MedEvidence! Truth Behind the Data

A Timely Discussion About Atopic Dermatitis (Eczema)

• Dr. Erich Schramm, Dr. Michael Bernhardt • Episode 357

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Dermatologist and clinical researcher Dr. Michael Bernhardt joins Dr. Erich Schramm to unpack the rapidly evolving science of atopic dermatitis. The two doctors discuss the symptoms, science, and treatments for atopic dermatitis, including how much clinical research has changed the landscape and improved outcomes. The two get into how the immune system drives the disease, and how new therapeutic drugs target those systems in way thats more than just skin deep.

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Announcement:

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.

Erich Schramm, MD:

Hello, and welcome back to another episode of the MedEvidence Podcast. I'm your host, Dr. Erich Schramm. I'm a board-certified family physician and longtime clinical research investigator with the ENCORE Clinical Research Group. And I'm very excited to be sitting across the table again from one of my favorite dermatologists and esteemed clinical research colleagues, Dr. Michael Bernhardt. Welcome back to another episode of the MedEvidence Podcast.

Michael Bernhardt, MD:

Great to be back. It's been a little while.

Erich Schramm, MD:

Yeah, it has been. So just getting caught up on things. We've done a couple of few of these before.

Michael Bernhardt, MD:

Right.

Erich Schramm, MD:

And remember the kind of the origin story for this was, you know, on Fridays, we have opportunity to work together, collaborating on patients and studies. And it came out of that that, you know, we spent a lot of time discussing, you know, topics, clinical research reports, and all the things that are coming down the pike. And people realized that, you know, we'd get into very detailed descriptions and discussions about, you know, disease pathways, and it was very educational. And they said, hey, you know, you guys should go and do a podcast because you know, we just we just like hanging out, two docs, talking about, you know, research and talking about our patients. And sure enough, and I looked at Mike and I said, gee, Mike, we should do some podcasts. And I said, Well, how many podcasts had you done at that time? And I believe your answer was

Michael Bernhardt, MD:

I think I had a my grand total was um zero.

Erich Schramm, MD:

Right, it was zero, somewhere between zero and one. And then the question was zero, right? How many podcasts I'd actually hosted? And the answer was for me a big zero. And so based on that kind of experience, we thought it would be a great idea to plunge forward and do these kind of podcast series. And I'm, you know, I'm kind of saying that in a facetious way, but quite honestly, you know, you really have a, you know, you're not just a dedicated clinician, but you're a clinical researcher, an educator. And so, you know, you when you come into the office, um, I feel like you really do bring a lot to the staff, including myself, but also to the patients. You know, you really do have quite a very holistic view of patient care, and so I really really admire and respect that.

Michael Bernhardt, MD:

As do you.

Erich Schramm, MD:

There you go.

Michael Bernhardt, MD:

Right back at you.

Erich Schramm, MD:

Right back at you. Back at you, buddy. So today we're gonna be talking about atopic dermatitis. And, as you like to do with these talks, you always do a great job, kind of foundational, explaining a good definition for atopic dermatitis, and then maybe running through, you know, the epidemiology, etiology, and then you know, maybe even go back and forth on a few different things.

Michael Bernhardt, MD:

Sounds good. So we've come a long way with atopic dermatitis, and and honestly, thanks to clinical research, you know, and and you know, it's so popular to bash the pharmaceutical companies. But like I tell the residents, you could be the best carpenter in the world, but if you don't have a hammer, nails, a skill saw, and a level, you're not gonna be able to do anything. And without the companies actually make the drugs that we can use, you know, we're back in the Stone Age. So we've had a lot of really great progress with Atopic in about the last eight or ten years. You know, they've drilled down and kind of found some very significant pathways that drive the disease condition. You know, Atopic is known, quote unquote, as the itch that rashes, right? I think that's from the textbooks around back when when I had a full head of hair. And I think our next talk's gonna be about hair loss.

Erich Schramm, MD:

It's gonna be a hair loss. I mean, you know, it's really interesting. You that's that's the phrase that comes to mind because I was one of your residents at one time, and that was one of those clinical pearls that stuck in my head and found it very helpful, you know, throughout throughout my career. So I that's the great great pearl, right?

Michael Bernhardt, MD:

Yeah, a lot of times each will precede, you know, what you can see and what you can feel. Um and it's common, starts in kids, very common in kids. Usually in the young kids, six months or so, periorificial, you know, around the mouth, and and then it spreads to the anticubital folds, you know, the bends of the elbows, the bends of the knees. And these kids can be pretty miserable. They really can be miserable, and it makes the whole family miserable. And you know, back in the day, all we had was topical steroids and moisturizers and antihistamines. And and the thing is, antihistamines are only marginally ineffective in this kind of itch because a lot there are other itch pathways between the skin and the brain, you know, via the spinal cord that go through mechanisms other than histamine. You know, gavinergic pathways, what they call the cowhage pathway. And and we found that a lot of these cytokines or these cycling intermediaries that help start the fire that that transmits itch to the brain, are totally independent of histamine. Right? So we have molecules like interleukin 31, which is a primary pruritogen of the skin, molecules like interleukin 4 and interleukin 13, which drive the whole inflammatory cascade. And now they're they're starting to drill a little deeper and they're looking at other molecules like one of the studies that we're trying to get, which is a combination of blocking interleukin 4 and blocking another molecule called TSLP. And I always, always, always mutilate the real name of this thing, you know. So I I'm just gonna stick with TSLP. It's like FOMBO, strombo, fymbic, strombic, lymphopuetin, or something like that. That's right.

Erich Schramm, MD:

Sound sounds like a little bit this afternoon we're gonna sit down and

Michael Bernhardt, MD:

I've tried to study it a hundred times. I still mutilate that. But TSLP, IL-25, and IL-33 are what are called uh alarmins, A-L-A-R-M-I-N-S. And alarmins are these little cytokine fragments that are released with any kind of irritation to the epidermis. Right. And they act like as the alarm clock. That's why they call them alarmins, and tell the rest of the inflammatory cascade, hey, wake up, there's something going on here that doesn't belong, and it triggers the whole itch scratch cycle. So uh right now we have great drugs that are FDA approved down to age six months of age. For example, a drug like dipolumimab, FDA approved down to six months of age. It's an injectable and it works great at shutting the process off.

Erich Schramm, MD:

That's IL-4 & IL-13.

Michael Bernhardt, MD:

It blocks IL-4 & IL-13.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

And then the 13 inhibitors, I think, are are only FDA approved down to I have to check and see whether it's 12 or or whether it's approved for adolescents or just adults. I don't not sure off the top of my head. The 13 inhibitors are also available. And then there's a new class of drugs for atopic dermatitis called JAK or JAK inhibitors. And those are orals. So in those kids and young adults who are the ones who predominantly have this who can't tolerate an injection, there's an oral form, but the you know, there's risk to benefits, and they all have this side effect risk.

Erich Schramm, MD:

How do you think in terms of when you're grading severity, mild, moderate, severe, you know, do you have some distinct parameters that you're looking in that and helping you to decide what kind of therapies you're going to be looking at with a patient?

Michael Bernhardt, MD:

And and the way when I'm teaching, when I'm teaching residents, I always tell them that you know a lot of there's no definitive diagnostic test for atopic dermatitis. You do a skin biopsy, it shows inflammation, what they call spongiosis, which is microfluid in the epidermis. Um maybe you'll see some eosinophils, which are cells that get upregulated when there's an allergic process. You can do some blood tests, may help, may not help. The one I use as a yardstick is IgE. Yeah. Right? And IgE is helpful if it's elevated. If it's normal, it doesn't really help you. And people have to remember there's two pathways. There's an allergic pathway and there's an auto-inflammatory pathway that's autonomous from allergy. So there's no real diagnostic test. It's a clinical conundrum. And you know, you look at the person, you see, uh, you know, are you itching? Well, if someone's sitting there scratching themselves to death, it's kind of a silly question to ask. But you ask, how bad is the itch? And criteria for itching is if the itch is such that it prevents the person from sleeping at night or staying asleep at night, that's severe.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

That's severe disease. Um if it's in an in a kid or young adult, if it's impairing their ability to stay awake and function in school, um, if they can't go with their peers, if they're soccer players, they can't play soccer. A lot of times this is comorbid with asthma, so they start running around, they get bronchospasm. Um, that's severe. Right. All right. Uh kid's a basketball player and he can't lift his arm ups to shoot because his the his axillary area is so torn up that it rips his skin when he tries to shoot a basketball. Well, that's severe disease. And, you know, back in the day with these people, all we had was topical steroids and antihistamines. And you know, more often than not, they did not accomplish the full task that we wanted to have done.

Erich Schramm, MD:

Right. So, um, and just maybe we can talk a little bit about how important it is in terms of skin care and for these patients and um moisturizers and you know, I mean what what kind of soaps uh they should use or avoid. Uh maybe you talk about that.

Michael Bernhardt, MD:

So the to to get to that answer, you have to uh visualize the skin as like a five-layer cake, right? Think of the epidermis as a five-layer cake. The basement, the first layer is the basal cells, right? The basement layer, basal cells. And the um the next layer is the squamous cells, then there's the spinous cells, and it's the granular cells. And then on top of the cake, like a thick layer of saran wrap, you have the the stratum corneum, which is the outer barrier. Right. Right. So we always say in in atopic dermatitis as a disrupted barrier. And when you think about that and try to take it out of a nebulous concept to a concrete concept, what is disruptive? Well, you you look at the granular layer. The granular layer is called the granular layer because, and this is going to come as a shock to people out there, the cells have granules in them, right?

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

So everybody recovers.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

So these cells have granules. And the problem in the atopic world is that these granules, which are important for secreting uh filaggrin, which is a structural protein uh for the stratum corneum, and it also helps with junctional and tying the junction, the skin cells together, or they call it junctional adherence. Um and then there's what's called the odland bodies, which secrete um cholesterol and sterols and free fatty acids, which are like the intercellular cement substance, right? So when these granular, and we know that in atopic dermatitis, these granular cells are defective. Uh either A, they're secreting defective products, um, and or B, they don't secrete at all, they get jammed up. Okay. And when you're not secreting these sterols or or uh what they're called ceramides, the skin has a gap. Normal ceramides run about twenty to twenty-four carbon chains in length. So think of it as like, I don't know, uh a tire chain that has a certain length. All right. Okay. So for the tire chain to function, it's gotta have X amount of loops to it. So in atopic dermatitis, it's like X minus 10 in these loops.

Erich Schramm, MD:

So these are these are inherent to good skin health because it maintains the integrity of the skin in itself.

Michael Bernhardt, MD:

And even more importantly, sometimes when these tire chains come out too short, they can actually act as an inflammatory driver and uh and aggravate the situation. So that's what leads to this defective barrier. So moisturizing is super important. And the reason I always tell my patients to get a moisturizer with ceramides is because if these kids and young adults are not producing ceramides in such a way that they keep the barrier whole, you need to supplement that. So a moisturizer without ceramides is only kind of quasi-effective.

Erich Schramm, MD:

Is that you know if uh if I go to the pharmacy and I find this easy to find uh moisturizers with ceramides, or do I have to look on the backside and

Michael Bernhardt, MD:

now they they advertise it because every you know everybody's kind of hip to the need for ceramides.

Erich Schramm, MD:

Okay. So uh that's critical to maintain um good skin health, um, moisturizing. Uh what about soaps?

Michael Bernhardt, MD:

Uh try to keep them bland. You know, I'm I'm a big fan of white fragrance-free dove soap. Okay. It's got mineral oil in it, which is lubricating. Um, I'm not really a big fan of of any fancy soaps that have fragrance or color or dyes because people with atopic diathesis are more sensitive anyway. So things that normally wouldn't irritate you or me or or you guys in the room, you know, if you have atopic, it might set you off. Right. So try to keep it kind of on the bland side. On the mild side, not the wild side.

Erich Schramm, MD:

Uh uh shower uh cool or warm?

Michael Bernhardt, MD:

What any that means so if you take a shower that's too hot, it's gonna stimulate those itch fibers and trigger that whole itch scratch response. So try to keep it moderate. I know on a cold winter day you love to crank that hot shower up. We all do. And it does. It feels so good, but if you have atopic dermatitis, it's gonna set you off.

Erich Schramm, MD:

Okay. Uh good, good food for thought. Um, the other question that's coming to mind is um, can can you describe the like early versus late stage disease processes? Because you know, at some point that you haven't activated so much of that uh the auto-inflammatory or the the allergy arm of it, but it it does ramp up over a period of time, right?

Michael Bernhardt, MD:

Yeah, it's kind of cool because it's a it's kind of a multiphase disease, right? And we know that in the first phase it's inflammatory, and then it becomes quote unquote fibrotic. In other words, the skin thickens up. And the TH2, you know, there's two inflammatory pathways, right? At least, I'll say three.

Erich Schramm, MD:

Yeah, please remind me of those. So now we've talked about them.

Michael Bernhardt, MD:

And I'm sure there's going to be a zillion more, you know, by the time you guys are my current age, there'll be a zillion more pathways found out. But I mean, right now the three main highways that we look at is TH17, TH1, TH2. And remember, there's some plasticity between the TH1 and the TH2 pathway. Um so with atopic dermatitis, we're mostly talking about the TH2 pathway. And what we find is that one of the little interesting things that we see in some of these TH2 diseases, they do end with thickening or fibrosis of the skin. Um we know that we're not sure of what what the exact mechanism of that is, but we know that in people with chronic atopic dermatitis, the skin will what we call licinofire, thicken. Right. Um now what's interesting is there is a newer biologic drug, nemolizumab, which doesn't block interleukin-4 or 13, which are the main drugs that we've been using. It blocks interleukin-31. Interleukin-31 is what's called a pruritogen. In English, to take it out of scientific ease and put it in English, pruritogen means something that makes you itch. Okay.

Erich Schramm, MD:

Okay.

Michael Bernhardt, MD:

So interleukin-31 is one of these primary pruritogens that really causes severe itching. It shares a receptor. So in other words, when these cytokines, if you think of cytokines as a key, right? They're floating around in your body, they're keys. They're looking for a little lock to go into in turn, right? So interleukin-31, that little key is looking for its receptor or its lock. Well, it shares a receptor with another molecule. This is pretty cool. Called Oncostatin M, which is Oncostatin M is a cytokine that or a receptor site that drives fibrosis. It also has other you know oncologic related properties that are just kind of being discovered that are not germane to this talk. Um but what it what it does is it does stimulate fibrosis.

Erich Schramm, MD:

At the level of

Michael Bernhardt, MD:

the receptor level.

Erich Schramm, MD:

At the receptor level.

Michael Bernhardt, MD:

So that may be one of the you know, activating IL-31 and oncostatin M may be one of the reasons that tickles that pathway of fibrosis. So these the couple of these drugs have been um FDA approved not just for atopic dermatitis, but another inflammatory fibrosing disease called prurigo nodularis, where people get these horribly itchy thumbtip size lumps on their on their trunk and on their arm on their extremities. And both these drugs work like a charm in terms of reducing not just the inflammation, but the thickening and the fibrosis.

Erich Schramm, MD:

Once a person, say they develop some of those thicker plaques um that you sometimes see, um, is that reversible? Can you how do you approach that?

Michael Bernhardt, MD:

With one of these injectables, either with um the 413 or the 13 inhibitors or the the 31 OSM inhibitor.

Erich Schramm, MD:

And that allows the skin to kind of re-engage and restore kind of a more normal.

Michael Bernhardt, MD:

You're taking the inflammatory onus away, and it with time it normalizes. Now, thicker fibrotic skin takes more time to normalize than just quote unquote itchy skin. With most of these drugs, the itching is gone within a day or two.

Erich Schramm, MD:

Right. And that's the main thing. Because if you're itching, it's never going to go away, right? If you if you continue to itchy.

Michael Bernhardt, MD:

Yeah, the itch relief is a godsend. You know, we're even seeing it now with some of the topicals, the topical JAK inhibitors, you know, ruxolitinib, and there's a new one that has some sort of name that I can't ever remember, um, "enzupco" or something like that. But they're topical JAK inhibitors. And they they're they're great for chronic eczema, they're great for chronic atopic dermatitis. Um we use ruxolitinib, topical ruxolitinib for um vitiligo. They stop itch in a matter of hours. I mean hours. They've done studies where they've charted it in 15-minute intervals, and you know, the the uh it's an inverted parabola and how quickly they respond. Wow. Yeah,

Michael Bernhardt, MD:

and we're using a lot of multisyllable words too.

Erich Schramm, MD:

No, I get that. You're must be Friday. It is. Well, we like that. Um and we've done uh and we're doing studies on ruxolitinib for hidradenitis suppurativa, by the way, which was another uh uh great podcast with you. So um, and we talked um in the past, we talked a little bit about um you've done some really good definitions to talk about um the JAK-STAT pathways um and uh really some great uh ideas some about understanding um inhibiting all the different types of inflammatory cytokines that that were found in these JAK inhibitors. And um and just so that when you I think when we left off on that, that we uh, or at least you were saying that that there's a very high comfort level to be using, especially a topical JAK inhibitor like ruxolitinib, um, we didn't have any really safety concerns with it. We thought it was or thought it was a very safe and effective treatment. Um, but you know, you have to do the studies, right? Yes, you can't.

Michael Bernhardt, MD:

I mean, all these drugs are are you know, all drugs have side effects. And when I'm doing talks, I always tell people that you can't skip over important safety information because A, it's important, B, it's safety, and C, it's information.

Erich Schramm, MD:

Right,

Michael Bernhardt, MD:

Right. So you always have to go over that. And and you know as a clinician, you'll see some regulatory things that sometimes make sense. Um but again, as a clinician, you don't always see the whole regulatory picture. Right. So FDA has the same warnings for the topical ruxolitinib in terms of of you know cardiovascular events, D V T, PE, thromboembolic phenomena that they do with some of the oral JAKs. Um so far there's not a plethora of literature that really um endorses that. And you know, I don't again, I'm only seeing it from a clinician viewpoint, not from a regulatory viewpoint. But I still um counsel patients as to the risks, including DVT, uh deep vein thrombosis, pulmonary embolism, even from the topical.

Erich Schramm, MD:

No. Right. Um Well, you have to, right, and that's a sign of a good idea. I think full disclosure for those patients.

Michael Bernhardt, MD:

So the easiest way to think about the JAKs if you want to kind of put the JAK-STAT pathway in perspective compared to blocking the cytokines.

Erich Schramm, MD:

Right, which we've talked about before.

Michael Bernhardt, MD:

But the cytokines is like you're putting the key in the ignition. Okay? If you don't have the right key, you can't turn on your ignition. Um the JAK-STAT pathway is that electrical conduit from the ignition to the starter of your car.

Erich Schramm, MD:

Okay.

Michael Bernhardt, MD:

All right, and that's the easiest way to think about it.

Erich Schramm, MD:

Okay, I like that. Uh-huh. Now, so um to that point, and thinking about um the four and thirteen inhibitors, now we got 31 inhibitor. Um, do you see that see that as being a potentially greater benefit than for the four and thirteen, or is there enough information out there to to come to some conclusion about it?

Michael Bernhardt, MD:

You know, they're all great drugs, right? And you prioritize based on patient age and in terms of what's appropriate for the patient. And the comorbidities. Um, you know, everybody's afraid of these JAK inhibitors, but there was a study published May, Journal of Clinical Allergy, that looked at abrocitinib, which is there's two main JAK inhibitors, pacritinib and abrocitinib, both great drugs. They both have done absolute wonders for people. But this particular study just focused on abrocitinib. And they were saying that in the low dose, the 100 milligram dose, the risk of cardiovascular and thromboembolic phenomena were no different in a younger population, the population under 65, um, which at that age to me is still a younger population. But in the under 65 population, there was no difference between the SEER data, the expected epidemiologic data. When patients are over 65, then the risks start to trend up a little bit.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

And when you have to go on the higher dose, the 200 milligram dose, the risks start to trend up a little bit. But for younger people on the low dose, um, based on this article, the data shows that that the morbidity is about equivalent to what you'd expect in the population.

Erich Schramm, MD:

Was that, to remind me, was that a kind of a pan-JAK inhibitor, or is that a more selective JAK inhibitor?

Michael Bernhardt, MD:

abrocitinib is more of a selective JAK-1. I mean, all these you know, all the drugs have some effect on multiple JAK sites, but you you look at how effect how much upregulation of the other JAKs and the difference between the JAK 1 and JAK2 upregulation is huge to the point where it's really just a selective JAK 1.

Erich Schramm, MD:

Right. And maybe, and just remind us um, you know, what are some of the the bad actor um cytokines that are downstream once JAK 1 is is out of the same.

Michael Bernhardt, MD:

Yeah, I mean so so all these things you're looking at like in interleukin 6, TNF Alpha, Interferon-gamma, uh those those there's others, but I mean bottom line is those guys drive a lot of the inflammatory cascade.

Erich Schramm, MD:

Great. So now we've got um so we've got uh a number of tools in the armament for atopic dermatitis with some uh really solid approaches with monoclonal antibodies. We've got oral JAK inhibitors

Michael Bernhardt, MD:

There was a meta-analysis last year that where they looked at at a upadacitinib. I think they did 45 studies, 15,000 patients, and they found basically the same thing that in low dose, the risk, the cardiovascular and the DVT PE risk was equivalent to what you'd see in the SEER data.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

And that, you know, when you bump up the dose, yeah, there's a corresponding increase in risk. But low dose in a younger patient population, you were pretty much at SEER data level.

Erich Schramm, MD:

Another uh question that comes to mind, and um getting back and talking about some of the other topicals out there, maybe you could talk about the calcineurin inhibitors and some of the other, you know, uh you know, we've used and pimecrolimus and some of these other things. And if there's were their place for those

Michael Bernhardt, MD:

So they're great drugs and they work and and they're they're a nice alternative to topical steroids. Um, you know, you you can't particularly in young kids, because young kids have a high surface to volume ratio. So if you saturate their skin with too strong a steroid, you can get some systemic effects. Right. You know, you can get some adrenal cortical suppression. Um, that's a lot of multisyllable words on a Friday afternoon. Anyway, you can get some adrenocortical suppression if you're just bathing the kid in in a mid or higher potency topical steroid multiple times a day. Right. Um so I mean a short blast if you need to bulldoze through it is fine, but if you can switch them off of that and get the equivalent of steroid sparing like we do with orals, with the topical calcinerium inhibitors, ELIDEL, which is pimecrolimus, and Protopic, which is uh tacrolimus, you can get pretty much the same mileage without that steroid risk.

Erich Schramm, MD:

Right. And so for the the parents that are out there listening and they're like, wow, well, how do you know uh how much uh topical steroid is too much or which is you know what's the right or the wrong uh topical steroid out there, I'd say, well, talk to your informed dermatologist to make sure that you know if there's really you know concerns about that. So that's that's a that's a good point. So uh we have a lot of options out there um aside from topical steroids, but like you said, they're always available there if you need it. So um we've talked about uh ways to keep the skin healthy and having good skin hygiene. Uh you've given us some really good uh background and talking about and understanding the uh the uh interleukin inhibitors, the monoclonal antibodies. We talked about um the uh how the JAK-STAT inhibitors um are out there and really being a very effective uh element. Um fantastic. Anything else that might be out you see coming down the pike?

Michael Bernhardt, MD:

You know, we use sometimes left people take bleach baths, which means you take a bathtub full of water just like you normally would and put a cap, maybe two caps, not a cup, not a C U P, a C A P, a cap or two of bleach. And the you know, when I tell people that they look at me like I'm either crazy or I have a third eye.

Erich Schramm, MD:

I've been looking around. I'm uh maybe there is a third eye that is that is a first, right?

Michael Bernhardt, MD:

Um and then I always say, well, there's a reason for it. And you know, why do we put chlorine, which is bleach, why do you put it in swimming pools? Because it kills bacteria.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

Right? So on the micro level, if you take a bleach bath once every week or two, you're gonna kill that staph that's on the skin. You know, like I was talking about before with the uh defective granular layer secretions, right? Normally the skin secretes what's called antimicrobial peptides, which reduce staph flora, and they do things to make it harder for the staph aureus, which is the main uh infection driver, to bind to skin. Well, in kids with atopic dermatitis with defective granular secretions, not only do they not have enough antimicrobial peptides to ward staph off, they actually have receptors on their stratum corneum that encourage staph binding. So these kids are more prone to staph carriage. Now, when you when you use a bleach bath once every week or two, you're killing that organism off in a way that does not cause drug resistance. Okay. And you're not going to put the kid at risk for a cap of bleach in the tub units. But um the other point I was going to make is that once you repair the barrier, when you're using the 413 or the 13 inhibitors or the JAK inhibitors, and you repair the barrier, particularly in the fourth, there's data that shows that with the 413 inhibitors, um, you actually reduce the kid's risk of infection because you've reintegrated the barrier.

Erich Schramm, MD:

Right. Do you ever see a time where you would put somebody on just oral antibiotics or any kind of prophylactic or any time, uh any time if you would consider any courses for oral antibiotics in that?

Michael Bernhardt, MD:

Yeah, when they're if they're starting to look impetenized, yeah, sure. Okay. Sure, sure. But I would definitely like to see them do a bleach bath. And then the other thing to remember, moms and dads out there, especially if any of you work with cement, right? The skin, when you're in a shower or bath, is like wet cement. And when you get out of that shower and bath, you've got about four or five minutes before that cement sets. And once the skin sets, it's less effective with the moisturizers. So when you get the child, yourself or your child out of the shower, pat dry, and then that's the time to put your moisturizer right on. Don't wait 20 or 30 minutes, put it on right after you get out, and you get a better result.

Erich Schramm, MD:

Wow. That's that's great. I mean, that's just great general, good skin care. Um back to thinking about um the JAK inhibitors and the monoclonal antibodies. Um, as far as um expectations for patients for healing, their timelines. Is there one that's a little quicker than the other, or is it all about the same?

Michael Bernhardt, MD:

They're all pretty good. Uh they're all pretty good. When you look at the studies, there's a lot of overlapping data with the low dose JAKs versus the 413 inhibitors. They're really pretty good. Um, some studies, some of the drugs have studies that show that itch reduction is a little faster with certain drugs. Um but by and large, by the time you see that person back. In two or four weeks, uh, they should be significantly more comfortable.

Erich Schramm, MD:

Wow.

Michael Bernhardt, MD:

And I typically give a drug about two, three months. And if they really haven't turned around, then we start talking about changing. Okay. Unless they just, you know, get obviously worse.

Erich Schramm, MD:

You know. Um great. So uh that's actually pretty impressive that we can take, and I've seen some really, really challenging cases with people with atopic dermatitis, especially those kids. And you know, it is a really challenging quality of life, and you know, you see those those patients plenty, and to think that in a matter of months that you can see such a such an amazing turnaround.

Michael Bernhardt, MD:

Weeks,

Erich Schramm, MD:

right?

Michael Bernhardt, MD:

Weeks,

Erich Schramm, MD:

right? Yeah. And um, you know, we we joke uh to say that you know, we talk about the three-headed monster in dermatology, which were uh atopic dermatitis, hidradenitis suppurativa, and psoriasis. And uh, you know, you're making that comment you'd said earlier that you know, here we had what did you say, institutionalized mediocrity for treatments up until a time that we ended up and you know these kind of game-changing therapies came out.

Michael Bernhardt, MD:

And yeah, these are these are true game changers. I mean, it's nice to have drugs that deliver on the promise, and that really work. They've been approved by the FDA after very rigorous, like studies that we did here. We were involved in the phase two for dupilumab, right? Very rigorous clinical trials, multi, you know, multiple randomized clinical trials, huge data sets with huge patient populations that are by and large safe and effective.

Erich Schramm, MD:

Right.

Michael Bernhardt, MD:

You know, it's a whole different world than even 15 years ago.

Erich Schramm, MD:

Right. Right.

Michael Bernhardt, MD:

In my day, when I first came out with someone with bad atopic dermatitis, we'd immediately just start on one of the injectables, one of the orals. You know, in those days it was tap water wet dressings with topical steroids, keep it on overnight, maybe some phototherapy, yada yada yada. And if you're better if you were lucky, they were at best twenty, thirty, forty percent better, which was you know not where we want to be.

Erich Schramm, MD:

Wow. So and that leads now uh to a great improved job uh you know, uh job satisfaction as a dermatologist.

Michael Bernhardt, MD:

Thanks to clinical research. Right. All this is thanks to clinical research.

Erich Schramm, MD:

Well, again, I appreciate your efforts and uh every Friday an opportunity to be able to learn from uh such a great educator and clinician as yourself, so always appreciate that. Thank you. So I understand the fourth headed monster is gonna be alopecia, right? Yeah, so we're gonna be uh jumping, doing a deep dive uh at an op uh in our next podcast talking about alopecia.

Michael Bernhardt, MD:

We haven't talked about restaurants yet.

Erich Schramm, MD:

Ah okay, all righty. Okay, you go first.

Michael Bernhardt, MD:

Okay. well, I would you know, I was in Mayo Hospital for about five days with a knee problem, and I found that of all the hospitals I've been in, their food's really pretty good. Um I'm not telling people it's the Mayo clinic. I'm not telling people to go get sick just so that they can get their food to say it out. But my wife loved the food at at Mayo Hospital.

Erich Schramm, MD:

Um did they have a wine pairing with that? But how did that work?

Michael Bernhardt, MD:

I don't think so. But all kidding aside, um the only new place that we've gone that's been really pretty good is uh is in St. Augustine, Andaman. Okay, what's that? It's uh Asian. Oh Asian Fusion, and um we've gone there three or four times, and the food's always been reliably great.

Erich Schramm, MD:

Okay. Well I'll have to look that up. So my go-to now, um so I like South Indian cuisine. And so I would direct people to the Honest South Indian restaurant that's over there on Bay Meadows. It's not very, it's not a fancy place.

Michael Bernhardt, MD:

It's called Honest South Indians.

Erich Schramm, MD:

Honest, huh? You know it's gotta be good, right? Honestly

Michael Bernhardt, MD:

Honestly,

Erich Schramm, MD:

yeah. So but yeah, so if you want to get a real sense for true, authentic, delicious South Indian food, that's that's the place to get.

Michael Bernhardt, MD:

My wife and kids love it, we're gonna go there.

Erich Schramm, MD:

Yeah. It can get hot and be warned it can be hot and spicy.

Michael Bernhardt, MD:

I'll tell them to keep it in the negative range. Cool, man.

Erich Schramm, MD:

Cool. Anything else uh you want to put out there?

Michael Bernhardt, MD:

I think we've covered pretty much everything you can cover.

Erich Schramm, MD:

We used all the big words that could possibly come to mind on

Michael Bernhardt, MD:

a lot of syllables for a Friday afternoon.

Erich Schramm, MD:

Maybe we've got to look up some things too to make sure we're we're on track. But thanks again, Mike. It's always such a pleasure to work with you.

Michael Bernhardt, MD:

My pleasure too man, enjoyed it.

Erich Schramm, MD:

We'll see you.

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