduated magna cum laud
(01:40):
from Harvard University and received his medical degree with honors
from Wheal Cornell Medical College in New York. He completed
his transitional residency at SCRIPS Mercy Hospital in San Diego, California,
and his ofph Themology residency at the top rated eye
hospital in the country, Bascom palmer I Institute in Miami, Florida.
He then completed his fellowship in vitrio retinal Surgery at
William Beaumont Hospital in Royal Oak, Michigan, recognized as one
(02:02):
of the premier RETNA training programs in the country. He
joined Texas Retina Associates in twenty fifteen and became Director
of Clinical Research for Texas Retina Associates in twenty twenty.
He's published numerous peer reviewed scientific papers, book chapters, and
national meeting abstracts on various ophthalmologic topics. He's an active
member of the Retina Society, Association for Research and Vision
and Ophthalmology in the Alpha Omega Alpha Honor Medical Society.
(02:25):
He serves on the Board of Directors of the Outpatient
off philmat Surgery Society on the Medical Executive Committee of
the Uphthalmology Surgery Center of Dallas. He also serves as
a manuscript referee for the standard scientific journal of his field, RETNA,
the Journal of Retina and Vitoris Disease and OSLI RETNA.
All Right, doctor Ashkin Abbey, welcome back to the podcast.
Thanks so much for joining me again.
Speaker 2 (02:46):
Great to be here.
Speaker 1 (02:48):
So last episode that we did together, we were talking
about cataract surgery and the context of macular degeneration as
well a bit in the context of RETINALDS attachment if
somebody's had a prior retinald's attachment. Today we're going to
focus on the treatment for dry macular degeneration, which is
still very practical but in some ways, perhaps a little
bit more theoretical in terms of how mainstream is it
(03:08):
at this point, or maybe I'm wrong and it is
already being used more frequently than I expected it to be. Typically,
I think most people tell their patients and again, you're
retina specialists. I'm a cornea specialist, so not my area expertise,
so my naivete is unfull display on many of these episodes.
I think most of us do kind of tell our
dry AMD patients listen, just bad luck, bad genetics, bad luck,
(03:30):
not great, and there's not much we can do. And
for the wet AMD patients, I might say, you know what,
the good news is, we can kind of treat this
to an extent. And for the dry AMD patients, I'll say,
the good news is you don't have wet AMD, and
you're trying to find the silver lining. But traditionally we
don't really have a great answer to dry macular degeneration,
whereas for wet AMD, obviously we've got anti vegets which
(03:51):
have revolutionized this. What do you routinely tell dry AMD
patients in terms of what their options are in terms
of preventing regression. Before we get into some of the
newer treatment models that might be emerging.
Speaker 3 (04:05):
Yeah, I mean the you know, I think a standard
is for patients who have an intermediate or worse Drymacica generation.
I do recommend that they all take the a RS
to formulation. I think we have enough strong data to
suggest that that does help to reduce the progression to
more advanced AMD.
Speaker 2 (04:23):
Whether it be a GA or wet AMD. You know.
Speaker 3 (04:26):
But there's the lifestyle modifications. I think, you know, people
probably should wear sunglasses when they're a sun. I think
UV light theoretically is going to be a problem here
for advancing the disease. It's not like we have great
data to support the use of the sunglasses, but I
think theoretically it makes enough sense that can't hurt probably
(04:49):
does help that I would. I do still recommend saying
sunglasses when they're in the sun. Obviously huge, huge, huge
modipower risk factors.
Speaker 2 (04:56):
Smoking cessation if.
Speaker 3 (04:58):
They obviously if they've already quit, great, but if they're
still smoking, definitely make it a point of empsis to
try to quit smoking as soon as possible. I think
they're I mean, just recently there's a study that showed
that the potential for possibly using ozepic for that even
and so we have new options for it, find ways
to try to make them quit, and I always remind them,
I say, you know, most of the studies say that
(05:20):
people have to quit and then relapse seven times over
before they finally quit smoking all together. So don't give
up even if you have had a relapse, keep going
out and try to quit all together because they can
save your vision over time. And I will say, even
just totally looking at the patients that I have that
I can smell cigarette smoke on them, they are some
of the toughest to treat in terms of their AMD
(05:41):
as well with when they're even in their whether they're
dry or wet, I think they just have a really
Usually they tend to have much more aggressive disease, and
they progress much more quickly, and they're much more difficult
to control if they have the wet am D side
of things as well.
Speaker 2 (05:54):
Furthermore, I would say diet. I think we have.
Speaker 3 (05:59):
Decent but not great data that you know, a Mediterranean
style diet could potentially be helpful in terms of reducing
the progression. Again, I will say it's decent data because
nutritional data can tend to be very difficult to validate
in a great way with gold standard evidence, but I
think there's been enough study of the Mediterranean diet for
(06:20):
it where I think, I say, if you're going to
pick something, Mediterranean diet is probably a decent one, and
usually it's generally pretty healthy overall for most patients too,
to consider to try to slow it down otherwise, you
know the standards that you know, everybody talks about leafy
green vegetables, omega threes through say fatty fish like salmon,
(06:41):
I have some potential for slowing things down, and then
I usually tell them to eat the rainbow. In terms
of fruits and vegetables, you know, multiply multicolored fruits and
vegetables are all good as well. With I would say,
again decent but not great data to support that as well.
Speaker 1 (06:57):
And I think it is helpful even when you do
say there might not be research or data to support
all these things that theoretically certain things make sense, like
sunglasses and anecdotally you've seen things in your practice, which
I'm sure many retina specialists have as well. Just because
a study hasn't been done or shown something, it doesn't
mean that we've discovered the truth. And that that factor
isn't important in the ideology of the progression of the disease,
(07:20):
So sunglasses, no smoking, Mediterranean diet, omegas and that kind
of stuff, which is important. And obviously the arid's formulation,
whichever multivitamin brand you want to choose. So more exciting
is some of the newer treatment options that are out
there or potentially are in development. Is most research out
there on some of the newer medications or agents. Is
it focused on people who have really really bad disease,
(07:43):
who are already counting fingers and these are more severe disease,
or are there treatments that are being tested right now
that are for your average I don't want to say average,
but the patient who's got kind of moderate drymacular degeneration,
not severe retino atrophy.
Speaker 3 (07:59):
Yeah, so it kind of goes across the spectrum now.
I mean, you know, if you look at the the
two we have two currently medications that we have approved
for the treatment of geographic atrophy and dry bacular generation.
Speaker 2 (08:15):
Both of those the clinical trials were a little different.
Speaker 3 (08:17):
So for one, which you call PEXI to Copeland that
the clinical trials for that were kind of.
Speaker 2 (08:23):
They took almost all comers.
Speaker 3 (08:25):
It was kind of just like everybody who has at
least a dis diameter of geographic atrophy or so whether
it's involving the phobia or not involving the phobia, whether
it's and whether it's even pretty large as well, and
you know, almost not count fingers, but maybe down to
say twenty two hundred vision even they would take them
if they had wet AMD and the other eye, they
(08:46):
still took them.
Speaker 2 (08:46):
They took everybody.
Speaker 3 (08:47):
Basically, it was it was very inclusive in terms of
the study they did for their phase three clinical trial,
which were the two trials.
Speaker 2 (08:53):
That were for them were called Oaks and Derby.
Speaker 3 (08:56):
And then if you look at the other complement inhibitor
that we have on the market currently, which is.
Speaker 2 (09:01):
A acid capped at piggle which is.
Speaker 3 (09:04):
A long name, but essentially it's called iSER Bay, which
is a C five inhibitor. That one the trial specifically
looked at patients who actually had not nonfobial involving girafhic atrophy,
so they had atrophy that was of a certain size.
It's about at least a disdiameter in size, but they
didn't want it to involve the phobia because that those
patients actually progressed the fastest in terms of losing their
(09:27):
having their atrophy progress more quickly than the ones who
have involving the phobia, So they wanted to show a
greater effect by treating those patients specifically. But those patients
see pretty well most of the time, you know, they're
usually their vision is pretty good because their phobia is
not involved yet with their GA. So even in the
ones that we've already had have on the market, now
we have different data sets in terms of how they
(09:48):
were approved, and we're they're looking at it from two
different ways in terms of people who had no not
so good vision and also good vision, but all in
the other trial mainly patients who had pretty good vision
already going in. Having said that, the future trials, the
current trials that we're doing, there's a decent number of
them that are excluding patients who have had wet AMD
(10:10):
in the other eye because they worry about it converting
to wet AMD during the trial for the treatment eye.
And obviously when you have one eye that types wet AMD,
you'r risk and the other eye goes up.
Speaker 2 (10:18):
A little higher to convert.
Speaker 3 (10:21):
Certain trials are doing the same thing where they're just
limiting the patient population just to the ones who have
GA not involving the phobia, and so you're only getting
the information for the ones who are progressing more quickly
because they again we want to show a better effect,
and patients that are already progressing and getting worse.
Speaker 2 (10:37):
And then but it definitely ranges.
Speaker 3 (10:39):
There are some trials that are including, like the previous
trial for pegsy to Copeland, they're including basically all comers
except for the ones maybe who didn't have who have
wet AMD in their fellow I think that one they're
excluding still a lot of those patients. So it is
definitely not just the really bad patients that are being
studied right now. They're actually looking at patients of all
(11:00):
sorts of the spectrum.
Speaker 2 (11:01):
Of the disease right now.
Speaker 3 (11:03):
But I will say the ones that they're looking at
for cell therapy, which is basically stem cells to treat
the atrophy, like transferring RP stem cells underneath the retina
to try to regenerate some of the retina that's been
lost to geographic atrophy. Those patients that are tending to
look for patients who are far worse off in order
to see more of a benefit in those kinds of
(11:25):
patients who have larger areas of ga more atrophy.
Speaker 1 (11:28):
So the stem cell treatments is probably what I was
referring to in terms of the ones who are really
really bad patients where they've got pretty pretty poor vision.
Whereas pegacy to Copeland that's for pretty severe atrophy that's
involving the phobia but maybe twenty two hundred county fingers vision.
And then the the iSER BAY, which I know is
the commercial name, just was easier to say than the
(11:50):
name you said, or that is for more moderate cases
where it's nonfobial involving geogratric atrophy.
Speaker 3 (11:57):
With so I will say that the both PEXI to
Copeland and the iSER A, those two inject those two medications,
they have an indication for any any geographic atrophy, so
you can use it for extra fobial or fobial involving
atrophy and geography atrophies try to slow down the progression
(12:18):
of the disease. It's just that their trial designs were
a little different.
Speaker 2 (12:21):
In how they got approval. Basically, it's what it comes
down to.
Speaker 3 (12:24):
But you can use siphobia or PEXI to Copeland for
a patient who has phobia sparing geographic atrophy, or you
could use aer or you can use either one for
involving the phobia as well.
Speaker 2 (12:35):
That's not a problem based upon the label.
Speaker 1 (12:37):
And are they injectables and how frequently are you using
these in patients? Is this something that is common you said,
it's been approved, Is it on the market, something that
you are you're using a fair bit of.
Speaker 3 (12:47):
Yeah, you know, it's the It's been steadily increasing in
terms of the number of pages I've been treating over
the course of the last probably year. I will say that,
you know, the patients are actually driving this a little
bit now because they're hearing about these new treatments and
they're coming in and asking for it, and so you know,
to say that we are definitely encouraging all patients to
(13:10):
use this, just like we do antibed Jeff, is I
think definitely not the case at this point. Right now,
we're looking at this as something that is a nuanced
conversation with the patient where you say we have something
now which we didn't two years ago, which you do now, right, So.
Speaker 2 (13:26):
That's already a big step forward. We have something to
offer you instead of saying.
Speaker 3 (13:30):
Oh, well, you know, mister Smith, your atrophy is getting worse.
I have nothing to I can't do anything for you.
I'll see you in six months or something like that.
I can now say, okay, we do have something now
for you that the trials that have been done have
shown that in the course of about two years of
treatment for the pegsy to Copeland, we can get maybe
(13:53):
about a twenty roughly about a twenty to twenty five
percent reduction in the rate of growth of the geographic
actually lesion by doing injections either once a month or
once every two months with PEXI to Copeland.
Speaker 2 (14:07):
Okay. And then if we do it.
Speaker 3 (14:09):
For a longer period of time, say we do it
for three years. Now we have a little bit more
data that shows that the effect, the treatment effect, actually
expands and increases as time goes on. So the more
you do it, the longer you do it, the more
of an effect you have in terms of reducing the
growth of the lesion itself and trying to preserve the
retinal tissue for longer. And the same goes for Iserbay
(14:31):
as well as you treat it. Although they started out
their trial with monthly injections, so they only did monthly
for the first year, so we don't have any data
about every other month dosing.
Speaker 2 (14:40):
For the first year.
Speaker 3 (14:41):
But then after this, after the first year, they went
to every other month dosing as well in addition to
monthly dosing to compare the two, and they did still
find a good effect in terms of reducing the rate
of growth of the lesion. Again, we're saying, you know,
in the range of twenty to twenty five to thirty
percent as time goes on. So you know this isn't
some sort of you know, massive massive change. You have
(15:01):
to tell every patient, well, listen, I can't give you
back the vision you've lost. What I can do with
these injections, And there's a lot There are a lot
of injections. I mean, it's a big burden on the
patient to come in either every month or every.
Speaker 2 (15:11):
Other month for these things.
Speaker 3 (15:12):
So I tell them it's a it's a It does
require you to come in regularly. If you don't come
in regularly, it's not really going to work. But if
you do do the injections regularly, you can see at
least a reduction in the loss of the tissue, which
probably will translate to keeping more of your vision. Over time, okay,
and then I usually will let them go and think
(15:34):
about it. I'll just give them the booklet and say
you can think about it, come back in a month
or two and we could probably decide if you.
Speaker 2 (15:39):
Want to do it then.
Speaker 3 (15:40):
But you know, it's a very different conversation than what
we've had for our web AMD patients, where it's just, oh,
you have fluid or blood on your retina. Treatment has
going to happen today. We'll see you in a month
and we're gonna do it again. And if we don't
do this, you're gonna lose a lot more vision. So
we need to do this right now. It's more do
you want to do this? Do you feel like it's
worth it? There are some risks as well. I mean
(16:00):
there's there with pexiocoplan. Right now, we've had a real
world reporting of some ecclusive vasculitis cases, which is concerning
that happens in about one in four thousand patients.
Speaker 2 (16:12):
Okay, so that has to be disclosed.
Speaker 3 (16:14):
That has to be discussed as well, because that those
cases of occlusive basculitis, some of them did extremely poorly
and you know, went to some of them went LP
or n LP afterward and we couldn't do anything about
it at that point. So that's also something that needs
to be discussed with the patient that we could have
potential for permanent vision loss with about a one in
four thousand on a first injection frequency based basis with
(16:35):
the pexia copeland, So all things that need be considered.
You know, obviously injections can cause an optimitis, rental tears,
and detachments as well, so all this needs to be
taken into into account for something that's not actually improving
the vision and maybe maybe is preserving the vision. But
right now, most of the data that we have to
(16:55):
support the visual kind of at least visual function benefit
of these injections is post talk analyses from these clinical trials,
but kind of more primary endpoint looking at vision. There
isn't good data from the critical trials to suggest that
there's primary endpoint data that we are preserving vision when.
Speaker 2 (17:19):
It comes to using these drugs.
Speaker 3 (17:20):
We kind of just have it based upon the more
of the anatomical changes that we're seeing.
Speaker 1 (17:25):
So a big paradigm difference that I'm hearing which will
influence these treatments is really that for a wet AMD
patient like you said, it's not just we're going to
do this to prevent it from getting worse. It's that
your vision could really improve to an extent if we
do these injections. Not always, but that's the hope. Whereas
with these treatments for the dry AMD for the geograghic agrophy,
(17:45):
it's almost a bit of a tougher sell, not that
you're trying to sell it, but it's a tougher sell
for the doctor to get behind and the tougher sell
to the patient because you're saying, listen, I can't get
your vision back. As you said, it's not like we're
going to get the fluid out of there and you're
going to see better. It's purely a profilac thing to
prevent progression. And that that sounds like a really important
difference in this discussion.
Speaker 2 (18:05):
Yeah.
Speaker 3 (18:06):
Absolutely, And again I think there are a decent number
of patients who, you know, they ask what can I do?
They're kind of interested, and all of a sudden we
talk about and they say, you know what, I'm not
interested anymore, you know, And I'd say, that's fine.
Speaker 2 (18:16):
We don't have to do this.
Speaker 3 (18:17):
You definitely don't have to do this, right Now, you know,
if the patient's ninety one years old and you know
it doesn't even know how many more years are left
and doesn't feel like coming in every month or two
if you get a shot in the eye, I don't blame.
Speaker 2 (18:29):
Her, you know.
Speaker 3 (18:29):
And especially it's not going to improve the vision. It's
not necessarily some sort of panacea for these patients.
Speaker 2 (18:35):
So yeah, it is. It definitely requires a lot.
Speaker 3 (18:37):
More care time than the web am B discussion because
wed AB discussion is just you have to do this,
and if you don't, we're going to be you know,
you're you won't see better, and you won't you probably
lose more vision. We can actually improve your vision with this.
It's the best thing you can do for this disease.
It's not a no brainer in these situations.
Speaker 1 (18:52):
For the dry cases, I might be off a little
bit on my definitions the path of physiology and such,
But when we're talking about geograph atrophy, I mean, I
know what it looks like, but how do you differentiate
that and some of the treatments available that we've discussed
for that versus somebody who's just got pretty extensive risen
which might not necessarily qualify under the definition of geographic atrophy.
Speaker 3 (19:14):
Yeah, I mean the you know, I think that if
you're looking at patients on an oct and if you
can see those little those transmission defects on the oct,
even small ones here and there, that's the beginning of atrophy.
Now you can get into into the weeds a little
bit more about whether it's complete atrophy something we call iRORA,
(19:35):
it's a sea aurra. But that's not necessary to talk
about unless you're in a deep academic discussion with the
retin a specialist. So for me, it's just when you're
looking at the patients on their oct and if you
start to see those transmission defects where you can see
kind of the light penetrating down into the choroid, the rps.
Speaker 2 (19:51):
Compromised, you're probably you're at the point where you're getting
some atrophy there. Even it could be mild atrophy if.
Speaker 3 (19:57):
The patient's coming into you and saying, I'm noticing even
though they're totally dry and they but they have kind
of large druisen, but they have and they may have.
Speaker 2 (20:05):
Some transmission defects.
Speaker 3 (20:06):
They're like, I'm noticing my vision, say I'm having a
harder time reading, or I'm having a I'm having a
harder time driving because I'm having some spots missing in
the vision when I'm trying to see when I'm trying
to drive and see the signs on the road, or.
Speaker 2 (20:19):
You know, there are certain things where like dim light.
Speaker 3 (20:21):
If they're having more difficulty in dim light and functioning
or seeing properly or reading, then I think you want
to start saying, okay, you know, it does look like
your atrophy is progressing, and you can usually compare I
don't know whichever data is, I'm sorry what imaging system
you use, but with either with you know, Heidelberg Cirrus,
most of the other one's top con as well, you
(20:42):
can do a kind of scan comparison, a line to
line comparison of your scans from say one from one
visit to a net to the next, and you could
see if there's been some progression of these transmission defects
and if they have gotten worse. You know, that's where
the discussion usually will open up for me, especially if
the patient comes in complaining about possibly considering doing something
(21:03):
and triguing that with a compliment in HIT or that
we have available right now.
Speaker 1 (21:07):
It's really really helpful and practical because a lot of
us who are not written A specialists really are just
looking at the OCT and we're not relying on anything
more more fatat more fat than that.
Speaker 3 (21:19):
Even retin A specialists or not, they're not using autofluorescence
and things like that that we, you know a lot
of times are using in the studies to look at
it and evaluate it. I mean, maybe when you start
doing that a little bit more, but you can get it.
You can lean a lot just from looking at the
OCT in a little bit more detail. You just have
to you know, it doesn't need to just be I
just need.
Speaker 2 (21:34):
To find fluid. If there's no fluid, no big deal.
Speaker 3 (21:36):
And now you've got to start looking a little bit
more at the RP looking to see if there's some
transmission defects and kind of correling that with what the
patient's complaining about.
Speaker 1 (21:45):
And that for me might be the greatest takeaway of
the conversation here that it used to be up until now,
it's been a lot easier in a sense to just
look at the OC fluid, no fluid and yes we
can do something. No, we can't really Aside from the
risk factors that we spoke about at the beginning of
the com but now there is heightened importance in I mean,
there was always heightened importance in listening to history and
(22:05):
looking at the oct thoroughly, but it's heightened importance in
that it actually will change, potentially the way we're advising
these patients on some of the management options available to them.
Speaker 2 (22:16):
Definitely. Yeah.
Speaker 1 (22:17):
Well, doctor ashkan Abbey, thank you so so much for
joining me again on this podcast. Really really useful information
and exciting to see where some of the newer innovations
are going to lead us to in terms of better
treating this extremely common disease as.
Speaker 2 (22:31):
You're aware of. Absolutely happy to do it.
Speaker 1 (22:35):
And thank you everybody for listening to another episode of
blind Spot. Have a great day.
Hey everybody, I'm zaeo Mednik and welcome to another episode
of Blindspot. This episode is sponsored by THEA Pharma Canada.
THEA pharm of Canada is the Canadian subsidiary of THEA,
Europe's leading pioneering and innovative eye health brand. Founded in
nineteen ninety four by Henri Chibre. With five generations of history,
the Chibret family has been dedicated to I care for
(00:32):
more than one hundred and fifty years. Their commitment to
improving lives is born of their pioneering spirit. They continue
to lead the worldwide preservative free movement in eye care.
They've created innovative delivery systems. They've focused on making products
accessible and cost effective for patients. They live this mission
every day because everyone should have the same opportunities to
see the world through healthy eyes. So thank you THEO
(00:54):
Pharmer Canada for supporting Blindspot for the past twenty plus years.
Macular degenera treatment has been revolutionized by anti veget medications.
When a patient comes in with wet macular degeneration, there's
something we can truly offer them, not only to prevent
vision from getting worse, but to actually restore vision. As well.
But when a patient comes in with dry macular degeneration,
(01:16):
there's little we can offer outside of Aeror's formulation, diet changes,
and lifestyle changes. There isn't a medication we've typically been
able to offer patients to prevent progression or to even
provide some sort of hope that things might not get worse.
But perhaps that is all changing. I'm joined today by
doctor Ashcan Abbey to discuss some of the newer treatments
for dry macular degeneration. Doctor Abbey graduated magna cum laud
(01:40):
from Harvard University and received his medical degree with honors
from Wheal Cornell Medical College in New York. He completed
his transitional residency at SCRIPS Mercy Hospital in San Diego, California,
and his ofph Themology residency at the top rated eye
hospital in the country, Bascom palmer I Institute in Miami, Florida.
He then completed his fellowship in vitrio retinal Surgery at
William Beaumont Hospital in Royal Oak, Michigan, recognized as one
(02:02):
of the premier RETNA training programs in the country. He
joined Texas Retina Associates in twenty fifteen and became Director
of Clinical Research for Texas Retina Associates in twenty twenty.
He's published numerous peer reviewed scientific papers, book chapters, and
national meeting abstracts on various ophthalmologic topics. He's an active
member of the Retina Society, Association for Research and Vision
and Ophthalmology in the Alpha Omega Alpha Honor Medical Society.
(02:25):
He serves on the Board of Directors of the Outpatient
off philmat Surgery Society on the Medical Executive Committee of
the Uphthalmology Surgery Center of Dallas. He also serves as
a manuscript referee for the standard scientific journal of his field, RETNA,
the Journal of Retina and Vitoris Disease and OSLI RETNA.
All Right, doctor Ashkin Abbey, welcome back to the podcast.
Thanks so much for joining me again.
Speaker 2 (02:46):
Great to be here.
Speaker 1 (02:48):
So last episode that we did together, we were talking
about cataract surgery and the context of macular degeneration as
well a bit in the context of RETINALDS attachment if
somebody's had a prior retinald's attachment. Today we're going to
focus on the treatment for dry macular degeneration, which is
still very practical but in some ways, perhaps a little
bit more theoretical in terms of how mainstream is it
(03:08):
at this point, or maybe I'm wrong and it is
already being used more frequently than I expected it to be. Typically,
I think most people tell their patients and again, you're
retina specialists. I'm a cornea specialist, so not my area expertise,
so my naivete is unfull display on many of these episodes.
I think most of us do kind of tell our
dry AMD patients listen, just bad luck, bad genetics, bad luck,
(03:30):
not great, and there's not much we can do. And
for the wet AMD patients, I might say, you know what,
the good news is, we can kind of treat this
to an extent. And for the dry AMD patients, I'll say,
the good news is you don't have wet AMD, and
you're trying to find the silver lining. But traditionally we
don't really have a great answer to dry macular degeneration,
whereas for wet AMD, obviously we've got anti vegets which
(03:51):
have revolutionized this. What do you routinely tell dry AMD
patients in terms of what their options are in terms
of preventing regression. Before we get into some of the
newer treatment models that might be emerging.
Speaker 3 (04:05):
Yeah, I mean the you know, I think a standard
is for patients who have an intermediate or worse Drymacica generation.
I do recommend that they all take the a RS
to formulation. I think we have enough strong data to
suggest that that does help to reduce the progression to
more advanced AMD.
Speaker 2 (04:23):
Whether it be a GA or wet AMD. You know.
Speaker 3 (04:26):
But there's the lifestyle modifications. I think, you know, people
probably should wear sunglasses when they're a sun. I think
UV light theoretically is going to be a problem here
for advancing the disease. It's not like we have great
data to support the use of the sunglasses, but I
think theoretically it makes enough sense that can't hurt probably
(04:49):
does help that I would. I do still recommend saying
sunglasses when they're in the sun. Obviously huge, huge, huge
modipower risk factors.
Speaker 2 (04:56):
Smoking cessation if.
Speaker 3 (04:58):
They obviously if they've already quit, great, but if they're
still smoking, definitely make it a point of empsis to
try to quit smoking as soon as possible. I think
they're I mean, just recently there's a study that showed
that the potential for possibly using ozepic for that even
and so we have new options for it, find ways
to try to make them quit, and I always remind them,
I say, you know, most of the studies say that
(05:20):
people have to quit and then relapse seven times over
before they finally quit smoking all together. So don't give
up even if you have had a relapse, keep going
out and try to quit all together because they can
save your vision over time. And I will say, even
just totally looking at the patients that I have that
I can smell cigarette smoke on them, they are some
of the toughest to treat in terms of their AMD
(05:41):
as well with when they're even in their whether they're
dry or wet, I think they just have a really
Usually they tend to have much more aggressive disease, and
they progress much more quickly, and they're much more difficult
to control if they have the wet am D side
of things as well.
Speaker 2 (05:54):
Furthermore, I would say diet. I think we have.
Speaker 3 (05:59):
Decent but not great data that you know, a Mediterranean
style diet could potentially be helpful in terms of reducing
the progression. Again, I will say it's decent data because
nutritional data can tend to be very difficult to validate
in a great way with gold standard evidence, but I
think there's been enough study of the Mediterranean diet for
(06:20):
it where I think, I say, if you're going to
pick something, Mediterranean diet is probably a decent one, and
usually it's generally pretty healthy overall for most patients too,
to consider to try to slow it down otherwise, you
know the standards that you know, everybody talks about leafy
green vegetables, omega threes through say fatty fish like salmon,
(06:41):
I have some potential for slowing things down, and then
I usually tell them to eat the rainbow. In terms
of fruits and vegetables, you know, multiply multicolored fruits and
vegetables are all good as well. With I would say,
again decent but not great data to support that as well.
Speaker 1 (06:57):
And I think it is helpful even when you do
say there might not be research or data to support
all these things that theoretically certain things make sense, like
sunglasses and anecdotally you've seen things in your practice, which
I'm sure many retina specialists have as well. Just because
a study hasn't been done or shown something, it doesn't
mean that we've discovered the truth. And that that factor
isn't important in the ideology of the progression of the disease,
(07:20):
So sunglasses, no smoking, Mediterranean diet, omegas and that kind
of stuff, which is important. And obviously the arid's formulation,
whichever multivitamin brand you want to choose. So more exciting
is some of the newer treatment options that are out
there or potentially are in development. Is most research out
there on some of the newer medications or agents. Is
it focused on people who have really really bad disease,
(07:43):
who are already counting fingers and these are more severe disease,
or are there treatments that are being tested right now
that are for your average I don't want to say average,
but the patient who's got kind of moderate drymacular degeneration,
not severe retino atrophy.
Speaker 3 (07:59):
Yeah, so it kind of goes across the spectrum now.
I mean, you know, if you look at the the
two we have two currently medications that we have approved
for the treatment of geographic atrophy and dry bacular generation.
Speaker 2 (08:15):
Both of those the clinical trials were a little different.
Speaker 3 (08:17):
So for one, which you call PEXI to Copeland that
the clinical trials for that were kind of.
Speaker 2 (08:23):
They took almost all comers.
Speaker 3 (08:25):
It was kind of just like everybody who has at
least a dis diameter of geographic atrophy or so whether
it's involving the phobia or not involving the phobia, whether
it's and whether it's even pretty large as well, and
you know, almost not count fingers, but maybe down to
say twenty two hundred vision even they would take them
if they had wet AMD and the other eye, they
(08:46):
still took them.
Speaker 2 (08:46):
They took everybody.
Speaker 3 (08:47):
Basically, it was it was very inclusive in terms of
the study they did for their phase three clinical trial,
which were the two trials.
Speaker 2 (08:53):
That were for them were called Oaks and Derby.
Speaker 3 (08:56):
And then if you look at the other complement inhibitor
that we have on the market currently, which is.
Speaker 2 (09:01):
A acid capped at piggle which is.
Speaker 3 (09:04):
A long name, but essentially it's called iSER Bay, which
is a C five inhibitor. That one the trial specifically
looked at patients who actually had not nonfobial involving girafhic atrophy,
so they had atrophy that was of a certain size.
It's about at least a disdiameter in size, but they
didn't want it to involve the phobia because that those
patients actually progressed the fastest in terms of losing their
(09:27):
having their atrophy progress more quickly than the ones who
have involving the phobia, So they wanted to show a
greater effect by treating those patients specifically. But those patients
see pretty well most of the time, you know, they're
usually their vision is pretty good because their phobia is
not involved yet with their GA. So even in the
ones that we've already had have on the market, now
we have different data sets in terms of how they
(09:48):
were approved, and we're they're looking at it from two
different ways in terms of people who had no not
so good vision and also good vision, but all in
the other trial mainly patients who had pretty good vision
already going in. Having said that, the future trials, the
current trials that we're doing, there's a decent number of
them that are excluding patients who have had wet AMD
(10:10):
in the other eye because they worry about it converting
to wet AMD during the trial for the treatment eye.
And obviously when you have one eye that types wet AMD,
you'r risk and the other eye goes up.
Speaker 2 (10:18):
A little higher to convert.
Speaker 3 (10:21):
Certain trials are doing the same thing where they're just
limiting the patient population just to the ones who have
GA not involving the phobia, and so you're only getting
the information for the ones who are progressing more quickly
because they again we want to show a better effect,
and patients that are already progressing and getting worse.
Speaker 2 (10:37):
And then but it definitely ranges.
Speaker 3 (10:39):
There are some trials that are including, like the previous
trial for pegsy to Copeland, they're including basically all comers
except for the ones maybe who didn't have who have
wet AMD in their fellow I think that one they're
excluding still a lot of those patients. So it is
definitely not just the really bad patients that are being
studied right now. They're actually looking at patients of all
(11:00):
sorts of the spectrum.
Speaker 2 (11:01):
Of the disease right now.
Speaker 3 (11:03):
But I will say the ones that they're looking at
for cell therapy, which is basically stem cells to treat
the atrophy, like transferring RP stem cells underneath the retina
to try to regenerate some of the retina that's been
lost to geographic atrophy. Those patients that are tending to
look for patients who are far worse off in order
to see more of a benefit in those kinds of
(11:25):
patients who have larger areas of ga more atrophy.
Speaker 1 (11:28):
So the stem cell treatments is probably what I was
referring to in terms of the ones who are really
really bad patients where they've got pretty pretty poor vision.
Whereas pegacy to Copeland that's for pretty severe atrophy that's
involving the phobia but maybe twenty two hundred county fingers vision.
And then the the iSER BAY, which I know is
the commercial name, just was easier to say than the
(11:50):
name you said, or that is for more moderate cases
where it's nonfobial involving geogratric atrophy.
Speaker 3 (11:57):
With so I will say that the both PEXI to
Copeland and the iSER A, those two inject those two medications,
they have an indication for any any geographic atrophy, so
you can use it for extra fobial or fobial involving
atrophy and geography atrophies try to slow down the progression
(12:18):
of the disease. It's just that their trial designs were
a little different.
Speaker 2 (12:21):
In how they got approval. Basically, it's what it comes
down to.
Speaker 3 (12:24):
But you can use siphobia or PEXI to Copeland for
a patient who has phobia sparing geographic atrophy, or you
could use aer or you can use either one for
involving the phobia as well.
Speaker 2 (12:35):
That's not a problem based upon the label.
Speaker 1 (12:37):
And are they injectables and how frequently are you using
these in patients? Is this something that is common you said,
it's been approved, Is it on the market, something that
you are you're using a fair bit of.
Speaker 3 (12:47):
Yeah, you know, it's the It's been steadily increasing in
terms of the number of pages I've been treating over
the course of the last probably year. I will say that,
you know, the patients are actually driving this a little
bit now because they're hearing about these new treatments and
they're coming in and asking for it, and so you know,
to say that we are definitely encouraging all patients to
(13:10):
use this, just like we do antibed Jeff, is I
think definitely not the case at this point. Right now,
we're looking at this as something that is a nuanced
conversation with the patient where you say we have something
now which we didn't two years ago, which you do now, right, So.
Speaker 2 (13:26):
That's already a big step forward. We have something to
offer you instead of saying.
Speaker 3 (13:30):
Oh, well, you know, mister Smith, your atrophy is getting worse.
I have nothing to I can't do anything for you.
I'll see you in six months or something like that.
I can now say, okay, we do have something now
for you that the trials that have been done have
shown that in the course of about two years of
treatment for the pegsy to Copeland, we can get maybe
(13:53):
about a twenty roughly about a twenty to twenty five
percent reduction in the rate of growth of the geographic
actually lesion by doing injections either once a month or
once every two months with PEXI to Copeland.
Speaker 2 (14:07):
Okay. And then if we do it.
Speaker 3 (14:09):
For a longer period of time, say we do it
for three years. Now we have a little bit more
data that shows that the effect, the treatment effect, actually
expands and increases as time goes on. So the more
you do it, the longer you do it, the more
of an effect you have in terms of reducing the
growth of the lesion itself and trying to preserve the
retinal tissue for longer. And the same goes for Iserbay
(14:31):
as well as you treat it. Although they started out
their trial with monthly injections, so they only did monthly
for the first year, so we don't have any data
about every other month dosing.
Speaker 2 (14:40):
For the first year.
Speaker 3 (14:41):
But then after this, after the first year, they went
to every other month dosing as well in addition to
monthly dosing to compare the two, and they did still
find a good effect in terms of reducing the rate
of growth of the lesion. Again, we're saying, you know,
in the range of twenty to twenty five to thirty
percent as time goes on. So you know this isn't
some sort of you know, massive massive change. You have
(15:01):
to tell every patient, well, listen, I can't give you
back the vision you've lost. What I can do with
these injections, And there's a lot There are a lot
of injections. I mean, it's a big burden on the
patient to come in either every month or every.
Speaker 2 (15:11):
Other month for these things.
Speaker 3 (15:12):
So I tell them it's a it's a It does
require you to come in regularly. If you don't come
in regularly, it's not really going to work. But if
you do do the injections regularly, you can see at
least a reduction in the loss of the tissue, which
probably will translate to keeping more of your vision. Over time, okay,
and then I usually will let them go and think
(15:34):
about it. I'll just give them the booklet and say
you can think about it, come back in a month
or two and we could probably decide if you.
Speaker 2 (15:39):
Want to do it then.
Speaker 3 (15:40):
But you know, it's a very different conversation than what
we've had for our web AMD patients, where it's just, oh,
you have fluid or blood on your retina. Treatment has
going to happen today. We'll see you in a month
and we're gonna do it again. And if we don't
do this, you're gonna lose a lot more vision. So
we need to do this right now. It's more do
you want to do this? Do you feel like it's
worth it? There are some risks as well. I mean
(16:00):
there's there with pexiocoplan. Right now, we've had a real
world reporting of some ecclusive vasculitis cases, which is concerning
that happens in about one in four thousand patients.
Speaker 2 (16:12):
Okay, so that has to be disclosed.
Speaker 3 (16:14):
That has to be discussed as well, because that those
cases of occlusive basculitis, some of them did extremely poorly
and you know, went to some of them went LP
or n LP afterward and we couldn't do anything about
it at that point. So that's also something that needs
to be discussed with the patient that we could have
potential for permanent vision loss with about a one in
four thousand on a first injection frequency based basis with
(16:35):
the pexia copeland, So all things that need be considered.
You know, obviously injections can cause an optimitis, rental tears,
and detachments as well, so all this needs to be
taken into into account for something that's not actually improving
the vision and maybe maybe is preserving the vision. But
right now, most of the data that we have to
(16:55):
support the visual kind of at least visual function benefit
of these injections is post talk analyses from these clinical trials,
but kind of more primary endpoint looking at vision. There
isn't good data from the critical trials to suggest that
there's primary endpoint data that we are preserving vision when.
Speaker 2 (17:19):
It comes to using these drugs.
Speaker 3 (17:20):
We kind of just have it based upon the more
of the anatomical changes that we're seeing.
Speaker 1 (17:25):
So a big paradigm difference that I'm hearing which will
influence these treatments is really that for a wet AMD
patient like you said, it's not just we're going to
do this to prevent it from getting worse. It's that
your vision could really improve to an extent if we
do these injections. Not always, but that's the hope. Whereas
with these treatments for the dry AMD for the geograghic agrophy,
(17:45):
it's almost a bit of a tougher sell, not that
you're trying to sell it, but it's a tougher sell
for the doctor to get behind and the tougher sell
to the patient because you're saying, listen, I can't get
your vision back. As you said, it's not like we're
going to get the fluid out of there and you're
going to see better. It's purely a profilac thing to
prevent progression. And that that sounds like a really important
difference in this discussion.
Speaker 2 (18:05):
Yeah.
Speaker 3 (18:06):
Absolutely, And again I think there are a decent number
of patients who, you know, they ask what can I do?
They're kind of interested, and all of a sudden we
talk about and they say, you know what, I'm not
interested anymore, you know, And I'd say, that's fine.
Speaker 2 (18:16):
We don't have to do this.
Speaker 3 (18:17):
You definitely don't have to do this, right Now, you know,
if the patient's ninety one years old and you know
it doesn't even know how many more years are left
and doesn't feel like coming in every month or two
if you get a shot in the eye, I don't blame.
Speaker 2 (18:29):
Her, you know.
Speaker 3 (18:29):
And especially it's not going to improve the vision. It's
not necessarily some sort of panacea for these patients.
Speaker 2 (18:35):
So yeah, it is. It definitely requires a lot.
Speaker 3 (18:37):
More care time than the web am B discussion because
wed AB discussion is just you have to do this,
and if you don't, we're going to be you know,
you're you won't see better, and you won't you probably
lose more vision. We can actually improve your vision with this.
It's the best thing you can do for this disease.
It's not a no brainer in these situations.
Speaker 1 (18:52):
For the dry cases, I might be off a little
bit on my definitions the path of physiology and such,
But when we're talking about geograph atrophy, I mean, I
know what it looks like, but how do you differentiate
that and some of the treatments available that we've discussed
for that versus somebody who's just got pretty extensive risen
which might not necessarily qualify under the definition of geographic atrophy.
Speaker 3 (19:14):
Yeah, I mean the you know, I think that if
you're looking at patients on an oct and if you
can see those little those transmission defects on the oct,
even small ones here and there, that's the beginning of atrophy.
Now you can get into into the weeds a little
bit more about whether it's complete atrophy something we call iRORA,
(19:35):
it's a sea aurra. But that's not necessary to talk
about unless you're in a deep academic discussion with the
retin a specialist. So for me, it's just when you're
looking at the patients on their oct and if you
start to see those transmission defects where you can see
kind of the light penetrating down into the choroid, the rps.
Speaker 2 (19:51):
Compromised, you're probably you're at the point where you're getting
some atrophy there. Even it could be mild atrophy if.
Speaker 3 (19:57):
The patient's coming into you and saying, I'm noticing even
though they're totally dry and they but they have kind
of large druisen, but they have and they may have.
Speaker 2 (20:05):
Some transmission defects.
Speaker 3 (20:06):
They're like, I'm noticing my vision, say I'm having a
harder time reading, or I'm having a I'm having a
harder time driving because I'm having some spots missing in
the vision when I'm trying to see when I'm trying
to drive and see the signs on the road, or.
Speaker 2 (20:19):
You know, there are certain things where like dim light.
Speaker 3 (20:21):
If they're having more difficulty in dim light and functioning
or seeing properly or reading, then I think you want
to start saying, okay, you know, it does look like
your atrophy is progressing, and you can usually compare I
don't know whichever data is, I'm sorry what imaging system
you use, but with either with you know, Heidelberg Cirrus,
most of the other one's top con as well, you
(20:42):
can do a kind of scan comparison, a line to
line comparison of your scans from say one from one
visit to a net to the next, and you could
see if there's been some progression of these transmission defects
and if they have gotten worse. You know, that's where
the discussion usually will open up for me, especially if
the patient comes in complaining about possibly considering doing something
(21:03):
and triguing that with a compliment in HIT or that
we have available right now.
Speaker 1 (21:07):
It's really really helpful and practical because a lot of
us who are not written A specialists really are just
looking at the OCT and we're not relying on anything
more more fatat more fat than that.
Speaker 3 (21:19):
Even retin A specialists or not, they're not using autofluorescence
and things like that that we, you know a lot
of times are using in the studies to look at
it and evaluate it. I mean, maybe when you start
doing that a little bit more, but you can get it.
You can lean a lot just from looking at the
OCT in a little bit more detail. You just have
to you know, it doesn't need to just be I
just need.
Speaker 2 (21:34):
To find fluid. If there's no fluid, no big deal.
Speaker 3 (21:36):
And now you've got to start looking a little bit
more at the RP looking to see if there's some
transmission defects and kind of correling that with what the
patient's complaining about.
Speaker 1 (21:45):
And that for me might be the greatest takeaway of
the conversation here that it used to be up until now,
it's been a lot easier in a sense to just
look at the OC fluid, no fluid and yes we
can do something. No, we can't really Aside from the
risk factors that we spoke about at the beginning of
the com but now there is heightened importance in I mean,
there was always heightened importance in listening to history and
(22:05):
looking at the oct thoroughly, but it's heightened importance in
that it actually will change, potentially the way we're advising
these patients on some of the management options available to them.
Speaker 2 (22:16):
Definitely. Yeah.
Speaker 1 (22:17):
Well, doctor ashkan Abbey, thank you so so much for
joining me again on this podcast. Really really useful information
and exciting to see where some of the newer innovations
are going to lead us to in terms of better
treating this extremely common disease as.
Speaker 2 (22:31):
You're aware of. Absolutely happy to do it.
Speaker 1 (22:35):
And thank you everybody for listening to another episode of
blind Spot. Have a great day.
Popular Podcasts
My Favorite Murder with Karen Kilgariff and Georgia Hardstark
My Favorite Murder is a true crime comedy podcast hosted by Karen Kilgariff and Georgia Hardstark. Each week, Karen and Georgia share compelling true crimes and hometown stories from friends and listeners. Since MFM launched in January of 2016, Karen and Georgia have shared their lifelong interest in true crime and have covered stories of infamous serial killers like the Night Stalker, mysterious cold cases, captivating cults, incredible survivor stories and important events from history like the Tulsa race massacre of 1921. My Favorite Murder is part of the Exactly Right podcast network that provides a platform for bold, creative voices to bring to life provocative, entertaining and relatable stories for audiences everywhere. The Exactly Right roster of podcasts covers a variety of topics including historic true crime, comedic interviews and news, science, pop culture and more. Podcasts on the network include Buried Bones with Kate Winkler Dawson and Paul Holes, That's Messed Up: An SVU Podcast, This Podcast Will Kill You, Bananas and more.
24/7 News: The Latest
The latest news in 4 minutes updated every hour, every day.
Dateline NBC
Current and classic episodes, featuring compelling true-crime mysteries, powerful documentaries and in-depth investigations. Follow now to get the latest episodes of Dateline NBC completely free, or subscribe to Dateline Premium for ad-free listening and exclusive bonus content: DatelinePremium.com