June 10, 2025 • 27 mins
Dr. Shannon Trotter sits down with Dr. Shawn Kwatra, a leading expert on chronic itch, to shed light on prurigo nodularis (PN)—a painful, often misunderstood condition frequently misdiagnosed as psychological.
Dr. Kwatra explains that PN is driven by a systemic inflammatory cycle between the immune system and nerves, creating an itch patients describe as worse than pain. He shares new insights into diagnosis, mental health impact, and cutting-edge treatments, including two FDA-approved biologics—dupilumab and nemolizumab—that offer real relief.
This episode brings awareness, compassion, and hope to those living with PN—and to the clinicians working to better treat it.
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Episode Transcript
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Speaker 1 (00:00):
any of these types of skin lesions nodules, but also
smaller bumps and someexcoriations from scratching.
And when we looked in thebloodstream of these patients,
we found there's rampantinflammation in their
bloodstream.
So, even though there's skinlesions, it's actually, I think,
a systemic disease.
You also get a comprehensivemetabolic panel to make sure
(00:21):
there's no liver or kidneydysfunction.
You can get a thyroid to makesure there's no thyroid disease
as well.
The macro of what you're seeingis that patients are scratching
.
This is an itch-scratch cycle,but what I call the
micro-itch-scratch cycle.
Speaker 2 (00:38):
Welcome to Dermot Trotter Don't swear about
skincare when host Dr Shannon CTrotter, a board-certified
dermatologist, sits down withfellow dermatologists and
skincare experts to separatefact from fiction and simplify
skincare.
Let's get started.
Speaker 3 (00:56):
Welcome to the Dermotrotter Don't Swear About
Skin Care podcast.
Today I've got a special gueston here, dr Sean Quatra.
He's a board-certifieddermatologist and the Joseph W
Burnett Endowed Professor andChair of the Department of
Dermatology at the University ofMaryland School of Medicine.
He has over 300 publicationsand is a global leader in
(01:18):
everything itchy, especiallychronic itch.
Welcome to the podcast, sean.
Speaker 1 (01:22):
Shannon, thank you so much for having me on today.
Speaker 3 (01:26):
We love having you here because we know anything
itchy is right up your alley.
One of the things that I reallywanted to talk more with you
about today is something that wecall prigonodularis.
That you know all too well, butsome of our audience members
may not even know that this isactually a clinical diagnosis or
something that we treat indermatology.
Do you mind kind of explainingwhat paragonodularis is?
Speaker 1 (01:47):
Sure.
So you know the word parigojust means itchy bump, and so
now actually, the diagnosisparagonodularis is really wide
encompassing.
It can be a patient thatpresents with nodules or smaller
bumps, papules or excoriations,and all you have to have is
(02:08):
chronic itch for six weeks orlonger.
Any of these types of skinlesions nodules, but also
smaller bumps and someexcoriations from scratching.
So it's actually incrediblycommon.
Our group did some of the firststudies on the population level
incidents and found that it wasa few hundred thousand people,
but every year it keeps going up.
(02:31):
And family medicine, internalmedicine, nephrology, liver docs
everyone's seeing these typesof patients, and so I actually
think that the disease istotally under-recognized and
that it even could affectmillions of people every year.
Every doc is seeing thesepatients.
(02:51):
Whether they know it or not,they're seeing these patients.
You guys are all seeing thesepatients and super easy to make
a clinical diagnosis biopsy notneeded.
Speaker 3 (03:00):
And so you talked a little bit how it presents and
sort of that.
It can be lots of differentpresentations.
A lot of people think it justhas to be bumpy, but you
described it can also justpresent as scratch marks or
excreation marks.
How do you most often seeprigonodularis present in the
patient and what are thesymptoms I mean beyond maybe
obviously itching, which mightbe quite obvious?
Speaker 1 (03:19):
Yeah, the itch is definitely the most dominant
feature that leads to sleep lossand quality of life disruption,
but oftentimes these lesionsalso sting a lot, they're
painful and there's manydifferent manifestations.
Usually you see nodules orbumps on the upper and lower
extremities.
We did a study that showed thatthese are the most common areas
(03:39):
where you develop these skinlesions.
But it can happen anywhere onthe body where you develop these
skin lesions, but it can happenanywhere on the body.
What's sad is sometimespatients are labeled as having
itching.
That's due to psychiatricfactors.
There's a term excoriationdisorder or I really don't like
(04:02):
this term and I don't thinkanybody should use it, but it is
an ICD-10 code ICD-9 codeneurotic excoriations which I
think is not respectful ofpatient.
But many of these patients whoactually have prionage lyris
have been inappropriatelylabeled as having their itch be
all in their head.
And I've seen these patientsand the number one question to
ask them is are you actuallyitchy?
(04:23):
And if patients are itchy, thenthey warrant therapy with one
of our multiple FDA approvedtherapies now for this condition
and many more that are comingalong, and I personally had many
patients who for 10 years ormore thought that it was just
all in their head.
They were very itchy, they gottreated and then they were
(04:44):
totally clear and I made it mymission to always talk about
this that we can't label people,as you know, having psychiatric
related itch.
We have to treat them.
Itch is really on thisneuroimmune axis and it's worth
it to try therapy One of our newsafe therapeutics that we have
(05:07):
approved for this condition.
Speaker 3 (05:10):
I really like that you highlight that because I
think you're right.
We see this a lot in patientsthat come in.
You know, and you probably seethis in patients multiple times
a day with dealing with so manypatients with paragonodularis.
But they'll say, yeah, you know, they've told me I'm crazy.
I've been to multiple doctors.
Nobody seems to be able tofigure out what I have.
And I think that awareness thatyou talked about, that people
(05:30):
just put this on their radar,that this is a true diagnosis
and the downside is, as youtalked about the mental health
aspect, is just having itch forthat long.
Imagine the stress and anxietyor even depression it might
cause a patient.
And so, yeah, there is thatconnection to mental health.
But exactly right to highlighthow it's not really all in their
head.
This is a true thing going onin their skin physiologically.
(05:52):
That explains that itch, thatthe the bumpy part you know a
lot of patients will ask aboutthey'll, and maybe you can
clarify this a little bit.
Do you kind of look at this asa primary process of the disease
itself or do you feel like,because of that chronic itching
scratching, it gets createdthroughout the process?
Or is it a combination of both,because they're always asking
how do you explain these bumpsthat are coming up on my skin?
Speaker 1 (06:13):
That's a great question, and oftentimes they're
actually symmetrically locatedon the extremities.
So there is a thought thatthere actually is a neural
plexus and the origin of theselesions is related to those
different points.
But what we also know is thattwo-thirds of patients this is a
(06:33):
study from our group areactually itchy, both in the
nodules or skin lesions, butalso in normal appearing skin,
and when we looked in thebloodstream of these patients,
we found there's rampantinflammation in their
bloodstream.
So even though there's skinlesions, it's actually, I think,
a systemic disease processwarranting a systemic therapy.
(06:56):
And I think one of the biggestproblems with the management of
these patients is that sometimesproviders stick with topicals
only targeting these lesions fortoo long and not recognizing
this is actually a systemicdisease process.
Speaker 3 (07:14):
And that's fascinating because we were
learning more and more aboutthis in dermatology right in
general, about the skinconditions we treat.
We used to you know, not to usethe cliche but I think they're
only skin deep only to learnmore about sort of this chronic
inflammation and, like youmentioned, more systemic or
widespread throughout the body.
Now you mentioned that neuronalplexus component.
Do you mind explaining that alittle bit more for our
(07:35):
listeners that are thinking well, what is he talking about?
Nerves, like again, becausesome people hear that nerve
component like again I'm notanxious about you know, or maybe
I get anxiety from itching somuch, but where does that nerve
component kind of play a rolefor patients?
Speaker 1 (07:48):
Sure.
So there's actually nerves thatgo all the way out to that
outermost layer of the skin, theepidermis and the dermis.
We call them thinly myelinatedA-delta fibers and unmyelinated
C fibers.
Many of us learn this inneurology or anatomy.
I think all those classes Istruggled with having to
(08:09):
memorize all the cranial nervesI don't know if you remember
that.
Speaker 2 (08:12):
Oh yeah, oh yeah.
Speaker 1 (08:14):
I really struggled.
I still remember being in thelibrary in medical school going
over them, but they areimportant.
I actually thought they wouldn'tbe important, but they're very
important to what we do asdermatologists because those
nerves go from that outer layerof the skin to the dorsal
ganglion, they cross over in thespinal cord and they go to the
brain and that is how theimpulse of itch is transmitted.
(08:35):
And the macro of what you'reseeing is that patients are
scratching.
This is an itch-scratch cycle,but what I call the
micro-itch-scratch cycle is avariety of different immune
cells that we have, likeeosinophils and T-cells and
basophils in the skin thatsecrete a lot of cytokines, like
IL-4 and 13 or IL-31.
(08:56):
They stimulate the nervesbecause their receptors are on
there.
The nerves releaseneuropeptides and the
neuropeptides actually causeimmune cells to secrete
cytokines and you have thiscycle, and so chronic itch and
paragonidolaris is a combinationof dysfunction of these immune
cells and the nerves.
And the nerves actually are theendpoint of transmitting itch,
which is the debilitatingsymptom that the patient
(09:19):
experiences.
So your nerves are very centralto the disease and in these
patients you're trying to find atherapy that can tamp down on
both the immune and the neuralparties that are responsible for
transmitting chronic itch.
Speaker 3 (09:36):
So fascinating too.
I mean I think people againjust think of it just being so
simple.
But the way you describe it, Ithink a lot of patients, as you
know too, would put it on thesame level of pain.
You know where they've maybehad significant pain before,
maybe an injury or surgery.
And it's very impressive howpeople will just talk about,
yeah, but this itch nothingcompares to how impactful itch
(09:58):
has been in my life.
I mean worse than pain.
I can remember treatingpatients with skin lymphoma when
I was in fellowship and some ofthese folks itch to the extent
of, you know, even contemplatingsuicide because of how terrible
itching can be.
You know, with itching you kindof talked about kind of that
physiologic reason why we itchand again how it's a little bit
different, you know, andprigonodular is, do you see some
(10:20):
differences to with itching,with different skin types, kind
of going along the spectrum oflighter skin to darker skin, and
how itch impacts them maybe alittle differently, and just the
physiology of it.
Speaker 1 (10:32):
Yeah, no, it's a great question To start.
Chronic itch, I absolutelyagree, is incredibly
debilitating and we did a studywith our itch patients showing
that a chronic itch patient hasthe disruption on quality of
life equivalent to a patient whohas chronic heart failure,
who's had a stroke or is onhemodialysis.
So that's very significantburden that our patients are
(10:57):
experiencing.
And I always ask patients whatis the worst itch or the peak
pruritus or itching that you'vehad in the last 24 hours at any
moment, zero to 10?
And that number, especially ifit's a seven or higher, conveys
severe itch, oftentimesinflammation in the blood.
You know people are notsleeping well.
That's a great marker in theblood.
(11:17):
You know people are notsleeping well.
That's a great marker.
What we've also found is thatitch can have different
presentations in time.
So we know, from atopicdermatitis and eczema in
African-American patients, youcan often have more bumpy or
papular disease on extensorsurfaces.
Paragonagylaris inAfrican-American patients
oftentimes has more thickenedlesions, more fibrotic lesions,
(11:38):
almost even keloidal in terms ofthe degree of fibrosis.
So it's very interesting, um,the significant skin thickening,
um, so there's just a varietyof different disease
manifestations.
Uh, we know the itch process issimilar, but what's so special
about paragonagularis is youalso have the double whammy of
(11:59):
not only having terrible itch,but also having these
disfiguring nodules that canimpair you psychosocially as
well.
It's really, you know, theworst of the worst.
Speaker 3 (12:07):
Yeah, I mean think about it, because you know
people are staring at you if yousee these bumps.
I remember having patients comein with PN and they're
constantly wearing you knowsleeves to cover up their arms
because they're embarrassed orthey'll just get labeled a
picker right, and lots of peopleare self-proclaimed pickers.
But we know this is so muchmore than that and what our
patients experienceno-transcript patients more.
Speaker 1 (12:45):
It's a great question .
So patients with prigonodularishave certain diseases that are
more common, for example type 2diabetes, and type 2 diabetes in
particular, I think makes sense, because you have high blood
glucose, you can have damage tothe peripheral nerves and that
can actually almost set off thisitch-scratch cycle by having
(13:06):
damage to the nerves that canthen release neuropeptides that
secrete cytokines from theimmune cells.
So type 2 diabetes is one ofthese common areas, but we know
there's other things like evenCOPD, chronic obstructive
pulmonary disease, hypertension,cardiometabolic diseases.
We know that hepatitis C, hiv,are more common as well.
Actually, our group did thefirst genetic study of
(13:27):
paragonodularis patients andfound that it's genetically
encoded whether you're morelikely to itch in general and
develop skin lesions or nodulesconsistent with paragonodularis,
or if you just have itching onnormal appearing skin, and so
that's why the workup forparagonodularis is exactly
similar to the workup foritching without a rash.
(13:50):
You're going to get a completeblood count to look at
hematologic parameters.
I also look at the eosinophilcount always because that's a
good indicator, if it's high, ofgood type 2 inflammation.
You also get a comprehensivemetabolic panel to make sure
there's no liver or kidneydysfunction.
You can get a thyroid to makesure there's no thyroid disease
(14:10):
as well, and then in certainpatients with risk factors, you
can get a comprehensivemetabolic.
You can get, in addition to acomprehensive metabolic panel,
you can get the hepatitistesting tests for HIV.
Those are all things that maybe associated with the disease.
But what I think actually, andwhere I think the science is
taking us, some of the sciencethat we're doing is that in a
(14:32):
prigonodularis patient you haveinflammation that's in your
whole bloodstream, and Iactually believe that a lot of
these diseases that areassociated with prigonagularis
can occur or worsen if thedisease is untreated.
So we actually found thatpatients with prigonagularis are
more likely to subsequentlydevelop chronic kidney disease
and have renal failure.
(14:53):
So I actually think there's amissing piece here.
It's not just that thesediseases are associated with
trigonodularis or itching, it'salso that the uncontrolled
inflammation from this diseasecan then cause damage to other
organs, and I think that's aparadigm we're exploring and
we've done studies with bothdupilumab and emolizumab showing
(15:13):
that they can reduce systemicinflammation in these patients,
and really looking forward tomore real-world studies that
looks at this more in depth aswell.
Speaker 3 (15:24):
That's going to be one of the key points, you know,
I think, for people to takehome from our conversation,
because that is something Idon't think that association
there is in the minds of mostyou know practicing primary care
physicians or somebody, andeven just the of most you know
practicing primary carephysicians or somebody where,
and even just the dermatologistsyou know, to really think of
this condition beyond what we'veknown and really just apply it
like we have to other, you know,skin conditions we treat like
(15:45):
psoriasis or hidronitissepharitiva or things like that.
I do think people are really,you know, look at this
superficially so that systemicpiece and maybe how it worsens
other internal issues.
Hate to say it, we try to getaway from internal medicine and
derm, but I just don't think wecan.
You know these things areintimately connected.
People try to run, we dosometimes, but I think it's
going to catch up to us,especially with PN.
(16:07):
Now that we've talked a littlebit, you know, obviously, about
kind of how it looks, a littlebit on the pathophysiology sort
of the diagnosis to it, I wantedto dive in a little bit deeper
and talk kind of about the broadspectrum, you know, of
treatment and how you mightapproach somebody that comes in
and you're thinking, yeah, youclinically have prigonodularis.
Where do you kind of start andhow do you look at the different
(16:27):
tools that are available to usto really control this disease
for patients?
Speaker 1 (16:33):
So I pretty quickly, when I'm evaluating these
patients, can get a good senseof how severe their disease is,
and I think everybody should beusing clinical bedside markers
and asking people about theiritch.
Again, zero to 10, what's theworst itch you've had in the
last 24 hours?
You get a number.
If it's seven or higher, evenfive, you know that you're
(16:54):
having pretty severe disease andyou need to be in the systemic
realm.
I think topical steroids arealways reasonable as an adjunct
therapy.
Phototherapy is a reasonabletherapy as well, but they're
just slow.
So to tell you the truth rightoff the bat, I'm usually going.
If people have more than, say,20 or so nodules, lesions and an
(17:15):
itch around seven or higher,I'm immediately going to one of
our two FDA approved therapies.
So we have both dupilumab,which is an IL-4 receptor alpha
blocker that blocks IL-4 and 13,which we know are increased in
these patients, and then alsorecently we've gotten the FDA
approval of nemolizumab, whichtargets the itchy cytokine IL-31
(17:35):
, and it's a blocker of IL-30and receptor alpha.
We're very lucky to havemultiple agents approved for
prigonodular.
Shannon, if I'd asked you that10 years ago, I don't think you
would have thought that waspossible, would you no way, not
at all yeah.
It's amazing, and so we havethese two drugs that actually
(17:57):
don't require regular laboratorymonitoring.
They're very targeted, muchsafer, so we've tried in the
past like methotrexate as adiaphragm any of these agents.
So we're very, very lucky andwhat I'm trying to do is make
sure that we decrease the amountof time that our patients are
suffering, cause still I seepatients every single clinic,
even earlier today have goneyears just with topical steroids
(18:18):
and been suffering before theyget to start on these systemic
agents, other agents that weshould know about.
There's some off-label studieson oral JAK inhibitors.
I actually presented some dataon oral provacitinib and also
topical ruxolinib that are beingdeveloped for this.
So exciting to have new optionsin the pipeline.
And then there certainly aredifferent off-label therapeutics
(18:42):
.
Some things that people like todo are inject steroids.
I think that's reasonable,especially if you have less
number of spots that you caninject the steroids.
Injection or intralesionalcorticosteroids are more
effective in PN than topicalsbecause, if you think about it,
there's this dead layer of skinat the top, the hyperkeratosis
it's very hard to get throughthat and the epidermal
(19:04):
acanthosis to get to where theaction is lower layers, the
epidermis and dermis, where youhave a lot of inflammation, the
acinophils T cells, fibroblasts,that are releasing these
cytokines.
So that's's the reason thattopical steroids don't work as
effectively and oftentimes youcan do the intralesional
therapies.
But especially a lot of skinand color patients, you worry
about hypopigmentation in thosepatients.
(19:25):
So in general, topicals are alittle bit more challenging
depending on the particularagent.
I go for one of these two newFDA approved therapeutics and
then adjunctive therapies likenarrow band phototherapy can be
helpful.
It's just a little slow, Ithink, but reasonable adjunctive
therapy for patients who havetrouble getting insurance
(19:45):
approval can always consider,you know, methotrexate therapy
or cyclosporine for a very shortperiod of time.
Again, these agents are veryuntargeted and not really needed
in this current landscape wherewe have more targeted
therapeutics currently.
Speaker 3 (20:02):
And from the standpoint I don't know if you
get this question a lot, I feellike often patients come in
they're like, okay, I know aboutthese options, Are there any
other natural options or thingsthat you think are worthwhile?
Or should I be watching thingsin my diet?
Or is there a supplement youwould recommend?
And again, knowing not alwaysthat is the evidence as strong
as what we have, obviously, forour clinical trials and approved
(20:23):
drugs Are there any types of,you know, treatments in that
sort of arena that you entertainor may offer to patients as an
option?
Speaker 1 (20:30):
You know, shannon, I'm gonna give you a story.
I recently tried a lavenderspray.
My wife she's also adermatologist yeah, she was like
there's no way this works.
Speaker 3 (20:40):
I was having a little thing, they were telling me,
you just want to prove her wrongSean.
Speaker 1 (20:44):
They were saying hey, this will help you sleep.
And my wife's like what are?
Speaker 2 (20:48):
you doing what do?
Speaker 1 (20:48):
you get, and I was like, no, I'm going to try it.
And it knocked me out.
And from that moment on too, Iwas like you know what?
We're going to be really superopen to all sorts of alternative
things and I've been.
I've been telling patients allabout turmeric powder, all sorts
of things.
Um, but no, absolutely.
I think that there's a role foralternative therapeutics.
We have a study where we lookedat the gut microbiome and found
(21:11):
some very interesting resultsin prognodular patients that
we're going to be publishingsoon.
Speaker 2 (21:16):
But the one thing I tell these patients is we want
to limit processed foods.
Speaker 1 (21:20):
So what we think is going on is that gut microbiome
is actually signaling and cantrigger itch by signaling
through the vagal nerve, andwhat we are finding is that
there's a lot of these fungalspecies that are upregulated in
praga nodularis patients, andwhat we think is that they're
tied to food deserts andprocessed foods.
(21:41):
So I tell all my patients ifyou can have a handful of
blueberries and eat some spinachor other greens and I'm talking
to myself also, because I lovefrench fries every day You're
eating chips, I'm eating chips,but I'm telling people to eat
blueberries and spinach.
I'm a hypocrite.
But as so we know that thosethings will help, will they cure
(22:02):
you alone?
No, probably not.
But of course those are greatthings that you can do that can
help a lot.
I think the unbalanced diet hascaused so many problems.
We can see, with the rise ofthe dry night, a spur of tea,
but I think probably gosimilarly as well.
Whatever we can do to makeourselves healthier overall.
But is there one alternativetherapy?
That's magic bullet?
Maybe we just don't know whatit is yet.
Speaker 3 (22:24):
Maybe it's lavender.
I was going to say for sleep wefound out.
Speaker 1 (22:29):
You have to try it.
Oh my God.
Speaker 3 (22:31):
I do love lavender a little bit, the essential oil
thing.
I don't always know if it'llknock me out, but it does.
It is relaxing, I'll give youthat.
I'll give you that.
We've talked more about kind ofthe medical piece, anything you
recommend if somebody issuffering from pregnenitis
adjusting maybe the mentalhealth aspect of how it impacts
their life that you typicallyemploy into your treatment
(22:51):
strategy.
Speaker 1 (22:53):
I think it's really important to get help if you
need it and to ask that question.
You talked a little bit earlierabout suicidal ideation.
You talked a little bit earlierabout suicidal ideation.
I was giving a talk and adermatologist came up to me and
they said they had treated oneof these patients with something
we all use, a triamcinolone.
We made a medium potencytopical steroid you know most
(23:15):
dermatologists use this veryoften and they'd had some time
to see the patient back and theyactually did commit suicide.
Oh my, and it's very toughhearing that.
I actually have a lot ofpatients that see me, that put a
lot of pressure and say, hey,if you can't help me, I'm
(23:36):
considering to kill myself, andit highlights how severe this
disease is, how much of animpact we can make.
But it also, I think to yourquestion, highlights how
important it is that we askpatients and refer them to get
care and someone to talk to andsomeone to evaluate them and
have a good relationship withpsychologists and psychiatrists
(23:57):
in our area and can referpatients and let them know that
there's a huge mental burden.
If you're itching and you can'tsleep, of course you know
you're more likely to haveanxiety and depression and then
that can be tough to get out of.
Even if we get the itch betterquickly, it's hard to get out of
that.
So I think, having that levelof empathy and asking I know
that we're very busy in ourclinics, but simple questions
(24:19):
there's anxiety and depressionscales.
A simple check-in takes a fewseconds but it is important, I
think, to do that and also tomake sure that we're being
aggressive with therapy.
I think that's very importantas well.
Speaker 3 (24:33):
Yeah, I like how you talk about that because it is a
very holistic approach I thinkthat we have to take as
dermatologists.
You can't silo out, you know, Ithink, all the skin diseases we
treat, the impact they have onsomebody's life, whether it's at
work or their ability to sleep,or just their mood, or, you
know, the development ofdepression or anxiety.
You know, I think that'ssomething we have to take very
(24:55):
seriously because I think youknow it's their busy days and
people sometimes gloss over thator our patients don't maybe
recognize it.
So for us to be able to pullthat out, get them to the right
place, to add that into theirtreatment regimen, that really
shows how we're committed toreally treating disease and the
patient entirely.
So really love that.
You highlight that.
And before we kind of end here,I did want to ask where do you
(25:15):
think we'll be in 10 years fromnow?
You know we already talkedabout where we were 10 years ago
.
10 years from now, in thetreatment of PM, where do we
think we'll be, or what do youthink is the most promising
treatment advancement that'llcome forth?
Speaker 1 (25:26):
You know, now that we have a pipeline, I think that's
the hardest thing to have avalidated scale, approved drugs,
a design of clinical trials.
We're going to see a ton of newtherapies and the mast cell has
actually emerged as being veryimportant.
It's unregulated in the lesionsof these patients and we know
the mast cell releases all theseitchy mediators and I think PN
(25:48):
is going to be one of thosediseases where we have mast cell
modifying drugs being approved.
There's multiple in developmenttargeting brutinine, tyrosine
kinase, also triptase and CKIT.
There's many different anglesof targeting the mast cell.
So I'm very hopeful to look atthat.
I also think many of the drugsthat are going to be approved
(26:08):
for atopic dermatitis may alsogo in for pyrogonadularis things
like OX40 and OX40 ligandinhibitors.
Many of the other newmonoclonal tri-specifics I think
could be great forparagonadularis as well.
So I'm very, very excited aboutall of the new therapeutics and
(26:31):
to see how this field develops.
Speaker 3 (26:33):
And maybe lavender spray right.
Speaker 1 (26:34):
Lavender spray.
Maybe I might do a clinicaltrial on it.
Speaker 3 (26:40):
Well, you'll just prove your wife right.
She'll appreciate that, likeall of us wives out there do.
Well, thank you so much, sean,for coming on the podcast.
This has been great to reallyget this broad overview of PN
really help people understand, Ithink, this entity a lot better
.
It deserves a lot moreattention than it's received in
the past and it's exciting tofinally see that people are
really looking more into it andreally providing patients with
(27:01):
relief.
Speaker 1 (27:10):
For our listeners out there.
If they want to find you, doyou mind sharing with how they
can locate you?
Sure, I'm on LinkedIn at DrSean Quattro, also Instagram and
X, so feel free to follow me.
Speaker 3 (27:14):
Well, thanks again for coming on the podcast and
stay tuned for the next episodeof Dermot Trotter.
Don't swear about skincare.
Speaker 2 (27:22):
Thanks for listening to Dermot Trotter For more about
skincare.
any of these types of skin lesions nodules, but also
smaller bumps and someexcoriations from scratching.
And when we looked in thebloodstream of these patients,
we found there's rampantinflammation in their
bloodstream.
So, even though there's skinlesions, it's actually, I think,
a systemic disease.
You also get a comprehensivemetabolic panel to make sure
(00:21):
there's no liver or kidneydysfunction.
You can get a thyroid to makesure there's no thyroid disease
as well.
The macro of what you're seeingis that patients are scratching
.
This is an itch-scratch cycle,but what I call the
micro-itch-scratch cycle.
Speaker 2 (00:38):
Welcome to Dermot Trotter Don't swear about
skincare when host Dr Shannon CTrotter, a board-certified
dermatologist, sits down withfellow dermatologists and
skincare experts to separatefact from fiction and simplify
skincare.
Let's get started.
Speaker 3 (00:56):
Welcome to the Dermotrotter Don't Swear About
Skin Care podcast.
Today I've got a special gueston here, dr Sean Quatra.
He's a board-certifieddermatologist and the Joseph W
Burnett Endowed Professor andChair of the Department of
Dermatology at the University ofMaryland School of Medicine.
He has over 300 publicationsand is a global leader in
(01:18):
everything itchy, especiallychronic itch.
Welcome to the podcast, sean.
Speaker 1 (01:22):
Shannon, thank you so much for having me on today.
Speaker 3 (01:26):
We love having you here because we know anything
itchy is right up your alley.
One of the things that I reallywanted to talk more with you
about today is something that wecall prigonodularis.
That you know all too well, butsome of our audience members
may not even know that this isactually a clinical diagnosis or
something that we treat indermatology.
Do you mind kind of explainingwhat paragonodularis is?
Speaker 1 (01:47):
Sure.
So you know the word parigojust means itchy bump, and so
now actually, the diagnosisparagonodularis is really wide
encompassing.
It can be a patient thatpresents with nodules or smaller
bumps, papules or excoriations,and all you have to have is
(02:08):
chronic itch for six weeks orlonger.
Any of these types of skinlesions nodules, but also
smaller bumps and someexcoriations from scratching.
So it's actually incrediblycommon.
Our group did some of the firststudies on the population level
incidents and found that it wasa few hundred thousand people,
but every year it keeps going up.
(02:31):
And family medicine, internalmedicine, nephrology, liver docs
everyone's seeing these typesof patients, and so I actually
think that the disease istotally under-recognized and
that it even could affectmillions of people every year.
Every doc is seeing thesepatients.
(02:51):
Whether they know it or not,they're seeing these patients.
You guys are all seeing thesepatients and super easy to make
a clinical diagnosis biopsy notneeded.
Speaker 3 (03:00):
And so you talked a little bit how it presents and
sort of that.
It can be lots of differentpresentations.
A lot of people think it justhas to be bumpy, but you
described it can also justpresent as scratch marks or
excreation marks.
How do you most often seeprigonodularis present in the
patient and what are thesymptoms I mean beyond maybe
obviously itching, which mightbe quite obvious?
Speaker 1 (03:19):
Yeah, the itch is definitely the most dominant
feature that leads to sleep lossand quality of life disruption,
but oftentimes these lesionsalso sting a lot, they're
painful and there's manydifferent manifestations.
Usually you see nodules orbumps on the upper and lower
extremities.
We did a study that showed thatthese are the most common areas
(03:39):
where you develop these skinlesions.
But it can happen anywhere onthe body where you develop these
skin lesions, but it can happenanywhere on the body.
What's sad is sometimespatients are labeled as having
itching.
That's due to psychiatricfactors.
There's a term excoriationdisorder or I really don't like
(04:02):
this term and I don't thinkanybody should use it, but it is
an ICD-10 code ICD-9 codeneurotic excoriations which I
think is not respectful ofpatient.
But many of these patients whoactually have prionage lyris
have been inappropriatelylabeled as having their itch be
all in their head.
And I've seen these patientsand the number one question to
ask them is are you actuallyitchy?
(04:23):
And if patients are itchy, thenthey warrant therapy with one
of our multiple FDA approvedtherapies now for this condition
and many more that are comingalong, and I personally had many
patients who for 10 years ormore thought that it was just
all in their head.
They were very itchy, they gottreated and then they were
(04:44):
totally clear and I made it mymission to always talk about
this that we can't label people,as you know, having psychiatric
related itch.
We have to treat them.
Itch is really on thisneuroimmune axis and it's worth
it to try therapy One of our newsafe therapeutics that we have
(05:07):
approved for this condition.
Speaker 3 (05:10):
I really like that you highlight that because I
think you're right.
We see this a lot in patientsthat come in.
You know, and you probably seethis in patients multiple times
a day with dealing with so manypatients with paragonodularis.
But they'll say, yeah, you know, they've told me I'm crazy.
I've been to multiple doctors.
Nobody seems to be able tofigure out what I have.
And I think that awareness thatyou talked about, that people
(05:30):
just put this on their radar,that this is a true diagnosis
and the downside is, as youtalked about the mental health
aspect, is just having itch forthat long.
Imagine the stress and anxietyor even depression it might
cause a patient.
And so, yeah, there is thatconnection to mental health.
But exactly right to highlighthow it's not really all in their
head.
This is a true thing going onin their skin physiologically.
(05:52):
That explains that itch, thatthe the bumpy part you know a
lot of patients will ask aboutthey'll, and maybe you can
clarify this a little bit.
Do you kind of look at this asa primary process of the disease
itself or do you feel like,because of that chronic itching
scratching, it gets createdthroughout the process?
Or is it a combination of both,because they're always asking
how do you explain these bumpsthat are coming up on my skin?
Speaker 1 (06:13):
That's a great question, and oftentimes they're
actually symmetrically locatedon the extremities.
So there is a thought thatthere actually is a neural
plexus and the origin of theselesions is related to those
different points.
But what we also know is thattwo-thirds of patients this is a
(06:33):
study from our group areactually itchy, both in the
nodules or skin lesions, butalso in normal appearing skin,
and when we looked in thebloodstream of these patients,
we found there's rampantinflammation in their
bloodstream.
So even though there's skinlesions, it's actually, I think,
a systemic disease processwarranting a systemic therapy.
(06:56):
And I think one of the biggestproblems with the management of
these patients is that sometimesproviders stick with topicals
only targeting these lesions fortoo long and not recognizing
this is actually a systemicdisease process.
Speaker 3 (07:14):
And that's fascinating because we were
learning more and more aboutthis in dermatology right in
general, about the skinconditions we treat.
We used to you know, not to usethe cliche but I think they're
only skin deep only to learnmore about sort of this chronic
inflammation and, like youmentioned, more systemic or
widespread throughout the body.
Now you mentioned that neuronalplexus component.
Do you mind explaining that alittle bit more for our
(07:35):
listeners that are thinking well, what is he talking about?
Nerves, like again, becausesome people hear that nerve
component like again I'm notanxious about you know, or maybe
I get anxiety from itching somuch, but where does that nerve
component kind of play a rolefor patients?
Speaker 1 (07:48):
Sure.
So there's actually nerves thatgo all the way out to that
outermost layer of the skin, theepidermis and the dermis.
We call them thinly myelinatedA-delta fibers and unmyelinated
C fibers.
Many of us learn this inneurology or anatomy.
I think all those classes Istruggled with having to
(08:09):
memorize all the cranial nervesI don't know if you remember
that.
Speaker 2 (08:12):
Oh yeah, oh yeah.
Speaker 1 (08:14):
I really struggled.
I still remember being in thelibrary in medical school going
over them, but they areimportant.
I actually thought they wouldn'tbe important, but they're very
important to what we do asdermatologists because those
nerves go from that outer layerof the skin to the dorsal
ganglion, they cross over in thespinal cord and they go to the
brain and that is how theimpulse of itch is transmitted.
(08:35):
And the macro of what you'reseeing is that patients are
scratching.
This is an itch-scratch cycle,but what I call the
micro-itch-scratch cycle is avariety of different immune
cells that we have, likeeosinophils and T-cells and
basophils in the skin thatsecrete a lot of cytokines, like
IL-4 and 13 or IL-31.
(08:56):
They stimulate the nervesbecause their receptors are on
there.
The nerves releaseneuropeptides and the
neuropeptides actually causeimmune cells to secrete
cytokines and you have thiscycle, and so chronic itch and
paragonidolaris is a combinationof dysfunction of these immune
cells and the nerves.
And the nerves actually are theendpoint of transmitting itch,
which is the debilitatingsymptom that the patient
(09:19):
experiences.
So your nerves are very centralto the disease and in these
patients you're trying to find atherapy that can tamp down on
both the immune and the neuralparties that are responsible for
transmitting chronic itch.
Speaker 3 (09:36):
So fascinating too.
I mean I think people againjust think of it just being so
simple.
But the way you describe it, Ithink a lot of patients, as you
know too, would put it on thesame level of pain.
You know where they've maybehad significant pain before,
maybe an injury or surgery.
And it's very impressive howpeople will just talk about,
yeah, but this itch nothingcompares to how impactful itch
(09:58):
has been in my life.
I mean worse than pain.
I can remember treatingpatients with skin lymphoma when
I was in fellowship and some ofthese folks itch to the extent
of, you know, even contemplatingsuicide because of how terrible
itching can be.
You know, with itching you kindof talked about kind of that
physiologic reason why we itchand again how it's a little bit
different, you know, andprigonodular is, do you see some
(10:20):
differences to with itching,with different skin types, kind
of going along the spectrum oflighter skin to darker skin, and
how itch impacts them maybe alittle differently, and just the
physiology of it.
Speaker 1 (10:32):
Yeah, no, it's a great question To start.
Chronic itch, I absolutelyagree, is incredibly
debilitating and we did a studywith our itch patients showing
that a chronic itch patient hasthe disruption on quality of
life equivalent to a patient whohas chronic heart failure,
who's had a stroke or is onhemodialysis.
So that's very significantburden that our patients are
(10:57):
experiencing.
And I always ask patients whatis the worst itch or the peak
pruritus or itching that you'vehad in the last 24 hours at any
moment, zero to 10?
And that number, especially ifit's a seven or higher, conveys
severe itch, oftentimesinflammation in the blood.
You know people are notsleeping well.
That's a great marker in theblood.
(11:17):
You know people are notsleeping well.
That's a great marker.
What we've also found is thatitch can have different
presentations in time.
So we know, from atopicdermatitis and eczema in
African-American patients, youcan often have more bumpy or
papular disease on extensorsurfaces.
Paragonagylaris inAfrican-American patients
oftentimes has more thickenedlesions, more fibrotic lesions,
(11:38):
almost even keloidal in terms ofthe degree of fibrosis.
So it's very interesting, um,the significant skin thickening,
um, so there's just a varietyof different disease
manifestations.
Uh, we know the itch process issimilar, but what's so special
about paragonagularis is youalso have the double whammy of
(11:59):
not only having terrible itch,but also having these
disfiguring nodules that canimpair you psychosocially as
well.
It's really, you know, theworst of the worst.
Speaker 3 (12:07):
Yeah, I mean think about it, because you know
people are staring at you if yousee these bumps.
I remember having patients comein with PN and they're
constantly wearing you knowsleeves to cover up their arms
because they're embarrassed orthey'll just get labeled a
picker right, and lots of peopleare self-proclaimed pickers.
But we know this is so muchmore than that and what our
patients experienceno-transcript patients more.
Speaker 1 (12:45):
It's a great question .
So patients with prigonodularishave certain diseases that are
more common, for example type 2diabetes, and type 2 diabetes in
particular, I think makes sense, because you have high blood
glucose, you can have damage tothe peripheral nerves and that
can actually almost set off thisitch-scratch cycle by having
(13:06):
damage to the nerves that canthen release neuropeptides that
secrete cytokines from theimmune cells.
So type 2 diabetes is one ofthese common areas, but we know
there's other things like evenCOPD, chronic obstructive
pulmonary disease, hypertension,cardiometabolic diseases.
We know that hepatitis C, hiv,are more common as well.
Actually, our group did thefirst genetic study of
(13:27):
paragonodularis patients andfound that it's genetically
encoded whether you're morelikely to itch in general and
develop skin lesions or nodulesconsistent with paragonodularis,
or if you just have itching onnormal appearing skin, and so
that's why the workup forparagonodularis is exactly
similar to the workup foritching without a rash.
(13:50):
You're going to get a completeblood count to look at
hematologic parameters.
I also look at the eosinophilcount always because that's a
good indicator, if it's high, ofgood type 2 inflammation.
You also get a comprehensivemetabolic panel to make sure
there's no liver or kidneydysfunction.
You can get a thyroid to makesure there's no thyroid disease
(14:10):
as well, and then in certainpatients with risk factors, you
can get a comprehensivemetabolic.
You can get, in addition to acomprehensive metabolic panel,
you can get the hepatitistesting tests for HIV.
Those are all things that maybe associated with the disease.
But what I think actually, andwhere I think the science is
taking us, some of the sciencethat we're doing is that in a
(14:32):
prigonodularis patient you haveinflammation that's in your
whole bloodstream, and Iactually believe that a lot of
these diseases that areassociated with prigonagularis
can occur or worsen if thedisease is untreated.
So we actually found thatpatients with prigonagularis are
more likely to subsequentlydevelop chronic kidney disease
and have renal failure.
(14:53):
So I actually think there's amissing piece here.
It's not just that thesediseases are associated with
trigonodularis or itching, it'salso that the uncontrolled
inflammation from this diseasecan then cause damage to other
organs, and I think that's aparadigm we're exploring and
we've done studies with bothdupilumab and emolizumab showing
(15:13):
that they can reduce systemicinflammation in these patients,
and really looking forward tomore real-world studies that
looks at this more in depth aswell.
Speaker 3 (15:24):
That's going to be one of the key points, you know,
I think, for people to takehome from our conversation,
because that is something Idon't think that association
there is in the minds of mostyou know practicing primary care
physicians or somebody, andeven just the of most you know
practicing primary carephysicians or somebody where,
and even just the dermatologistsyou know, to really think of
this condition beyond what we'veknown and really just apply it
like we have to other, you know,skin conditions we treat like
(15:45):
psoriasis or hidronitissepharitiva or things like that.
I do think people are really,you know, look at this
superficially so that systemicpiece and maybe how it worsens
other internal issues.
Hate to say it, we try to getaway from internal medicine and
derm, but I just don't think wecan.
You know these things areintimately connected.
People try to run, we dosometimes, but I think it's
going to catch up to us,especially with PN.
(16:07):
Now that we've talked a littlebit, you know, obviously, about
kind of how it looks, a littlebit on the pathophysiology sort
of the diagnosis to it, I wantedto dive in a little bit deeper
and talk kind of about the broadspectrum, you know, of
treatment and how you mightapproach somebody that comes in
and you're thinking, yeah, youclinically have prigonodularis.
Where do you kind of start andhow do you look at the different
(16:27):
tools that are available to usto really control this disease
for patients?
Speaker 1 (16:33):
So I pretty quickly, when I'm evaluating these
patients, can get a good senseof how severe their disease is,
and I think everybody should beusing clinical bedside markers
and asking people about theiritch.
Again, zero to 10, what's theworst itch you've had in the
last 24 hours?
You get a number.
If it's seven or higher, evenfive, you know that you're
(16:54):
having pretty severe disease andyou need to be in the systemic
realm.
I think topical steroids arealways reasonable as an adjunct
therapy.
Phototherapy is a reasonabletherapy as well, but they're
just slow.
So to tell you the truth rightoff the bat, I'm usually going.
If people have more than, say,20 or so nodules, lesions and an
(17:15):
itch around seven or higher,I'm immediately going to one of
our two FDA approved therapies.
So we have both dupilumab,which is an IL-4 receptor alpha
blocker that blocks IL-4 and 13,which we know are increased in
these patients, and then alsorecently we've gotten the FDA
approval of nemolizumab, whichtargets the itchy cytokine IL-31
(17:35):
, and it's a blocker of IL-30and receptor alpha.
We're very lucky to havemultiple agents approved for
prigonodular.
Shannon, if I'd asked you that10 years ago, I don't think you
would have thought that waspossible, would you no way, not
at all yeah.
It's amazing, and so we havethese two drugs that actually
(17:57):
don't require regular laboratorymonitoring.
They're very targeted, muchsafer, so we've tried in the
past like methotrexate as adiaphragm any of these agents.
So we're very, very lucky andwhat I'm trying to do is make
sure that we decrease the amountof time that our patients are
suffering, cause still I seepatients every single clinic,
even earlier today have goneyears just with topical steroids
(18:18):
and been suffering before theyget to start on these systemic
agents, other agents that weshould know about.
There's some off-label studieson oral JAK inhibitors.
I actually presented some dataon oral provacitinib and also
topical ruxolinib that are beingdeveloped for this.
So exciting to have new optionsin the pipeline.
And then there certainly aredifferent off-label therapeutics
(18:42):
.
Some things that people like todo are inject steroids.
I think that's reasonable,especially if you have less
number of spots that you caninject the steroids.
Injection or intralesionalcorticosteroids are more
effective in PN than topicalsbecause, if you think about it,
there's this dead layer of skinat the top, the hyperkeratosis
it's very hard to get throughthat and the epidermal
(19:04):
acanthosis to get to where theaction is lower layers, the
epidermis and dermis, where youhave a lot of inflammation, the
acinophils T cells, fibroblasts,that are releasing these
cytokines.
So that's's the reason thattopical steroids don't work as
effectively and oftentimes youcan do the intralesional
therapies.
But especially a lot of skinand color patients, you worry
about hypopigmentation in thosepatients.
(19:25):
So in general, topicals are alittle bit more challenging
depending on the particularagent.
I go for one of these two newFDA approved therapeutics and
then adjunctive therapies likenarrow band phototherapy can be
helpful.
It's just a little slow, Ithink, but reasonable adjunctive
therapy for patients who havetrouble getting insurance
(19:45):
approval can always consider,you know, methotrexate therapy
or cyclosporine for a very shortperiod of time.
Again, these agents are veryuntargeted and not really needed
in this current landscape wherewe have more targeted
therapeutics currently.
Speaker 3 (20:02):
And from the standpoint I don't know if you
get this question a lot, I feellike often patients come in
they're like, okay, I know aboutthese options, Are there any
other natural options or thingsthat you think are worthwhile?
Or should I be watching thingsin my diet?
Or is there a supplement youwould recommend?
And again, knowing not alwaysthat is the evidence as strong
as what we have, obviously, forour clinical trials and approved
(20:23):
drugs Are there any types of,you know, treatments in that
sort of arena that you entertainor may offer to patients as an
option?
Speaker 1 (20:30):
You know, shannon, I'm gonna give you a story.
I recently tried a lavenderspray.
My wife she's also adermatologist yeah, she was like
there's no way this works.
Speaker 3 (20:40):
I was having a little thing, they were telling me,
you just want to prove her wrongSean.
Speaker 1 (20:44):
They were saying hey, this will help you sleep.
And my wife's like what are?
Speaker 2 (20:48):
you doing what do?
Speaker 1 (20:48):
you get, and I was like, no, I'm going to try it.
And it knocked me out.
And from that moment on too, Iwas like you know what?
We're going to be really superopen to all sorts of alternative
things and I've been.
I've been telling patients allabout turmeric powder, all sorts
of things.
Um, but no, absolutely.
I think that there's a role foralternative therapeutics.
We have a study where we lookedat the gut microbiome and found
(21:11):
some very interesting resultsin prognodular patients that
we're going to be publishingsoon.
Speaker 2 (21:16):
But the one thing I tell these patients is we want
to limit processed foods.
Speaker 1 (21:20):
So what we think is going on is that gut microbiome
is actually signaling and cantrigger itch by signaling
through the vagal nerve, andwhat we are finding is that
there's a lot of these fungalspecies that are upregulated in
praga nodularis patients, andwhat we think is that they're
tied to food deserts andprocessed foods.
(21:41):
So I tell all my patients ifyou can have a handful of
blueberries and eat some spinachor other greens and I'm talking
to myself also, because I lovefrench fries every day You're
eating chips, I'm eating chips,but I'm telling people to eat
blueberries and spinach.
I'm a hypocrite.
But as so we know that thosethings will help, will they cure
(22:02):
you alone?
No, probably not.
But of course those are greatthings that you can do that can
help a lot.
I think the unbalanced diet hascaused so many problems.
We can see, with the rise ofthe dry night, a spur of tea,
but I think probably gosimilarly as well.
Whatever we can do to makeourselves healthier overall.
But is there one alternativetherapy?
That's magic bullet?
Maybe we just don't know whatit is yet.
Speaker 3 (22:24):
Maybe it's lavender.
I was going to say for sleep wefound out.
Speaker 1 (22:29):
You have to try it.
Oh my God.
Speaker 3 (22:31):
I do love lavender a little bit, the essential oil
thing.
I don't always know if it'llknock me out, but it does.
It is relaxing, I'll give youthat.
I'll give you that.
We've talked more about kind ofthe medical piece, anything you
recommend if somebody issuffering from pregnenitis
adjusting maybe the mentalhealth aspect of how it impacts
their life that you typicallyemploy into your treatment
(22:51):
strategy.
Speaker 1 (22:53):
I think it's really important to get help if you
need it and to ask that question.
You talked a little bit earlierabout suicidal ideation.
You talked a little bit earlierabout suicidal ideation.
I was giving a talk and adermatologist came up to me and
they said they had treated oneof these patients with something
we all use, a triamcinolone.
We made a medium potencytopical steroid you know most
(23:15):
dermatologists use this veryoften and they'd had some time
to see the patient back and theyactually did commit suicide.
Oh my, and it's very toughhearing that.
I actually have a lot ofpatients that see me, that put a
lot of pressure and say, hey,if you can't help me, I'm
(23:36):
considering to kill myself, andit highlights how severe this
disease is, how much of animpact we can make.
But it also, I think to yourquestion, highlights how
important it is that we askpatients and refer them to get
care and someone to talk to andsomeone to evaluate them and
have a good relationship withpsychologists and psychiatrists
(23:57):
in our area and can referpatients and let them know that
there's a huge mental burden.
If you're itching and you can'tsleep, of course you know
you're more likely to haveanxiety and depression and then
that can be tough to get out of.
Even if we get the itch betterquickly, it's hard to get out of
that.
So I think, having that levelof empathy and asking I know
that we're very busy in ourclinics, but simple questions
(24:19):
there's anxiety and depressionscales.
A simple check-in takes a fewseconds but it is important, I
think, to do that and also tomake sure that we're being
aggressive with therapy.
I think that's very importantas well.
Speaker 3 (24:33):
Yeah, I like how you talk about that because it is a
very holistic approach I thinkthat we have to take as
dermatologists.
You can't silo out, you know, Ithink, all the skin diseases we
treat, the impact they have onsomebody's life, whether it's at
work or their ability to sleep,or just their mood, or, you
know, the development ofdepression or anxiety.
You know, I think that'ssomething we have to take very
(24:55):
seriously because I think youknow it's their busy days and
people sometimes gloss over thator our patients don't maybe
recognize it.
So for us to be able to pullthat out, get them to the right
place, to add that into theirtreatment regimen, that really
shows how we're committed toreally treating disease and the
patient entirely.
So really love that.
You highlight that.
And before we kind of end here,I did want to ask where do you
(25:15):
think we'll be in 10 years fromnow?
You know we already talkedabout where we were 10 years ago
.
10 years from now, in thetreatment of PM, where do we
think we'll be, or what do youthink is the most promising
treatment advancement that'llcome forth?
Speaker 1 (25:26):
You know, now that we have a pipeline, I think that's
the hardest thing to have avalidated scale, approved drugs,
a design of clinical trials.
We're going to see a ton of newtherapies and the mast cell has
actually emerged as being veryimportant.
It's unregulated in the lesionsof these patients and we know
the mast cell releases all theseitchy mediators and I think PN
(25:48):
is going to be one of thosediseases where we have mast cell
modifying drugs being approved.
There's multiple in developmenttargeting brutinine, tyrosine
kinase, also triptase and CKIT.
There's many different anglesof targeting the mast cell.
So I'm very hopeful to look atthat.
I also think many of the drugsthat are going to be approved
(26:08):
for atopic dermatitis may alsogo in for pyrogonadularis things
like OX40 and OX40 ligandinhibitors.
Many of the other newmonoclonal tri-specifics I think
could be great forparagonadularis as well.
So I'm very, very excited aboutall of the new therapeutics and
(26:31):
to see how this field develops.
Speaker 3 (26:33):
And maybe lavender spray right.
Speaker 1 (26:34):
Lavender spray.
Maybe I might do a clinicaltrial on it.
Speaker 3 (26:40):
Well, you'll just prove your wife right.
She'll appreciate that, likeall of us wives out there do.
Well, thank you so much, sean,for coming on the podcast.
This has been great to reallyget this broad overview of PN
really help people understand, Ithink, this entity a lot better
.
It deserves a lot moreattention than it's received in
the past and it's exciting tofinally see that people are
really looking more into it andreally providing patients with
(27:01):
relief.
Speaker 1 (27:10):
For our listeners out there.
If they want to find you, doyou mind sharing with how they
can locate you?
Sure, I'm on LinkedIn at DrSean Quattro, also Instagram and
X, so feel free to follow me.
Speaker 3 (27:14):
Well, thanks again for coming on the podcast and
stay tuned for the next episodeof Dermot Trotter.
Don't swear about skincare.
Speaker 2 (27:22):
Thanks for listening to Dermot Trotter For more about
skincare.
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