Episode Transcript
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Speaker 1 (00:01):
Welcome to the
Dermatrotter Don't Swear About
Skincare podcast.
We've got an exciting episodehere for you today.
We've got Dr Raj Chovatiya.
He's actually a clinicalassociate professor at Rosalind
Franklin University, chicagoMedical School, and founder and
director of the Center forMedical Dermatology and
Immunology Research in Chicago,illinois, and I'm so excited to
(00:24):
have him on here today.
So welcome to the podcast, raj.
Speaker 2 (00:27):
Thank you so much for
having me, Shannon.
It's a real pleasure to finallymake it to your VIP guest list.
Speaker 1 (00:33):
Well, you've made it.
You're up at the top as a VIP,so it was worth the wait to get
you out here and on the podcast.
And I really wanted to bringyou on because in the
dermatology space and patientsare aware of that and some of
them out there might even be onone of these drugs you know this
kind of you know, elusive classof the JAK inhibitors that you
know a lot of noise has beenmade about, obviously with
dermatologists and otherspecialists, but then a lot of I
(00:55):
think you know fear amongstpatients about what do these
drugs really mean and are theyright for me?
And what I wanted to do isbring on today to really just
bring some clarity to what thesedrugs are and how they might be
able to help patients and maybealleviate some of those
concerns people have.
So I'm just going to getstarted with asking you just
kind of outright you know, whatexactly is a JAK inhibitor and
how does it work?
Speaker 2 (01:16):
Great question, and
you know it seems somewhat basic
when we're talking about thisfrom healthcare provider to
healthcare provider, but you'dbe surprised how many folks who
haven't had a chance to reallyuse JAK inhibitors or
participate in studies or thinkabout them actually find this to
be a little foreign as well.
So I like to describe JAKinhibitors as really a small
molecule that works on theinside of cells that are
(01:37):
overactive in your immune system.
Now there's other cells inwhich they're relevant, but at
least for the purposes of ourdisease treatment, really, we
like to think about this drugclass working across multiple
different types of immune cells.
Now, the reason why that'simportant is that, you know,
some people might be morefamiliar with our injectable
biologic therapies.
We've had them for longer.
They're big antibodies that yougo inject directly into the
(02:00):
bloodstream and or thesubcutaneous area.
They bind to very specificsignals that hang around on the
outside of our cells.
But JAK inhibitors do a littlesomething different.
Rather than very specificallytargeting one signal or the
other, they actually work at alower point in that pathway,
across multiple cells formultiple signals, and so the way
(02:21):
the human body is designed.
It's a very cool feature ofevolution, is there's really
only a small handful of waysthat signals are transmitted
through cells.
You can almost think of it as arelay race.
You got someone handingsomething off to someone,
someone handing something off tosomeone else.
Eventually this goes into thepowerhouse of the cell, the
nucleus, where there'stranscription, translation and
proteins and stuff made.
(02:41):
So transcription factors areactivated as a result of the
Janus kinase family in a lot ofcells or the JAK family.
Jak inhibitors essentially juststop this relay race at a
different point for a lot ofdifferent signals and stop
inflammation in severaldifferent ways, and that's one
of the reasons why they're avery exciting class of drug that
can work across so manydifferent kinds of diseases of
(03:06):
drug that can work across somany different kinds of diseases
and now that you're talkingabout those kind of diseases or
you know states that we kind ofreally look to do treatment
where particular in the skin.
Speaker 1 (03:14):
you know, are we
looking at obviously now where
we use JAK inhibitors and wheredo you think we're going in the
future?
Speaker 2 (03:19):
So some of the oldest
studies for JAK inhibitors were
actually psoriasis and, as itturned out, JAK inhibitors were
just okay for psoriasis.
It turns out that there's someother signals that work through
non-Janus kinase mediatedpathways that are important here
, and so they didn't really gothat far forward.
But what ended up happening is,in a lot of different case
reports, case series and justuses of other Janus kinases in
(03:42):
the real world, people found outhey, some of my patients with
eczema seem to be doing better,Some of my patients with
vitiligo seem to be doing better, Some of my patients with
alopecia areata seem to be doingbetter.
And this is kind of how thewhole Jack inhibitor revolution
started and thus began a seriesof phase two and phase three
clinical trials for a wholebunch of new small molecules in
(04:05):
oral and topical format to lookat a variety of different
dermatologic diseases.
So in today's day and age wehave oral gynase kinase
inhibitors that are approved forthe treatment of atopic
dermatitis as well as alopeciaareata, and we have topical
gynase kinase inhibitors thatare approved for the treatment
of vitiligo and atopicdermatitis.
(04:26):
Now this list is growing prettyrapidly.
We're going to soon have oraltreatments that are approved for
hydradenitis suppurativa andvitiligo.
We're going to see topicalspotentially moving into this HS
realm and perhaps some even lesscommon dermatologic diseases
like our lycanoid diseases maysee an approval there too.
But the next man up is going tobe a disease called chronic
(04:47):
hand eczema, where hopefullywe'll have a new cream that's
also a Janus kinase inhibitorlater this year.
So whether or not it's a classof drug that you feel very
equipped to talk about, you'regoing to have to because they're
touching so many disease statesthat we see in our everyday
clinic.
Speaker 1 (05:03):
So if a patient is
kind of walking through the
clinic and you take a look atthem and say, okay, yeah, you've
got atopic dermatitis, I thinka JAK inhibitor would be
appropriate for you, how wouldyou explain that it's going to
help, maybe in terms of theiractual rash or their itch or
quality of life?
What are the expectations thatyou really talk to them about,
about improvement, that theymight see?
Speaker 2 (05:24):
A question that comes
up all the time, because, at
the end of the day, in everyatopic dermatitis visit, I try
to make sure patients understandthat they have multiple
treatment options, and I have noidea, really, when they walk in
through the door, which one isgoing to be the right one for
them, because a lot of it isdependent upon how they feel,
based on what you say.
So you have so much power as ahealthcare provider to really
(05:44):
provide information that allowspeople to make the right choice.
And so when we're talking aboutJanus kindness inhibitors,
let's refer to oral therapiesfor moderate to severe disease
for a moment.
These are going to be oncedaily pills that are available
in a couple of different doseslow doses and high doses that
allow us to very flexibly treatthe signs and symptoms of
disease and to just preparesomebody for what might happen.
(06:08):
One of the coolest things aboutoral Janus kindness inhibitors
is how fast they work and howpotent they are.
So, when it comes to thinkingabout itch as the primary
symptom of atopic dermatitis,most of our Janus kindness
inhibitors have data showingthat it's really we're talking
about days that you're startingto see somebody actually having
a clinically meaningfulimprovement in itch, and then,
when we start thinking aboutsignificant milestones for
(06:31):
improvement of the actualinflammation that you see in the
skin lesions, this is reallyonly on the order of a few weeks
.
So, frankly, you may have a lotof information in the course of
, let's say, a month, comparedto another type of therapy that
works a little slower, a littledifferently, where it may take
you several months to figure outwhat's going on.
Now, the other cool part isthat, even if we don't get to
(06:56):
where we want to, we have theability to go to an even higher
dose as well.
And that's the other part Ilike to remind folks as well is
that, even though I say allthese good things, it's one of
those.
Wait, there's more.
We may be able to even escalateyou to another dose too.
Speaker 1 (07:09):
So with knowing that
and the flexibility in dosing
and the improvement that youknow might actually be seen for
these patients.
You know, I like to talk alittle bit of like the elephant
in the room, if you will.
You know, for the JAKinhibitors what everyone kind of
fears, not only, I think, someof the healthcare providers
listening out there, but ourpatients that are aware of this.
You know, box warning.
That does appear on the Jackinhibitor class.
(07:31):
Do you mind explaining a littlebit about even you know what a
box warning is, other medicinesthat might have a common things?
You know, like an ibuprofen,and what does it really, you
know, mean Like why do theyactually have one, just to put
it in context for a patient?
Speaker 2 (07:48):
So this is a.
This is a good piece of bedtimereading here, so I'll try to
give maybe a medium version ofthis story, but what I want to
tell anybody listening out thereis this is actually relevant,
because some shortened versionof this is a part of every
conversation I have with mypatients, because it's really
the only way to provideappropriate context for what
looks crazy and scary on labelsbut may not actually be as
worrisome for many of the peoplethat are walking through your
(08:10):
office as you might think.
So when it came to Janus kinaseinhibitors, this is a large
class of medications and sort ofthe granddaddy of this class
was a medication calledtofacitinib, a small molecule
that was a pan-JAK inhibitor,meaning that had activity across
all four JAK proteins, and itwas originally approved for
rheumatoid arthritis.
And in those studies let's saya couple of decades ago or a
(08:31):
decade and a half ago what theyfound was that huh patients were
doing better.
But there seemed to be theserare events and not the kind of
rare events we totally lovePeople that potentially may have
some major adversecardiovascular issues,
potentially some blood clots,maybe some malignancies, maybe
even some death related to thoseas well, but these are very
(08:52):
rare signals.
In any clinical trial no matterwhether you're thinking about
people at high risk or low riskit's hard to spot some of these
particular events.
And so there was a mandatedstudy that was done to look at
people that were compared tostandard of care therapy versus
this medication, tofacitinib,that were followed for several
years and what they wanted to dowas understand, from a safety
(09:14):
standpoint, is this really arisk we should worry about or
not?
And for this type of study, thedeck was really stacked,
because, at the end of the day,if you wanted to catch these
kinds of events, if you had aregular population, you'd this
study for like 100 years, right,and like no one's sticking
around for 100 years, let metell you that right now.
And so they took people thatwere all over the age of 50,
(09:34):
that had a variety ofcardiovascular risk factors,
that were all onimmunosuppressive therapy with
methotrexate.
About half of them were on sometype of corticosteroid therapy
as well, and so already thisisn't sounding like your average
atopic dermatitis population,but all these parameters were
true, and they all hadrheumatoid arthritis a very
different disease state andthese patients were treated with
(09:56):
either tofacitinib or aninjectable medication called the
TNF-alpha inhibitor, somethingthat we used to use a lot of in
dermatology for psoriasis, butis used a lot as first-line
therapy for people withrheumatoid arthritis.
These people were then followedover the course of several
years.
Some people managed to stay ontherapy for a few consecutive
years, and what they were reallytracking was a variety of
(10:17):
non-inferiority margins for someof those adverse events that I
listed and, as it turned out,there seemed to be a relatively
higher, increased incidence ofmajor adverse cardiovascular
events, infections, malignancies, venothrombolic events and even
death.
Now the funny thing is that,across all these groups, it's
(10:38):
possible that the overall rateof these events is still a
little lower than patients withrheumatoid arthritis, just
because they already are asicker patient group, especially
older patients.
But compared to the TNF-alphainhibitors, these events were a
little higher, and so this ledto the FDA making a boxed
warning on all JAK inhibitorsoral, topical, any way, shape or
(11:03):
form that.
Hey look, because of thismedication that is related to
the rest of this class.
Here's things that you reallyneed to be worried about,
potentially in people who mighthave certain risk factors, or
tobacco users former or currenttobacco users in the case of
smoking and so this wordingrepetitively appears on both our
topical Janus kinase inhibitorslike ruxolitinib, as well as
our oral Janus kinase inhibitorsfor atopic dermatitis,
(11:24):
upatacitinib and abracitinib.
Now, what does this mean to meas somebody who is in
dermatology, talking to anatopic dermatitis patient?
Well, it's something that Ihave to talk about and address,
but what's interesting is if youfollow most of these adverse
events in patients with atopicdermatitis.
It's a very, very differentstory and we can touch on that
if you'd like, but I think whatI want the listening audience to
(11:46):
think about is probablyeverything I just spent a few
minutes talking about.
You can boil that down into afew sentences to give your
patients some context.
Hey, you look at the paper thatcomes with this drug.
You might see some big, scarysounding words.
They're going to be in big,bold letters in a big black box.
What exactly does that mean?
Well, a medication that isessentially related to this
(12:07):
medication the first one of thisparticular family was studied
in patients with a differentdisease, patients who are older,
sicker on other medications,with a lot of different risk
factors, and they found thatthere was increased rates of
some of these scary soundingthings infections, malignancy,
thromboembolic events, and sothat's put on there just to give
everybody reminder that thatwas seen.
(12:27):
Now, what does this mean for you?
The eczema, homobolic events,and so that's put on there just
to give everybody a reminderthat that was seen.
Now, what does this mean foryou, the eczema patient that's
sitting in front of me?
These were all events that wereseen extremely uncommonly in
patients that were treated withatopic dermatitis, whether in
monotherapy or in combinationwith topical steroids, and in
some follow-up studies thatwe've looked at.
When you take a look at thewhole population of eczema
patients, these are probablysomewhere in the ballpark of
where you might expect to seesome of these rates.
(12:49):
So what does that mean for me?
Well, we'll talk about yourhealth every time that I see you
, and I want to know aboutwhat's going on with you, but my
concern is not that high for X,y and Z reason, and that's
about it.
That's how you can actuallyvery succinctly present this to
a patient without causing anyunnecessary alarm.
Speaker 1 (13:06):
I love that because
you know, unfortunately, with
box warnings, you know they'reimportant, the FDA feels like
it's important for us to know.
But you really put it incontext, you know for the
patient, just to get that youknow more realistic
understanding.
And I think, too, you'rereassuring them that yes, this
is something that's highlighted,but again, you're not as
concerned because you knowdifferent population and looking
at them and how they're beingtreated.
(13:27):
So that gives people, I think,a nice balance and may help them
feel a bit more comfortableabout starting a medication like
a JAK inhibitor that carriesthat box warning.
You know, if you think aboutsomebody who you know you've
talked about going on a JAK,you've sort of convinced them.
You've had that spiel right nowthat were there, okay, feeling
good about this.
And you know, with regards tosome of those safety, you know
(13:53):
concerns around JAKs.
What do you talk to them about?
Sort of the lab work piece.
You know why are you doing it,what type of labs are you
planning to order and how oftendo you tend to follow them?
Speaker 2 (13:58):
Sure.
So labs are actually prettyeasy with JAK inhibitors because
there's a few things you'regoing to get in the beginning,
maybe a little bit of stuffafter being on therapy for a few
months, and then at that pointit's really totally up to you.
So at baseline, for any patientthat's going to be on a
systemic oral JAK inhibitor,you're going to want to do a
little bit of infectious workup,very similar to what you might
be used to with some of ourpsoriasis therapies.
(14:19):
This would be looking at TBstatus, oftentimes through a
blood interferon release assay,hepatitis B, hepatitis C status.
At that point there's somesubtle differences between all
the drugs.
So what you might see on thelabel for abracitinib,
baricitinib, upatacitinib, oreven what you might see for
(14:39):
duraxolitinib, whatever getthere, whatnot they all have
slightly different nuances andso you might have a different
lipid monitoring.
So some of them are about onemonth from starting and baseline
.
Some of them are, look at,three months.
You might have slightdifferences in terms of whether
you're looking at a CBC or ablood test.
You might have a differentnuance in terms of whether
you're particularly taking aliver function test.
Some people like to throw inmetabolic panels in there too.
(15:02):
That part I won't bore everybodywith the details.
Read the label because I thinkit can be giving you good
guidance.
But here's the thing Don'tover-order labs.
If you order your labs atbaseline and at an appropriate
follow-up time, every one ofthese labels says at that point
it's as clinically directed, andI take the FDA.
If we're going to complain aboutboxed warnings, I'll take them
(15:23):
for their word.
If they say it's as clinicallydirected, then I'm definitely
incorporating that to mypractice and as someone who's
sort of been with a lot of thesedrugs in various phases of
development or participated inmany of these studies, I can say
that for lab aberrations notsuper common Typically if
they're going to happen it'susually within the first month
or two and in most of thesestudies patients were resolving
or resolved for many lab changes.
(15:44):
With JAK inhibitors inparticular, it's kind of a I
won't make a blanket statementbut for most of the oral jack
inhibitors it was really aroundprobably the six to eight week
mark that maybe you might seesome of these things.
But that's the reason why I tryto push some of my lab checks
to be a little after that, justbecause then you're not going to
catch something that you don'twant to have to follow up on.
Anyway, I'm sure you're a lotlike me where you hate to have
(16:05):
to deal with labs.
Speaker 1 (16:08):
And patients hate
that too.
As you know, it's a lot ofundue anxiety.
You know, when you findsomething and you try to explain
to them well, but based on theevidence, like it can be
transient these things tend tobounce back.
This is just where we initiallysaw it, and so maybe it's
better to check a little furtherout, just so we avoid that
predicament for the patient.
So, in addition to labs, though, if you have somebody coming,
okay, I get the box warning,okay, I get it.
(16:29):
I understand that.
That's you know in the context.
I'm okay, I get the lab piece.
Okay, what about the sideeffects?
What are you going to tell them, raj, about side effects that
they should just be on thelookout for and make you aware
of if they're experiencing anyof?
Speaker 2 (16:40):
them.
So with our JAK inhibitors.
Really there's only a fewthings that truly seem to be
drug related from the am Islightly concerned route, and
the rest of them are all justkind of adverse events that you
think about with clinical trials.
So I'd say that in terms oflike the big and bad and I use
that in quotations I mentionedherpetic infections with my
patients because that's probablyreal to various degrees, based
(17:03):
on the JAK inhibitor and basedon the dose.
If you have a history of herpessimplex or genital herpes, I
like to remind them let's makesure that you have your
valacyclovir on hand in case youdo have a breakout, because a
small percentage of people mighthave a breakout with this
particular therapy.
Shingles is another one.
Herpes zoster, right, that isseen at low rates does seem to
be dose dependent and it maydepend on the drug itself, but
(17:24):
that's also a possibility.
So I like to talk to mypatients if you're age
appropriate getting the shinglesvaccine, otherwise just keeping
a lookout for this or if it'ssomething they want to even
consider.
I will not start therapy, butit's at least something I like
to put in the back of their mind.
The last one is infections.
Now, those count as infections.
(17:47):
But typically when I sayinfections, upper respiratory
tract or sort of even lowerrespiratory tract infections
were things that were seen inthese studies.
It's tougher because we seethese across a lot of studies as
well, but it's at leastsomething I mentioned.
After those three, I don'tspend as much time on those
boxed warning elements as onemight think.
I spend more time on what'sspecific to that drug.
So let's take upatacitinib, forexample, the one at the top of
that list acne.
We see that in various degreeswith all of our JAK inhibitors.
But this is probably thesignature event of upatacitinib.
(18:10):
Seen it several times in thereal world usually ends up
resolving without muchintervention or maybe the mild
use of washes or topicals.
It's not usually a majortreatment stopper for my
patients.
In the case of abracitinib,it's sort of this nausea,
headache kind of picture with alower degree of acne.
Is this usually somethingthat's a major stopper for my
patients?
Not really.
(18:30):
They take it with food andwater and usually it ends up not
being a lasting side effect.
The others have similarsignature side effects but
almost all of them have adverseevent lists that have the
regular old stuff that you'dexpect from any other drug.
Speaker 1 (18:43):
When you mentioned
the shingles vaccines, I do
think for a lot of people thatthat scares them or they know
somebody obviously who's had itand how miserable they
potentially were with actuallyhaving shingles.
If you recommend getting thevaccine, do you recommend
starting, obviously, thatinitial vaccination prior to
getting on drug and then are youcomfortable with them doing it
while on drug or do you havethem take a break for that
(19:05):
second shot?
Speaker 2 (19:06):
Yeah, we know how
difficult it is to get people in
the office in the first place,and once they're there, I really
want to make it worth theirtime and effort, because they
sought me out to be able to helpthem.
So I'll get started on therapyIf I have samples to give them
that day.
We'll get samples going on thatday If they decide that they
want to pursue a shinglesvaccine.
The great news is that we nolonger have to think about the
live vaccine anymore.
(19:27):
Pretty much everybody gets thenon-live version.
Most of our drugs have data fornon-live vaccination.
In the case of upatacitinib,it's not specifically from the
atopic dermatitis program, butit's from the rheumatologic
disease program, and there theylooked at people with vaccine
responses.
There wasn't much of adifference, and so for non-live
vaccines, I don't tend to make abig deal about people taking
(19:47):
gigantic breaks For livevaccinations.
That's a separate story andthere's less of those.
So I guess measles is back inour discussion in the lexicon.
Speaker 1 (19:55):
Yes.
Speaker 2 (19:55):
And so perhaps it's a
separate topic, separate time,
but by and large I do not delaytherapy for someone who needs it
, even if they might beappropriate for a shingles
vaccine.
Speaker 1 (20:07):
So now that you've
got that patient in front of you
, you know you've gone throughkind of the whole spectrum of
how this works.
The box warning talked aboutsome lab work, side effects.
If you still have a patientsort of hesitant, what's your
advice to a patient?
Or do you really just kind oftailor to, obviously where their
hesitation arises?
But is there something that youcommonly see that you have, you
know, sort of a way to approacha patient to just make them
(20:29):
feel better about going on oneof these drugs?
Speaker 2 (20:36):
You know, oftentimes
for patients with atopic
dermatitis they're used togenerally being pretty healthy
that they had ever really beenon big guns or systemic
therapies in the first place,and so some of the reticence
comes from there.
For others, this is their nextstep after something they used
and they're a little bummed thatthat particular treatment
option didn't work, and sothey're a little nervous about
what if this doesn't work aswell.
I'd say, in all of these cases,to your point, you're going to
be tailoring your conversationto the individual patient in
(20:58):
front of you, but I like toremind my patients is look, this
is one of the greatest times inhistory to have atopic
dermatitis, and it's only goingto keep getting better.
I may not be able to tell youwith exact certainty what the
next few months looks like onthis therapy, but I think this
one gives you the best chance tomeet your goals and my goals in
terms of what we're trying toget to.
We have the ability to see eachother as often or as infrequent
(21:18):
as you'd like, and even if thisdoesn't give you the best chance
of getting better which itmight, because this disease
sometimes can be unpredictablewe have a lot of other choices
or combinations that we can try,and I think, something as
simple as you, acknowledging thefact that sometimes we don't
have all the answers, becauseatopic dermatitis is what we
call a heterogeneous disease,meaning that immunologically it
(21:39):
doesn't always behave exactlythe same, unlike psoriasis,
patients have a lot more buy-inbecause you know, if it was
super simple, somebody wouldhave taken care of their problem
for them already and theywouldn't be here talking to you
about using an oral JAKinhibitor.
Speaker 1 (21:52):
Fantastic.
Well, you know, now that weknow where JAK inhibitors are I
know you mentioned just brieflyin the future is if you could
predict you know five years fromnow where we'll be for JAK
inhibitors in dermatology.
You know, I know you alluded tothis a little bit earlier.
Where do you think we'll be inthis space with JAKs?
Speaker 2 (22:07):
I mean, it sounds
like JAK inhibitors have the
potential ability to touch upone of our common inflammatory
diseases and even some of ourless common ones too.
So we're definitely, over thenext few years, hopefully going
to see some approvals for newerJAK inhibitors in other
inflammatory disease states.
So hydradonitis suppurativa Itouched on is a big one with a
few in development.
(22:27):
Additionally, we're going tosee some real approvals for
vitiligo, which we've never hadbefore, which is really helpful
for people that may haveextensive disease Additional
systemic indications.
We're going to be seeing JAKinhibitors for parigonodularis
as well, a condition that we'vereally learned a lot more about
over the last few years as we'vehad therapies available In our
topical world.
We're going to definitely seeother inflammatory diseases with
(22:51):
having a topical jack as anoption.
This includes milder elementsof HS potentially.
We saw some recent readouts forPN data, so maybe that's going
to be an option for our patients.
Potentially to some otherindications whether you're
thinking about certain types ofscarring alopecias, maybe
thinking about like annoyeddiseases that I'd mentioned and
others that we never really hadtreatments for.
(23:11):
People are looking into that aswell, and I also mentioned
disease states that we nevereven thought about as disease
states chronic hand eczema,which largely speaking has been
a X us disease that we have notreally fully recognized but are
beginning to appreciate assomething we see quite a bit.
It's another heterogeneousdisease that probably is going
to benefit a lot with topicaljack inhibitor inhibition.
Speaker 1 (23:32):
Wow, I mean, it's
just truly exciting.
You know, I think that's where Ireally wanted to bring you on,
to help you know, not only ourhealthcare providers that listen
, but just patients, because Ithink we need to get on the same
page about this class.
I think there's been a lot offear mongering and just
misunderstanding, and part ofthat is you know some of the
studies, the labeling, but whenyou put it in context, like you
just did, I think that it paintsa much brighter future for
(23:56):
these drugs obviously wherethey're going, but really where
they are for the here and nowand how they can benefit our
patients, especially with atopicdermatitis.
So thank you so much, Raj, forcoming on and chatting with us
today.
I know a lot of people up thereare going to feel a lot better
about prescribing those JAKs andfor those patients getting
ready to take them, I thinkthey're going to feel more
confident in the drug as welland what it can do for them.
(24:16):
For our listeners out there, ifthey want to find you, can you
let them know where you'relocated online or elsewhere, if
they want to track you down?
Speaker 2 (24:23):
Sure thing.
So, first and foremost, thanksso much for having me on.
It's been a real pleasurehaving, for having this
conversation, one that I lovehaving, and for anybody that
wants to learn more.
This is one of severaldisease-related areas I've
probably been doing a lot ofeducation on over the years.
You can look for me on myvarious handles RajMDPhD on
LinkedIn, where I like to sharecontent that I've made on X as
(24:43):
well, though not entirely active.
I have my own webpage where Itry to keep track of some of the
stuff I've done as well.
In case you want to pick up onthat and it's literally
rajmdphdcom as well, and justlooking for me, we'll find my
clinic page for our clinicthat's located in Chicago as
well.
Speaker 1 (24:58):
Well, thanks again,
raj, it was great having you on
the podcast, and for all of youout there, stay tuned for the
next episode of Dermot Trotter,don't Swear About Skincare.