A (2:44)

We're not running a department.

C (2:46)

We're not running a department.

A (2:47)

That's right. We're not. We're not chairs. Like fairs.

B (2:49)

Exactly. So, yeah.

A (2:52)

So.

B (2:53)

So four patients locally advanced basal cell debulking, then vismota jib. So after. So after they're debulking, they got. A week later, they got a punch biopsy so they could look at the tissue. And so what they found was, you know, interesting. Just that process of the sur. Sort of trauma from debulking really upregulated, you know, a bunch of, like, notch and went signaling associated genes, like patched and hey, two, and, you know, other. Other genes. But what was really impressive was the clinical response in these patients. So way better than you would think. So basically, three patients had significant clinical response. One was lost to follow up, like a typical likely advanced basal cell patient. And then about a year later, one of the patients needed surgical intervention. But, you know, we think about, like, I think we traditionally think, maybe I'll give them bismodogib, I'll shrink down that tumor, then I'll do some surgery. But this actually suggested that it might make sense to debulk it, then put them on medication and then bring them back and think about doing surgery.

A (4:03)

And again, the idea is that the debulking causes the tumor to express stuff that makes it more responsive to the chemo. That's the idea, yes.

B (4:17)

Yeah. So it actually makes it more likely to respond than if you didn't do the surgical debulking. I think we still need more data on this, but, you know. And how much surgical debulking do you need to do? Canadian C. But I like the idea of, you know, sort of this idea of sensitizing the tumor with something that's relatively straightforward.

C (4:37)

Yeah. I always thought sensitizing would be like a miquimod or, you know, the TVEC stuff that we were talking about. It may. You just go in there and just shave it all down. Right, right.

A (4:49)

Part of what I wondered here is when they debulk this, how did they get it to stop bleeding? Like, would that. I guess that's pottery.

B (4:58)

Lots of aluminum chloride.

A (5:00)

The patients all have Alzheimer's now, but it's okay. They get their. Their BCC are better.

C (5:07)

I had a BCC Quality of life.

A (5:12)

Their BCC specific quality of life is great. We're all going to get dementia whenever we're.

C (5:19)

You know, we deserve it.

A (5:22)

We deserve it now. All right, all right, Patton, what do you. So. So the takeaway there, unlike one of our prior episodes where we decided that a Mickey curettage followed by imiquimod, not derms on drugs approved does look like pre vismodead JIB debulking. Provisionally approved. Provisionally approved.

B (5:42)

Awaiting a study of greater than four patients.

A (5:45)

You know what, with RFK having gotten approved, we might be the new fda. You know we could just.

B (5:52)

For all of dermatology, we could be.

A (5:54)

The new FDA approved. Nope. Next.

C (5:57)

All right, all right. My first six packs was a pre proof article from the November JAD of last year titled COVID 19 infection is associated with an elevated risk for autoimmune blistering diseases while COVID 19 vaccination decreases the risk. A large scale population based COHORT study of 112 million individuals. Wordy, wordy title. It's by Kerman et al. In the intro the authors refer to a Meta analysis from 2024 suggesting COVID vaccine could be associated with new onset or exacerbation of AIBD autoimmune blistering diseases. So what do we tell our patients? I had patients with new onset BP after getting COVID vaccine and they would say, well, will the booster flare my BP or not? And I'd be like maybe. And they'd be like maybe it will or maybe it won't. And I'd be like, yeah, no, I needed a better. I needed a better answer than that. Believe it or not, it was a retrospective cohort study that used trinetic software to study millions of patients in the United States. So starting date of January 2020 up through I think like May, slash June of 2024, three groups of patients diagnosed with COVID those who received the COVID vaccine and control patients. So just had a health encounter without any documented history of COVID 19 or vaccination within six months of the index date. They then performed propensity score matching, came up with three comparisons. So thought was right. COVID 19 infection, it's going to be worse than controls. You get an infection, your immune system gets all fired up. If this is getting too scientifically technical, I apologize. You get AIBD as a result, Right? And that's what the first forest graph shows. Figure 2a. Patients diagnosed with COVID 19. 50% more likely to develop an AIBD as a result. Stronger association for Pemicus compared to with bp. Hazard ratio for pemus was really high. Hazard ratio for BP was lower, but it was still statistically significant. Top three plots. Primary analysis Authors did a bunch of sensitivity analyses. I'm not going to get into that just for sake of time. The next forest plot is COVID infection versus vaccination. That's Figure 2C. Overall hazard ratio of 3.13. Higher hazard ratio for pemphigus, really high, like 5.5. So 5.5 hazard ratio of the infection versus vaccination of giving you an IBD. Right. So why did I skip over Figure 2B? Because it's. It's the dramatic effect. This is the most exciting part of the paper. Right. Like I said, I don't get out much. So figure 2B. COVID vaccine versus controls risk of developing a IBD was almost halved by getting the vaccine compared to control patients. And that was surprising to me. You would think, you know, between a control group and the vaccine, vaccine's going to ramp up your immune system a little bit and it's probably going to be a higher risk of AIBD in those patients. And the opposite was true. It was mostly the result of pemphigus because the hazard ratio for BP was numerically lower in the vaccinated patients, but it wasn't significant. So if patients are asking about COVID vaccine, will it increase my risk? You can tell patients, we have one study, and it showed that with a particular condition, vaccination actually appeared to be protective. And so take that, RFK vaccine protective.

A (9:27)

So what do you think? Wait, first, what is extended psm? That's one of the things in the.

C (9:35)

So you propensity score match because you say, okay, I want. I need somebody who's white, who's the same age, you know, same ethnicity, same age, few comorbidities. I think their first PSM was nicotine use, things like that. They just extended it. Liver disease, chronic fatigue. Yeah.

A (9:52)

So they were better matched than normal patients. Yeah, more.

C (9:56)

Matched them for more comorbidities.

A (9:58)

Huh. This is, It's. It's mechanistically really hard to think of how this. And yeah, I know you mentioned this already, but it's hard to think of how this is possible. It just.

B (10:10)

Except the vaccine is so. I don't know that with trinetics, you're capturing every COVID positive case.

C (10:17)

I think that. Right. I think that explains it. Right. These aren't controls in the sense of. Didn't ever have Covid. Right. They. They never saw their doctor about COVID They never took a COVID test. But, I mean, everybody got Covid.

A (10:33)

Yeah.

B (10:33)

They could have taken it at home and they just.

C (10:36)

Yeah, but still, even if you think about that, you're comparing. So that group of patients, those control patients would be. Okay, got Covid, but really weren't that sick. So basically didn't have, like, significant Immune activation. Whereas, I mean, some people got pretty sick getting the vaccine.

A (10:55)

And again, remind me, was it that Covid was Covid compared with vaccination, which one was. Covid was worse than vaccinated for pemphigus.

C (11:08)

It had that 5.5 hazard ratio. I mean, Covid was way worse, especially for pemphigus, but it was worse for BP as well.

A (11:16)

So. Anyway, it goes back to the answer we can always give. Why did I get this? It must have been a virus. Your immune system responded to a virus, and it just got overworked and the whole thing. So it confirms for us we can just make up, continue to use the virus excuse for everything.

B (11:36)

Makes it easy.

A (11:37)

So far, I think of you as our psoriasis expert did. So as the dermatitis guy, I saw tons of people who believed that their dermatitis got worse either after Covid or a COVID vaccine. I don't know. Like, I would always, you know, I always agree. Cause I was like, you know your body better than me. You think that know you timing was right. Sure. I could imagine that.

C (12:02)

Did.

A (12:03)

Did you feel like you saw that with psoriasis?

B (12:06)

Not as much. Everybody just wanted to get an excuse to work from home because they were on a biologic. That was my entire Covid life. As the psoriasis person, would you.

A (12:15)

Would you give out the. I. I'll give an excuse for almost anything, because I know you will.

B (12:19)

Yeah, it's generally, I'm not that nice. Haven't you figured that out?

A (12:23)

It's true. It's true. I will agree with that. All right, so let's go on to my first article. So this one was just fascinating to me. So diet and living environment is novel Etiological factors for melasma. Results from a retrospective case control study of 150 Chinese patients. First author was last name Xi. And the things that jumped out at me here. So they looked at a lot of different aspects, and some of them were a little bit odd. Like, you remodeled your house. You didn't remodel your house. Like, whatever. I kind of weeded those ones out as it's hard for me to come up with any plausible explanation. But the things that were really interesting. So if you had an abnormal menstrual cycle, you were more likely to have melasma. Okay, fine. If you had a previous sunburn or exposure to sun two hours a day, you were more likely to have melasma. Okay, fine. A regular sunscreen user was more likely to have melasma. Now, that's one that I think is probably reverse causation, where people notice, you know, maybe they're getting some pigmentation or something, so they start using lots of sunscreen cream. It's hard for me to buy that one, but the one that was most interesting. Well, I'm gonna throw in one more that just kind of. So cystic breast hyperplasia. So which I think of as a hyperestrogenmic state. Sure, estrogen is melanocyte responsive, but alcohol intake. Now, the number of people who. Who were significant alcohol consumers was relatively low in the study, but the relative risk of melasma for people who consumed meaningful amounts of alcohol was 20 fold higher. And so it. It does. Now, whenever I see a patient who's got melasma, I am going to, you know, ask them if they consume alcohol, and I'm gonna recommend to them if they do drink. And I'm not even talking like excessive drinkers. I'm just talking. They drink. I'm gonna recommend to them that they, you know, cut that out as much as possible. Cause again, mechanistically, I can. You know, alcohol has a lot of effects. I can imagine that, you know, it increases blood flow to your skin, and that increases heat to your skin, and that increases pigmentation, something like that.

C (14:47)

Other.

B (14:47)

A lot of. A lot of imagining.

A (14:49)

A lot of imagining they're drinking their.

B (14:51)

Alcohol outside in the sun while remodeling their house, maybe. Confound it.

C (14:56)

Which is not safe. You should not be drinking.

A (14:59)

Do that.

C (14:59)

Yeah, don't do that.

B (15:00)

Or while getting a mammogram to find your cystic hyperplasia. Who knows?

A (15:05)

So there were a few things that protected. So seborrheic dermatitis patients were less likely to have melasma. People who drank soft drinks, less likely to have melasma. Let's see here.

C (15:18)

And then that was a vitamin C effect. Right. Didn't they say a lot of the soft drinks have the vitamin C?

A (15:25)

Well, so I'm going with caffeine. Because coffee intake also reduced your risk of melasma.

C (15:32)

Interesting.

A (15:32)

So I'm going with.

B (15:33)

Don't people use caffeine and, like, skin brightening topical things, too?

A (15:38)

I didn't even think about that.

C (15:40)

Yes, I thought the moving to a new place was kind of interesting because they said in the paper, when you move, most of the time, you're moving, like, to a nicer place. So you're moving, like, out of the city into a more sort of like, not in the city. And they felt that maybe the higher pollution and things like that in the City affected. It was an interesting paper. I mean, I. The alcohol. Interesting. Maybe I'll mention it. I'll probably mention it, right?

A (16:10)

Because I was looking for, like, what can I talk to people about? Because I'm not going to be like, well, did you move? Oh, you shouldn't have.

B (16:17)

Like to remodel your house.

C (16:20)

Yeah. Go back. Go back to your old place.

A (16:24)

So. But the, you know, the alcohol thing's useful. And then, you know, the caffeine intake, I can buy that. We know that coffee has a lot of, you know, there's a lot of data that coffee is beneficial for decreased cancer risk, decrease dementia. I can't remember. Decrease something. So coffee intake might be good, but. All right, that was our primary takeaway from there. So less alcohol, maybe more coffee for your melasma patients. And let's move on to our Next study here, Dr. Faris.

B (16:59)

All right, so this is the impact of antibiotic therapy in psoriasis patients with active streptococcal infection. A prospective study. So this is the Journal of Dermatology, Bon Clanny et al. So this was, you know, we all.

A (17:16)

Wait, wait, it was. It was Bon Chiani. That's an I, not an L. Okay, fine.

B (17:21)

Okay. Thank you for correct.

A (17:22)

Bunklani. Bonciani.

B (17:24)

Okay. Oh, Bonchiani. Okay, I was misreading it. Okay. So we all are taught, you know, strep infection is associated with psoriasis or gutate psoriasis or psoriasis flares. So they kind of tried to answer that question, but they had 155 psoriasis patients. And then they had, you know, sex matched dermatology, dermatology patients who didn't have psoriasis at about the same period. And what they did was they came in, they did a throat swab, they. To look for strep, and then they checked ASO titers. And so the patients who had strep infection with psoriasis received both topical treatment, which was basically betamethasone calcipa trio and an oral antibiotic, which was like amoxicillin or clarithromycin or clindamycin. And the people who didn't have strep, they just got the topical. So they, they included strep infection as positive ASO or a positive throat swab. So these are not like people coming in with terrible sore throats. It's sort of just like, did we find evidence of this? So, you know, I think the thing that was interesting was 25% of patients with psoriasis had a positive culture, half of them were ASO positive, whereas only about 13% of healthy controls were positive for that. More evidence of strep in the throat or, you know, positive asos and psoriasis patients. But they really did not see any. They didn't see more improvement with, like, antibiotics didn't make these patients do better. Now, they didn't have a control group. They decided it would have been unethical in an asymptomatic person who they happened to swab and have a positive test to not treat them. So they didn't have a control. Like, okay, this. This group gets antibiotics. This one didn't. So, you know, there was maybe some. The. The patients who got antibiotics, their PASI scores were a little bit lower, didn't reach statistical significance. I don't feel like this really gave me a whole lot of answers, but, you know, interesting. I thought the most interesting thing was just higher prevalence of positive throat cultures.

A (19:44)

And you guys. Neither one of you does sort of empiric, amoxicillin or anything else in your gut. Tate. Psoriasis patients.

B (19:54)

I don't.

C (19:55)

No.

A (19:55)

Didn't Cress in English teach us to. I feel like that's what we did in residency.

C (20:00)

I don't. I mean, cress. Maybe. I don't think English. Like, if you weren't symptomatic, but maybe I'm misremembering.

B (20:07)

I don't remember.

C (20:09)

It was very traumatic training under him.

A (20:10)

Oh, no way. I'm putting in a plug. The two greatest dermatology educators in the history of dermatology were Joe English and Doug Kress.

B (20:20)

That's right.

A (20:20)

We're amazing.

B (20:21)

We wouldn't be here. We wouldn't be there.

C (20:22)

We wouldn't be here for that.

B (20:24)

Any normal people would have rejected all three of us. So we're very lucky.

A (20:30)

I'll still never forget that day when I found out, my God, there's a do coming to do residency with me. Like, what? Where has my life gone? And it turns out Patton's.

B (20:40)

You've just lost your whole DO audience. Thanks, Matt.

C (20:42)

No, because there's a. It's a happy story. In the end, I converted him.

A (20:45)

It was a stereotyping that was. I learned my lesson.

B (20:50)

Like Patton, smartest of the three of us, right?

C (20:52)

Oh, right.

B (20:55)

Yeah. But no, interesting. The strep thing, you know, there's some data that, like, tonsillectomy may improve psoriasis, so there might be something there. I just think this wasn't the way to get at it.

A (21:04)

But, you know, I forgot about that. I've had Some old dermatologists tell me that they had patients back, you know, back in the day when we didn't have like amazing drugs, who they really saw tonsillectomies, not everybody. They didn't like tell their patients, go get your tonsils out. But they had their experience over a long time was that a tonsillectomy made a substantial number of psoriasis patients. Psoriasis much easier to treat. Yeah. Which is believable. It's believable. Okay, let's move on to our next patient here, our next study. So, Dr. Patton, why don't you go ahead.

C (21:41)

Yeah. Second six pack was January edition of seminars in arthritis and rheumatism titled use of biologic drug in the treatment of local scleroderma and systemic sclerosis in children. A scoping review by center et al. Why did I pick this? Because I, I do manage linear scleroderma in adults from time to time, not kids. But I figured it would be relevant. My treatment algorithm combines steroids and methotrexate. Maybe add mycophenolate somewhere down the line. So I, I saw the title and I'm like, huh, biologics. Like am I this, you know, prednisone, methotrexate, kind of old fashioned? Am I missing out? Like, are there biologics I need to start thinking of? This is the age of biolo. Even though the article discusses both localized scleroderma systemic sclerosis, I was just going to focus on the linear scleroderma part. Systemic sclerosis often managed by room. So it was a review that was conducted on 29 articles. Text goes through a bunch of numbers and the tables are hard to understand. They were for me. I'm not that smart. Almost all the patients were on or had been on corticosteroids and methotrexate. And a lot of patients also tried mycophenolate. So it still looks like those are first and second eyeing agents for localized scleroderma. Main points, there was a visual abstract. Most preferred biologic was abetasept 55.2 of patients. Abetasept is orencia, second most preferred.

A (23:04)

What's it do?

C (23:05)

Do you know what it's thing a beta sept is? It's a CTLA4 protein hooked up with IgG. So the CTLA4 protein binds to CD80 and 86 on the antigen presenting cell. Basically not letting the antigen presenting cell interact with the T cell and activating.

B (23:23)

It blocks CO stimulation.

C (23:25)

Thank you. I could have said it blocks close stimulation.

A (23:28)

So it's like the opposite of the cancer chemotherapy drugs.

C (23:35)

Yep.

A (23:35)

Okay. All right, all right, got it.

C (23:37)

All right. Second most preferred drug was tocilizumab. That is an anti IL6 antibody that was used in 48.3% of localized scleroderma patients. Main indication for using biologics was progressive skin disease. So it was kind of, you know, derm relevant. That's why they did it most frequently is because they were on some of those other medications and the skin disease was getting worse. They list these improvement rates. A beta SEP, 92.9%, tocilizumab, 77.4%. But, like, the number was really confusing. For a beta SEP, the response rate was only reported on 33.3% of patients. So close to 70% didn't have data on whether they improved or not. It's really hard to say that, like, you know, 92.9, like, oh, my gosh, that works awesome. But they didn't have data on 70% of the patients that were, you know, in this review. So tocilizumab data was available for close to 90% of the patients. So even though the improvement rate was lower, that number might be a little bit more reliable. I don't know how helpful this article was. It reassured me. Steroids and methotrexate probably still the way to go. Mycophenolate. If you're not getting that response, maybe consider a better tocilizumab. But I've never given those drugs, so I. I don't know how easy it would be. They're not FDA approved. They have both been evaluated in controlled trials. There was a phase 2 multi center randomized. A beta sept published in 2020. Primary endpoint of an improved skin score wasn't reached or it didn't reach statistical significance. Let me say that right. And then there was a phase 3 trial, tocilizumab, also published in 2020. Primary skin fibrosis endpoint wasn't met either, so. So I don't know. What do you guys think?

A (25:20)

Well, the adult ones you're treating, are they in coup de Saab or are they, like, over a joint or. It could be any of it.

C (25:26)

The last two that I treated, like I said, I don't treat a ton of this, but it was over. It was linear over a joint, elbow, hand affecting range of motion. Yeah, Okay.

A (25:39)

I do.

B (25:40)

I'm mostly sending these patients to rheumatology when they're at that point of, like, more needing more than methotrexate. But room Is.

C (25:49)

It can be weird though, right? I mean, some. The last one I saw had seen room and the, you know, rooms have their specialties. So they saw like, maybe it was a DM specialty room person and said linear scleroderma is derm. Like go and see them.

B (26:04)

Yeah, I guess I'm not given a beta sep or tocilizumab.

C (26:09)

No, that's.

B (26:09)

Yeah, yeah, yeah. Like at that point I'd be working with them, but yeah. Interesting. Maybe I'll think about it more.

C (26:15)

Yeah.

A (26:15)

So, Pat, I gotta ask. There was this beautiful cord diagram. Yeah, I know what, it's gorgeous. But what. I can't make heads nor tails of it.

C (26:25)

It was really about indications. And so it's easier if you go down to like infliximab, where there, there was like one patient on infliximab, or maybe it was rituximab and the chords go out as. Why was that person given infliximab? Well, there's three little cords to three different of indications. Progressive skin disease, maybe it was pulmonary. So it was basically that whatever drug it was being attached to, the indication for that particular drug. Honestly, I think that's why I picked the paper. That thing was, I want to. I want to get that on a T shirt. And then I would wear it and people would come up to me and ask me about my cool T shirt.

B (27:03)

That might be what happens. Yeah.

A (27:06)

All right. Patent easily dazzled by pretty colors. That's the takeaway. All right, so let's get to our last paper of the six pack. So this one was mine. And as regular listeners are probably starting to figure out, we are big proponents on derms, on drugs of oral reflumelast. So this was a real world 24 week prospective cohort study. And really there are a couple of things that were useful here. So first, how good is this drug? So oral reflumelast for anybody, again, who doesn't know about it, think Otesla, but free and more effective, but also probably a little more GI side effects is the way that I think about it. Mechanistically, it's identical. It's just higher potency. It is a PDE4 inhibitor and it went generic about a year or two ago. And so it's about six bucks a month if you get it through Mark Cuban's cost plus pharmacy. No labs, no immunosuppression. So this was people who went on oral reflumolast and how many of them. The key things here were how many got pass C75 and how many got passing 90? So if, if we look at the passing 75, it was over 50% of people. So it was between 50%. And so between half and two thirds got passy 75. So if we looked at it as observed, it was modified NRI. Basically, as observed it was 2/3. If we looked at it as non responder imputation, intent to treat analysis, it was half. And for passing 90 it was somewhere between a third and a half. So depending on how you looked at the stats. So a good drug, they actually had better numbers. There was a randomized double blind study or at least a randomized blinded study where they looked at intramuscular methotrexate versus roflumilast and actually got more like 75% of people to pass 75 and about half to passing 90. So just goes back to another thing. This is a really useful drug. If your patient has been on a biologic before, they're probably not going to be happy on it because it's slow, does give you some GI upset and doesn't work as well, but it's incredibly inexpensive. No immunosuppression is very safe drug. And so using it for psoriasis gives us. The main reason I think it's interesting is it gives us an idea of how effective it is. The main places I'm using it are more lichen, planus, granulomanulare, lichen, plano, pilaris, you know, stuff like that where we don't have better drugs. And then occasionally in psoriasis, whenever I can't get a better drug covered, you know, in any, anything that either of you kind of wanted to add about this. The main reason I wanted to do it was just it gives us a, again, more of an idea of how effective this drug is as a general idea of, you know, how well is it going to work for LP or whatever.

B (30:26)

I like it. You know, people say, oh, I like to add a Tesla to biologics. Like I can never get that covered. Right. So I will sometimes do this in combination with the biologic. I also thought, you know, baseline there are 58 patients. At week 12, there are still 52 in there. That's not that bad of a dropout rate for something that does have GI issues. So I thought it was interesting. I like having it in the toolbox.

A (30:51)

Yep.

C (30:51)

Yeah, I love having reflumelast. It's, I think we talked about that. Like it, for me, it is the new methotrexate. We use methotrexate for a bunch of stuff and it's a safe medication. I don't want to like overblow the side effects of methotrexate but you do have to do monitoring and you have to go through all those potential side effects. Or flumelastin. It's just, I love it. It's my methotrexate.

A (31:14)

There's data that it reduces cardiovascular morbidity and mortality in COPD patients. And I think, I, I don't know if I've mentioned this before but there's one study where they gave it to young healthy people and it made them smarter.

C (31:29)

Yeah. If you were smart enough you would remember that. You told us that.

B (31:33)

Clearly you're not taking enough.

A (31:34)

I need to, need to up my dose. It might help me. I have a friend who is on it. He had this crazy gingival plasmacytosis. So like friable red gums, you know, bleeding anytime he ate anything, trouble brushing his teeth because it was so bad. And I was like oh my God, you got gingival hyperplasia. You know, he went to see a good oral pathologist. Oral plasma cytosis, which is like I've seen six cases ever. This is incredibly rare. I wish I could put him on a Tesla. I think it would work. And I was like oh well you. But I can't get a cover. I was oh, try the reflumelast. Worked amazingly, amazingly. But like he's a healthy, you know, 53 year old guy. He lost like 40 pounds because it was just the GI, the nausea, the effects on going to the bathroom, the whole thing, it was like miserable.

C (32:30)

Wow.

A (32:31)

So yeah, it was interesting having a friend on it rather than a patient and kind of hearing what he had to say. Yeah. Well, I want to thank everybody for joining us this week. Hopefully you found the articles in our six pack interesting and that you will find them useful in your day to day practice. You know, if you've got questions, if you've got comments, ideas for topics we should cover on the show, shoot us an email @questionsoms on drugs.com Again that's questionsrms on drugs.com I do really want to recommend if you haven't been there, go check out the Scholars in Medicine platform. If you just Google Scholars in Medicine you will find it. They've got like 80 hours of really well done Durham lectures. A lot of content across the board in terms of meetings, abstracts, new stuff out of the journals. Just a fantastic educational platform that is at no cost to us as derms and, and especially send medical students people new to Derm, Massachusetts. You know, people, like I said, new into Derm. Just great platform, but all right, I hope you learned a few things. Hope you laughed once or twice. And mostly, I hope you're planning to join us next week. Till then, I'm Matt Zyrus.

C (33:50)

I'm Tim Patton.

B (33:51)

I'm Laura Faris. And we are Derms on Drugs.

A (33:54)

Sam.