Announcer:
0:00
Welcome to MedEvidence, where we help you navigate the truth behind medical research with unbiased, evidence-proven facts Hosted by cardiologist and top medical researcher, Dr. Michael Koren.
Dr. Erich Schramm:
0:11
Hello and welcome back to the MedEvidence podcast. I'm your host, Dr. Erich Schramm, sitting in for Dr. Koren today. For those who don't know me, I'm a board-certified family physician and longtime clinical research investigator with ECNORE Clinical Research Group. I'm also a seasoned cannabis physician involved in helping people following their healing journey with medical marijuana. I'm very excited to be here today with one of my favorite dermatologists, Dr Michael Bernhardt. Dr Bernhardt and I go back many, many years. He never gets tired of hearing the story about me being that family practice resident
Dr. Michael Bernhardt:
0:49
One of the smartest they ever had.
Dr. Erich Schramm:
0:51
Well, he's very generous, but recalling a very, very good experience with my clinical dermatology rotation and Mike was a fantastic teacher, of course, but importantly he was a really good role model, you know, demonstrating empathetic, patient-centered care. I learned a lot from Mike
Dr. Michael Bernhardt:
1:12
Thank you.
Dr. Erich Schramm:
1:13
And still do I get an opportunity to work with you every Friday afternoon, which is another extension, I would think of your teaching, which we can talk about. Your background
Dr. Erich Schramm:
1:30
So, for those who don't know Dr. Michael Bernhardt, he's been practicing clinical dermatology for several decades. In addition, he is a very seasoned clinical investigator, as I've alluded to, and I've had the pleasure of collaborating on a number of studies with Mike. In addition, he's got extensive background in clinical education and medical education and just recently completed his three-year stint at the Florida State University teaching residents, and that is no small task, I would say. So you're kind of this triple threat in the clinical world of research, clinical practice and, as well as doing your academics. So one of the things we're excited to be talking about today is hydradenitis suppurativa Now, that's a mouthful, so we like to refer to it as HS, and perhaps you could give us a little idea about HS-101.
Dr. Michael Bernhardt:
2:26
Sure, sure, I'd be glad to. But before we start on HS, I just got to tell you this stress ball is the perfect stress ball for a dermatologist because it's called Molecool M-O-L-E C-O-L-L Molecule Not molecule, but molecoll. So I highly recommend this for all you stressed out dermatologists.
Dr. Erich Schramm:
2:49
There we go.
Dr. Michael Bernhardt:
2:49
Very good, all right. So we're going to talk a little bit about HS.
Dr. Michael Bernhardt:
2:53
So the cool thing in the last 10 or 15 years that we've done is it used to be what I used to call the three-headed monster in dermatology. We'd have people with severe psoriasis, severe eczema or atopic dermatitis and hidradenitis. And we've really come a long way, largely because of some of the research that's done in clinical facilities like this with clinical trials. We had a lot of patients on the clinical trials for psoriasis. We did some of the phase 2 and phase 3s for atopic dermatitis. Now we're dealing with the last of the three-headed monsters and we're just now bringing it into the modern era of treatment with things other than antibiotics.
Dr. Michael Bernhardt:
3:39
So Hidradenitis; All right, so let's you know, if you guys know me, you know I can't free associate and think without being able to draw, because it just kind of facilitates a whole thought process. So this is the skin. The epidermis has several layers to it and then within the epidermis you've got the hair follicle, and feeding into the hair follicle is oil gland, what we call the sebaceous gland. This is a little dermal papillae, which is a bunch of blood vessels and collagen, which has all these little chemical intermediators that we call cytokines, which are like cell and cell signals that stimulate the hair shaft to grow. Okay, and at the same time that the hair shaft is stimulated to grow, basically the same cells that line the epidermis will also line the follicle.
Dr. Erich Schramm:
4:32
And some people are more follically challenged than others. I understand Preaching to the choir. I know I was going to say maybe that's the next four-headed monster to tackle, right?
Dr. Michael Bernhardt:
4:43
if I say hair today, gone tomorrow.
Dr. Michael Bernhardt:
4:45
I know from personal experience. So this is the oil gland and what basically happens in hidradenitis. Let's go clinical first before I draw. The average person with hidradenitis starts with lesions, typically in their teens, and it'll go for eight to 10 years before that person's diagnosed. These lesions are normally found in what we call the fusion planes, the armpit, the area under the breast, the crease of the groin and the perianal crease. That's the usual hot spots and what'll happen is a person will present to their family, they'll present to the emergency room or urgent care with boils and they'll get treated as boils. They get lanced, they get drained, they get put on an antibiotic and this will go on for typically 8 to 10 years before someone puts it together and says, hey, wait a minute, we've got the same lesions recurring in similar areas that are leaving tracks and scarring, leaving draining areas, and it's always in that same spot. You know the armpit, the inframammary crease. Boom, it's hidradenitis. And that's really the clinical hallmark of hidradenitis Recurrent, quote-unquote abscesses and boils.
Dr. Michael Bernhardt:
6:01
Same area goes on for a long time. Now why does it happen? Well, these cells that line the follicle, they swell up and form plugs and there's a lot of things that these cells will overreact to. Smoking is one, nicotine is one. Hormones testosterone, progesterone can drive it. Metabolic syndrome morbid obesity can drive that. We can get into more details about that in a little while. But those are the clinical drivers.
Dr. Erich Schramm:
6:35
All right Now seen, I understand, a little more so in women than men. Is that your typical experience?
Dr. Michael Bernhardt:
6:42
Yeah, my, experience is it's mostly females. You know, when you look at some of the clinical trials, a lot of clinical trial data will be skewed. A lot of them, you know, is predominantly Caucasian community in clinical trials. But my own personal experience, overwhelmingly the African-American community is overrepresented with this condition and usually has several underlying comorbidities obesity, diabetes that tend to drive this Metabolic syndrome, non-alcoholic steatohepatitis. We tend to see all that kind of overlap.
Dr. Erich Schramm:
7:15
How would you compare or contrast this to acne?
Dr. Michael Bernhardt:
7:19
So in the old days, back when I was a resident um, we used to call it acne inversa right, because it's not in the face or back, it's in these inverse areas, um, and in certain ways it overlaps. But when we start talking about the cytokines, the cytokine soup in hidradenitis is a little bit different than what we see in that acne. Of course, they're both both neutrophil-mediated conditions, right, they're both due to overexcitation, shall we say, of the oil secretion apparatus, but the cytokine milieu is a little bit different.
Dr. Erich Schramm:
7:58
Okay, we can talk a little bit more about that a little bit later. But also to underscore in primary care we treat a lot of this. See, you treat a lot of this and this can be really devastating to patients. I mean, it's painful scar formation, very poor quality of life for those patients with this.
Dr. Michael Bernhardt:
8:18
I've seen people's lives totally destroyed when you start talking to people about it. Patients cannot marry, they can't have a normal dating life or sex life. They have to be judicious about what kind of work they do because, if God forbid, you go in and get a great new corporate job and you have a bunch of these abscesses that decide to spontaneously open a drain and release a foul odor while you're in the middle of a board meeting. It's going to be tough for maintenance. So in terms of the areas of involvement, right, it's always and forgive my drawing, I'm not a very good artist but it's armpits, right inframammary crease, genital area and the gluteal crease, and sometimes they'll be associated with it. Sometimes they'll also have an associated pilonidal cyst. So when you see recurrent crops of abscesses in that area, I mean bang, that's hidradenitis until proven otherwise.
Dr. Erich Schramm:
9:16
Right and back 20 years ago as a rotating resident, we might have been looking at, you know, topical compresses, oral antibiotics. I won't say that's primitive. Maybe looking back now it seems kind of sort of primitive, but we just didn't have a whole lot to offer those patients.
Dr. Michael Bernhardt:
9:37
We didn't, and really up until two, three years ago it was the same thing Oral antibiotics, particularly doxycycline, because it drives down some of these enzymes called metalloproteinases that upregulate inflammatory markers. So we'd use a lot of doxycycline. We would use metformin to block the insulin growth factor. One pathway Humira was a huge first step in the right direction because Humira, which is a TNF inhibitor, was the first FDA-approved biologic that had some impact.
Dr. Michael Bernhardt:
10:12
And what we do is we quantify these lesions in terms of what's called a high scar, HISCR, which is hidradenitis remediation, basically. And what are we looking at? We're looking at a reduction of abscesses, nodules and tracts, and so if you have a 50% reduction of these abscesses and nodules, you've achieved what they call a HISCR 50, 75%, HISCR 75, and so on and so forth. So Humira was great because it was the first drug that gave us a HISCR 50. It actually worked. It was wonderful. And then, when the pandemic hit, the FDA got so slammed and so overworked with things related to COVID that a lot of non-COVID things got pushed on the back burner. So several drugs that we were waiting for approval. One was secukinumab, which is marketed as Cosentyx, and bimekizumba, which is Bimzelx, which involved 17 A inhibitors finally got the FDA approval and these drugs are kind of putting us in the modern era now.
Dr. Erich Schramm:
11:15
Right, and you were already talking about some of the bad actor cytokines that we often talk about when we have time on Fridays when we have an opportunity to do that. But getting back to the original Humira as a monoclonal antibody was a real game changer and we talked about that also in treating psoriasis.
Dr. Michael Bernhardt:
11:38
Oh, it was a huge game changer, right.
Dr. Erich Schramm:
11:41
And then, consequently, you know, do you see the newer agents as the new and improved version of Humira, or just a different version.
Dr. Michael Bernhardt:
11:52
Humira's a really cool. Drop my phone, sorry. That makes for a great podcast and great radio and TV. Sorry, but it didn't break. Yeah, these things are a game changer because you know there's several inflammatory mediators. I call them like the three or four amigos or the three musketeers. They always run together and wherever they run, trouble follows right. So whether you're talking about interleukin-6, whether you're talking about TNF-alpha, whether you're talking about 17A 17AF or the 17AF heterodimer Wherever these guys go, trouble follows. And we knew that 17A played a role in the inflammatory cascade in HS, and some of the newer data is showing that 17A WAP, while being a major driver, 17F and 17AF heterodimer may play even more of a role of amplification. Now, with that being said, the specific mechanism hasn't been quantified, so some of this is still kind of speculative, based on own personal interpretation of the data, you know. But we seem to know that this molecule 17A, 17F, 17AF really seem to upregulate the inflammatory cascade.
Dr. Erich Schramm:
13:09
Right, and maybe more so than TNF.
Dr. Michael Bernhardt:
13:14
Yeah, well, TNF is upregulated.
Dr. Erich Schramm:
13:15
Right, but maybe 17A and F, being a more potent stimulator, would you say, is a better target for treating in terms of its anti-inflammatory responses.
Dr. Michael Bernhardt:
13:28
I think it's emerging, as in the latest literature, it's really kind of evolving into the given a choice that would be my first choice to target in terms of mediators. Now, the problem is that you know this from practicing medicine that if the patient has certain comorbidities, it carves out certain classes of drugs, which is why it's good to have both the TNF inhibitors as well as the 17A or 17F inhibitors, because the person may have certain premorbidities that prevent us from using one drug by the other.
Dr. Erich Schramm:
14:05
Right and kind of the premise for those therapies is they're monoclonal antibodies directed specifically at these targets, but not every treatment out there is a monoclonal antibody, so what other ways are there to affect the inflammatory pathway? These cascades without. What are some of the other therapies out there that don't involve monoclonal antibodies?
Dr. Michael Bernhardt:
14:29
Well, let's start with the monoclones first a little bit. I mean, the nice thing is that there's two drugs that target 17A and 17AF, right? So the sekukinumab targets 17A, bimekizumab targets 17AF. And that's important because there's about because there's an article that was just published in the British Journal that in the dermis that surrounds the follicle there's huge amounts of 17 F being secreted by the skin around the follicle, which is an upregulatory drives more inflammation. Okay, so that's important, but some people can't tolerate this drug. So we know that 17A, which is also secreted by dendritic cells, will drive inflammation. Now you have the 17A, 17AF. They'll all interact and also upregulate TNF, which is also secreted by some of these dendritic cells, secreted by some of these dendritic cells. So if someone can't tolerate the 17A or the 17AF drug, at least we have the TNF inhibitor to fall back on.
Dr. Michael Bernhardt:
15:38
So when we're
Dr. Michael Bernhardt:
15:38
looking at drugs outside of the biologics right. So I know that right now there's some clinical trials in the pipeline and the next generation of drugs are going to be the JAK inhibitors. We don't have a JAK inhibitor oral FDA approved yet for treating HS. I've heard some scuttlebutt that there's things in the pipeline. There is a clinical trial going on. It's going to be starting, I think, here within the next month or so with a topical JAK inhibitor, ruxolitinib, which is marketed as Opzelura.
Dr. Michael Bernhardt:
16:10
It's a JAK1-2 inhibitor and it's going to be used for mild to moderate disease, not those severe where people have hypertrophic keloidal scarring and 100 abscesses, but more with the follicular occlusion and occasional papules Right, and that's a topical cream. It's already got the FDA approval for things like eczema and vitiligo. So it's not, you know, it's not like the first scene in Hamlet where the three witches are brewing something and taking, you know, the wing of a bat and the eye of a newt and putting it together and saying, here, try this, you know. So it's not anything like that. This is already an approved drug looking at it for an unfulfilled need and you know the theory with HS is if we can intervene early and catch things in the mild to moderate stage and not let people go to that severe stage, you can hopefully decrease disease progression and at the same time decrease morbidity.
Dr. Erich Schramm:
17:06
So in the case of using topicals, these would be just at specific sites, affected sites.
Dr. Erich Schramm:
17:17
Or do you see that it might have some greater systemic absorption that would?
Dr. Michael Bernhardt:
17:19
I'll have to check with the medical science liasons to to see what the degree of absorption is. My overall impression is that I don't think you can be getting enough to get a systemic pop from the drive. I think that it's just more of a localized absorption.
Dr. Erich Schramm:
17:33
Cool, maybe you could talk a little bit about JAK and JAK STAT and what the heck is that?
Dr. Michael Bernhardt:
17:40
Oh, JAK STAT All right. Wasn't it a song by the Rolling Stones? No, it was
Dr. Erich Schramm:
17:44
Jumping Jack. Yes, there you go.
Dr. Erich Schramm:
17:45
There you go. Right, that's right. Yes, there you go. There you go. Yeah, right, that's right.
Dr. Michael Bernhardt:
17:48
Somebody got that wrong on Jeopardy last night. They asked the final question was what band got the best new performing? Or it was the quick category was Grammys, what band got the best new performers in the sixth Grammy and then the 35th and the 67th? And of course, one person put the Rolling Stones. It was the Beatles. Okay, I'm a big Beatles fan. Okay, so of course it was the Beatles. You know that. So, JAK STAT, has absolutely nothing to do with the Rolling Stones, so all right, so I'm going to have to draw.
Dr. Erich Schramm:
18:23
Okay, there we go. I was hoping you were going to pull that out now.
Dr. Michael Bernhardt:
18:27
Yeah, it shuts me up, right? If I'm drawing and I have my back, I can't be talking, right, all right? So everybody, get your cup of coffee and start waking up, all right? So here we go. So let's pretend that this is a cell and let's pretend, for the sake of argument, that this is what we call a Th17 cell.
Dr. Erich Schramm:
18:50
T helper 17. That's part of the immune system.
Dr. Michael Bernhardt:
18:54
There are mainly three classes of active cells and inflammation for our purposes, right Th1, cells and inflammation for our purposes, right TH1, that drives the type 1 pathway. Th2, which drives the eczema pathway, interleukens 4,13, so on and so forth, and then the TH17 cells which drive the IL17 pathway .
Dr. Erich Schramm:
19:20
Right. We talked about that in psoriasis as well.
Dr. Michael Bernhardt:
19:24
So we're going to pretend that this lousy drawing of a chocolate chip cookie is really a Th17 cell. And if you in your mind's eye visualize like a beach ball with the port that you put your mouth on to blow the beach ball up, so that port is what we call the cell receptor. So the receptor will bind circulating things that float in the bloodstream. In this case these things are interleukin-17 molecules, which act as an antigen. So what's an antigen? Something that stimulates a reaction. So the antigen, the 17 antigen, binds to the receptor. And when that antigen binds to the receptor it activates the receptor. So that's a separate one-hour lecture I'll avoid, but let's just say it activates the receptor.
Dr. Michael Bernhardt:
20:17
And in the course of activating the receptor there are these little enzymes that sit on the receptor, kind of like if you picture a stick with a glob of honey on it, the glob of honey would be the JAK enzyme system. Okay, so when these enzymes get activated, there's another set of enzymes within the cell called STAT S-T-A-T, signal transduction and translation. They will automatically join together and then move to the cell nucleus where they induce upregulation of the inflammatory molecule. So the way I like to describe it is the receptor gets activated. So, in other words, the catcher's mit has caught the baseball. So, the baseball being the antigen, the catcher's mitt has caught the baseball and in the course of catching the baseball, instead of bringing your arm back and throwing the ball, the receptor gets activated and the STATS join together. I'd like to say boy meets girl, they run off to a nice happy place, which is the nucleus, and they make this Interleukin-17.
Dr. Erich Schramm:
21:29
The baby comes out, okay.
Dr. Michael Bernhardt:
21:30
Right, and that's what drives the inflammation that we see pretty much in hidradenitis as well as psoriasis.
Dr. Erich Schramm:
21:37
Right. So right now you could look at that and say OK, well, there's two things you could do to affect that. One would be to block IL-17 with an antibody or,
Dr. Erich Schramm:
21:47
Or we could go back and look at some of these intracellular mechanisms and look at that and think that might be a really good opportunity, because you know thinking about JAK what some of the bad actors that JAK produces in where we talked about IL-1, TNF, it's a long list of cytokines that JAK produces, not just IL-17, but it produces a wide variety of bad actors there.
Dr. Michael Bernhardt:
22:21
As I'd say, the whole enchilada.
Dr. Erich Schramm:
22:27
What would be the potential downside if you shut JAK down altogether? Would there be any necessarily downside?
Dr. Michael Bernhardt:
22:32
Yeah, I mean, all drugs have side effects, right, otherwise they'd be sold in the candy counter. So when you're blocking JAK, there's all sorts of things that you have to be cognizant of right.
Dr. Michael Bernhardt:
22:45
JAK inhibitors affect certain blood counts, platelet counts, lipid profiles, the main thing that we worry about, particularly in people over the age of 65, and this is more with the pills, this isn't really with the cream, this is more with the pills, although the FDA has mandated a class-wide warning, even with the cream, that we have to be just as vigilant. But the reality of the reality scope is people are much more at risk to severe side effects from the pills than they are from the cream. All right, so do we worry about deep vein thrombosis. Pulmonary Embolism, cardiovascular disease. I just reviewed an article yesterday, it came out in May Journal of Clinical Allergy and Immunology where it showed that most of the time when you're on these pills, in younger people, the side effects profile is considered manageable. When you get into the over 65 cohort, these drugs have to be used appropriately with moderate to severe disease with a good history, good physical exam, making sure there's no predisposing factors, and used with caution. And it's our obligation as learned intermediaries to transmit this risk benefit to the patient and their potential surviving spouse, depending on the circumstance.
Dr. Erich Schramm:
24:01
Right and to be clear, when you're talking about oral medications, you're specifically referring to the JAK inhibitors.
Dr. Michael Bernhardt:
24:05
They're all JAK inhibitors Correct. So I mean they're helpful.
Dr. Erich Schramm:
24:10
What would be a few examples of that, just so people might have heard,
Dr. Michael Bernhardt:
24:14
severe atopic dermatitis.
Dr. Michael Bernhardt:
24:15
You know there are several drugs already approved, FDA approved, that are JAK inhibitors and they're game changers for people, the life-changing drugs. That's we're in dermatology, we use it the most Now the topical, which is the same one that we're going to be doing the clinical trial on for topical hidradenitis, mild-moderate hidadrenitis. The topical is a great drug. It's a great drug. We use it for atopic dermatitis and vitiligo.
Dr. Michael Bernhardt:
24:44
It's been a huge game changer for vitiligo. I mean, we had nothing that worked for vitiligo, zip, zero and nada. And up until about two or three years ago, people came in with vitiligo. The spiel they get from me is hey, if it's been there longer than two years, good luck. Well, we've turned that around, you know, with the topical JAK inhibitor, topical ruxolitinib, we've got people repigmenting and it's amazing, there's nothing short of amazing, and hopefully we can achieve the same thing in mild to moderate hidradenitis by using the topical JAK, without having to get into some of the systemic concerns. Right, you know it's FDA approved down to age of 12. So it's appropriate for adolescence. So hopefully this will be a nice addition to the armamentarium.
Dr. Erich Schramm:
25:33
Right. Well, let me ask you an investigator question, because occasionally patients will read about this and say hey, we know that this topical works for this condition and this condition. Why can't we just, why can't you just prescribe it for, hey, this other condition, right, why can't? If it works for vitiligo and atopic derm, hey, just write me a script for my HS. Why can't we just do that?
Dr. Michael Bernhardt:
25:58
It doesn't have the FDA approval, there's no scientific data, there's no randomized clinical trials that says, hey, it's going to work, right, you know. And these things are expensive and the side effect risks, and that's what I mean. Everything has to be used appropriately and that's the beauty of doing the randomized clinical trials, so then we can know that we're giving this drug to this patient for a good reason, right, with an anticipation of results.
Dr. Erich Schramm:
26:25
Right. Now. Of course, as investigators, you know we have a certain level of reassurance when we are already familiar with a medication or a compound and say, OK, you know, we've got a lot of experience with this, but, your understanding, we're looking at that in a different application, so you can't just go and decide. You shouldn't be just going and deciding.
Dr. Erich Schramm:
26:45
you're going to treat people without having a good understanding about the approval cost
Dr. Michael Bernhardt:
26:51
If you go off label and just shoot from the hip. I mean, usually you want to do a literature search first and just make sure there's some appropriate literature Like, for example, androgenetic alopecia.
Dr. Erich Schramm:
27:08
For those of you that said we're all pointed at our relatively hair-free scalps.
Dr. Michael Bernhardt:
27:15
So like for androgenetic, alopecia and I had this discussion with at least two people this morning. Right Off-label use of low-dose minoxidil it works.
Dr. Michael Bernhardt:
27:23
It's great Is a quackery to use it because there's no FDA approval. No, the drug went generic. Once a drug goes generic, no company is going to pony up the money that it costs to run the randomized clinical trials and go through the FDA hurdles Okay, fine. But you can pull out 10 or 15 articles which there are that show, hey, this works. And here's the side effect profile. So you're not just making something up and it works. It works well. There's risks when you get over a certain dosage, but for by and large low-dose drug for guys and young men that have hair loss, it's a great drug. People, alopecia areata, it's a great drug. It works. Here's your side effect profile. But you're not just making something up. You've done the literature search. You've pulled 10 or 15 articles, you've read the risk-benefit ratio and you can have an intelligent discussion with a patient. So that's the difference between just saying, yeah, let's just try this. 40 years ago you could do that. But what was this joke that I heard? It's not a joke.
Dr. Michael Bernhardt:
28:26
There was a story back in the mid-1970s that, the way that methotrexate got the approval from the FDA for psoriasis, a group of dermatologists went up to the FDA and said we'd like to use this for psoriasis. Okay, that won't happen. Now, boys, that's not happening anymore. But half a century ago that's what people did to start using drugs. Hey, this worked. I've used it on a dozen patients. Everybody's doing great. It's getting approved, okay, fine, that doesn't happen anymore. So, like, when we do this trial, we'll be one site. There are multiple sites of interviews in the AHS trial and it's randomized, so we don't know what cream the person's getting, because that's what we call blinded. We don't know what person's using and we look at the results and we don't know.
Dr. Michael Bernhardt:
29:45
So the results can't be tweaked, there's no cheating in the system. It is what it is, if it's not, it's not. If it works, great. If not, back to something else.
Dr. Erich Schramm:
29:45
And to be clear
Dr. Erich Schramm:
29:45
so for us as unbiased investigators, we just want to get to the truth.
Dr. Michael Bernhardt:
29:46
Which is what science is. It's exercise in empiric skepticism to search for truth.
Dr. Erich Schramm:
29:52
That's right.
Dr. Erich Schramm:
29:55
Anything else you'd like to add to your JAK STAT?
Dr. Michael Bernhardt:
29:59
Yeah, I mean I think we covered the JAK STAT basis right. JAK get activated, STAT, STATS , translocate to the nucleus and upregulate cytokine cascade. So going back to HS, right, let's go back to HS because there's some cool things about HS. So, from my readings and my thought process, HS, I think, is a two-phase disease and that's why it's been so challenging to treat right. So you have the initial inflammatory phases, which is when people come in with the draining tracts and the big tender lumps and bumps right, what we call abscesses and nodules, and that's really driven by 17A and 17AF, at least based on what we see on current research levels. And then what happens is it transforms and turns into this scarring process which can be quite severe.
Dr. Michael Bernhardt:
30:54
I mean, some of these scars are so bad that people can't lift their arm. If it's in the axillary crease or what we call the armpit, they have restriction of leg movement if it's in the groin, and that, based on what I've read, seems to be a different set of chemical mediators that seems to be a little bit of interleukin-1 and transformation growth factor beta. That's trying to for some crazy means trying to get the skin to recreate the epidermis inside the dermis, inside the outer layer and the lower layer. Why would it be doing that? You know the computer system is misprogrammed, obviously. So the thinking is that if you can shut down the inflammation in the 17A, 17AF phase, you don't get to the interleukin-1 transformation growth factor phase, so you don't get the big scarring. And that's what we're really trying to prevent.
Dr. Erich Schramm:
31:46
All right, so you're trying to back to what I meant when we were looking at your drawing. I said thinking in terms of trying to treat things more upstream. Right, Try to prevent as much of that, the inflammatory cascade.
Dr. Michael Bernhardt:
32:00
Exactly, exactly, yes, and it'll be really cool to see if the topical JAK can do as well as some of the monoclonals. Now again, the monoclonals are for the more severe disease.
Dr. Erich Schramm:
32:14
Right yeah.
Dr. Michael Bernhardt:
32:15
But it'd be really interesting to see how much progress we can make with just the topical. That'd be really cool, right, well, this is my new picture. By the way, I like this. This is called Snowstorm and House.
Dr. Erich Schramm:
32:25
I like that. You've really accurately recreated tha t. One of you are many talents right Educator, researcher, clinician, that's right, that's right. Well, so Mike, get to that point in the interview and I say, hey, any question you wish I'd asked or anything you'd like to add to what we've set up to this point.
Dr. Michael Bernhardt:
32:48
Well restaurant review. Ah, okay, Good okay, okay, this is the highlight. This is what everybody's wanting to find. I had dinner the other night at M Brothers in Mayo. I've got to tell you it was really good, really good. I'd give it a five star. You know, the same people do Matthews and do Medura's. They have M Brothers and it's a Mayo Clinic Absolutely great.
Dr. Erich Schramm:
33:12
Okay.
Dr. Michael Bernhardt:
33:12
Absolutely great.
Dr. Erich Schramm:
33:14
Do you have a recommendation?
Dr. Michael Bernhardt:
33:16
I had to steak. For all you vegetarians, for all you people that are watching cholesterol. I had the steak. Okay, it was pretty good Okay.
Dr. Erich Schramm:
33:23
Okay, so my turn. Okay, I'm actually a vegetarian, so you're looking right at one. How about that?
Dr. Michael Bernhardt:
33:27
What if you had steak? You're an indirect vegetarian right Because the steak ate the ketchup. There you go.
Dr. Erich Schramm:
33:33
That's right. It that's right. So I'm going to put a shout out for the Floridian in St. Augustine. Ok, I like this. It's a great kind of that Florida southern comfort cooking. It's got a lot of great vegetarian options and, for people who eat seafood, lots of great options. So I'm a go-to all the time there.
Dr. Michael Bernhardt:
33:59
The Floridian?
Dr. Erich Schramm:
34:00
The Floridian.
Dr. Michael Bernhardt:
34:02
Good to know
Dr. Erich Schramm:
34:02
Yes, sir, all right, so what's our next topic of discussion going to be in Dermotology role?
Dr. Michael Bernhardt:
34:08
What?
Dr. Michael Bernhardt:
34:09
do you want to talk about?
Dr. Erich Schramm:
34:11
Well, we're talking about our bald heads, but until we've got to come up with something better to help that,
Dr. Michael Bernhardt:
34:16
I'll talk about alopecia.
Dr. Michael Bernhardt:
34:17
Okay, I'll talk about the march of the hair follicles.
Dr. Erich Schramm:
34:20
Let's do that.
Dr. Michael Bernhardt:
34:21
Sounds good.
Dr. Erich Schramm:
34:21
Cool man, all right, sounds good.
Dr. Michael Bernhardt:
34:23
Hair today going tomorrow.
Dr. Erich Schramm:
34:24
There you go, all right.
Announcer:
34:25
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