A (5:01)

First I gotta say, Ferris, thank you. Unlike Patton, you regularly bring articles that I get something useful out of. Now here. Here's what I got useful out of this. So oral ivermectin combined with oral metronidazole is hands down the most effective therapy I've ever seen for rosacea in general. And that is, I'm convinced that almost all cases of Papillo postular rosacea are actually Demodex. Even if you get a negative Demodex prep, like, ridiculously useful. But every time I use it, I tell patients, hey, there's a good chance you're going to get a little worse for a week or so. And if you do, that's going to tell us that it's really working. It's going to work great in you. And I would always say I think it's because as we kill off the little mites, they're releasing toxins that are making you briefly get worse. And. Son of a. Son of a gun, you use this. This article gives support to what I have been making up for years, but it is my clinical experience. I would hear that from patients is why I started telling people that. So this helps explain something that I see not infrequently in regular people. And you would expect that this Masati reaction would be less common in people on immunosuppression since it's an immune, you know, immunologic response. So I thought it was super cool. This was really good. Thank you, Ferris.

B (6:31)

Yeah. Interesting paper. So that's good. And if we save one person from being treated for GVHD when they really had Demodex, it'll be worth it.

C (6:40)

It's true.

A (6:41)

Pat, you. You got anything you want to add?

C (6:43)

Nope. Loved it. Cool. Cool. Case reports. Picture's really impressive. They. They have that before and then after, and it's. It's an impressive response. Agree.

B (6:51)

Yeah.

A (6:52)

All right, Pat, what do you got?

C (6:54)

My. Another useless paper, apparently. So. Sorry, Matt. My first six pack is from November 2025 edition of Clinical and Experimental Dermatology and is titled Comparative Effectiveness and Safety of A and Dupilumab and Treatment Resistant Purigo Nodularis by Demir Boss et al. It was a retrospective multi COHORT study from 2024 to 2025. Patients had to have failed two prior systemic therapies, had to have 20 lesions and were excluded if they had atopic derm or any sort of atopic diathesis. Which is weird because they say that in the paper and then there's a graph and it said that two of the patients in the DUPY group had asthma. So, so they, they didn't really do that. I don't know, I don't know what's going on there. All patients had biopsies confirming PN. In the final analysis, 12 patients prescribed Dupy, eight prescribed Avro, 200 milligrams, eight prescribed UPA 30 milligrams. And they were, they were pretty different populations. DUPY patients were older, they had a longer disease duration. Those two things I think would have an effect on efficacy. Figure 1 shows a little line graph of the primary endpoint of PPNRs. So that's peak pruritus numerical rating scale. And all the medications worked. JAKS being faster and more effective, although I don't think statistically so more effective they were statistically, I think faster. Figure 3 shows decreases in nodule counts in all groups with again the JAKS being more effective. Like at six months, 11% of Dupy patients had a 50% decrease in the number of nodules versus 100% of the Abro and upadacit and patients. But again, I think that the difference in the baseline populations probably had a pretty big effect on that. So those were the primary endpoints, the PPNRs and the nodule counts. Secondary endpoints were patient reported outcomes. Patients in all groups reported improvements with more rapid responses in the JAK groups compared to the DUPY group. So kind of the same sort of story over and over again. Authors also did, this time by group interaction. I didn't understand it completely. It's like a way to measure treatment trajectories. A table three shows these numbers. So right degree of extra reduction seem to be similar between the three things like lesion clearance. Some psych scores, some treatment satisfaction scores did show differences between the groups. So that was it. It seems like maybe the Jacks are more effective in Perago nodularis compared to dupy. But I think different baseline characteristics make this hard to interpret. Yeah, I don't know. I, I, I, I always have a thing about, a weird thing about paragonodularis. When, when Doopie came out with that approval, I, I was kind of, I was almost a little bit puzzled. Like Prurigo nodularis is atopic derm. So of course this medication is going to work. Like I, I, I still to this day like diagnosing Prurigo nodularis, you're, you're kind of taking away a lot of potential medications. Because if you say this is a patient that has PN, like presentation of AT now have like 10 drugs, both topical and systemic. I mean, for me, paragon is atopic derm. So, you know, now we say like, Jack's probably. And the patients who are not responding to, you know, right now, if you just say paragon olaris, you got dupy, you got nemo. If you say they have atopic dermatitis, which, again, I don't like. I don't think that's fraud. I don't think you're making it up. I think paragon ogularis is really just a manifestation of atopic derm. Diagnose them with that. And then you have now Jacks, and we have evidence that they might even be quicker and maybe more effective.

A (10:37)

So I, number one, would agree with you completely. I think that PN is a type of, as. We should think of it as a subtype of atopic derm. Agree with you completely.

C (10:48)

On.

A (10:49)

However, I will say there are lots of itch experts who completely disagree and lots of atopic Durham experts who completely disagree with. But in the. None of them live in the real world. And I think that in the, in the real world, yes, I think we. We are doing our patients a disservice if we say this might be. It's like there's plenty of people who think this is a subtype of AD but I'm not going to call it that. I'm going to call it pn, no AD So that I limit your therapeutic options.

C (11:21)

Doesn't make any sense.

A (11:22)

Doesn't make any sense.

B (11:22)

I think they're two different diseases. Sorry, bad doctor. I think that it is. I think that there is this type 2 immunity cycle. And I think there's the nerve part and I think there's the. The T cell part, and I think atopic derm initiates in the inflammatory cytokine. Like that's the chicken or egg or whatever. That's a bad analogy. The whole point of the chicken and egg is you don't know which one it is. In my mind, it's the chicken first, but that's another.

C (11:51)

Well, where did the chicken come from, Laura?

A (11:54)

God, that's right. It had to be. I think it was the egg before the chicken, because what had to happen was a non chicken had got a mutation, a germline mutation, and then laid an egg that the first chicken came out of.

B (12:06)

Okay, okay, we're not going to do that. I think. I think that AD initiates in the inflammation, like initiates in the T cell. And I think that PN initiates in the nerve. That's what I have. But they're doing the same thing. Like, I think it's the same cycle, but I think it's like which, which chicken is which.

A (12:29)

So I agree with if so far I also agree with what you just said. And whenever I say that, I think it's a subtype of ad. Like, because I define AD as inadequate barrier function to protect your skin from non specific environmental insults. So I think there are. When I say, I think if you look at like the prurigo lesion itself, you're going to find barrier deficiency. And I think there are some prurigal patients who, if you look at non lesional skin, do not have any barrier deficiency. And that is a difference from atopic derm patients.

B (13:02)

Yes.

A (13:02)

And that's why I like, that's why I'm not like, like, I get the. Yeah, they might be different diseases. They are a different disease. And some people, there's some people who have both. There's some people who mostly have one, mostly of the other. Like, I get both sides of the argument. It just doesn't make any sense for a patient. Like if you can call it ad, you should. Because they have more therapeutic options.

C (13:25)

Yeah. And I think they're even in like the genome wide association studies. Like there's a lot of overlap between PN and ad. When they look at this, I think there's more signals for like fibrosis, just like genes and things like that in the PN patients. But you know, genes are disease and if there's overlap then I like, it's. It's kind of the same.

B (13:47)

I think it's all a spectrum and I am definitely like a lumper, not a splitter. So I'm like, fine.

C (13:52)

Every time I treat a PN patient now I'm going to be thinking which came first, the chicken or the egg.

B (13:57)

Exactly.

C (13:58)

I'm gonna, that's all I'm gonna be thinking about now. Man.

B (14:01)

Glad I can make you think.

A (14:03)

All right, let's. So my first one was a premalast in Japanese patients with palma plantar pustulosis. A RA Phase 3 trial. Basic takeaway. A premolast worked really well for pomaplantar pustulosis. The clinically useful takeaway is this tells us that rofluma last will work even better in palmoplantar pustulosis and be much cheaper. So we can't go any episodes without talking about oral roflum elast. And so my main takeaway from this was palmarplantar pustulosis patients if I can't get them on a good biologic or if the, or if the biologic doesn't work well enough, if I, if, if this biologic didn't work well enough then I'll add on the flumelast. If I can't get them on the biologic I will just give them oral reflumelast. It also suggests that topical reflumelast probably ought to help as well, but don't know for sure. Main thing was anytime there's anything that gives me another thing that I can say reflumast works for, I'm going to talk about it. That's it.

C (15:13)

Yep, I like it like it.

A (15:15)

Okay, next one was probably a little more controversial slash interesting. This one was a randomized double blind disebo controlled trial out of Iran. And I do specifically mention out of Iran as well as when articles come out of China because I see more articles from those places that end up being hard to believe and I just don't like there's a lot of pressure to publish and I just don't know like but so this article said Iran.

B (15:50)

That's as political as I'm going to get on that one.

A (15:52)

Oh, Iran not so Iran. Iran is not correct Iran.

C (15:56)

That's like cracker pronunciation Iran. Iraq.

B (16:00)

Yeah, exactly right. If you're Ohio roots showing through not sophisticated places like North Carolina and Tennessee.

A (16:13)

All right, so this study was intranasal corticosteroids, a promising new approach for adults with chronic idiopathic urticaria linked to aeroallergens double blind randomized clinical trial. So basically fairly small number of patients here, so 29 or placebo 40 got the intervention. And what was really interesting, the intranasal corticosteroids didn't help much but they did help. So the people who got intranasal corticosteroids, their urticaria activity score went down by like 5ish points. The people who didn't get it, their score went down by like 2ish points. And it, it was a difference. And like what I think is going on here because right you, you don't really get systemic steroid levels from intranasal. Intranasal budesoni. So this was intranasal Budeson. I basically the over the counter stuff, just two, two squirts a day in each. Not one squirt twice a day in each nostril. What I and I asked a couple of my allergist buddies about this and they were like that sounds like baloney but it's a randomized trial. So like, like, so mechanistically, if anything is happening, it's that you've got mast cells in your nose. And whenever the mast cells get activated by the aeroallergens, they're releasing not just histamine but also some cytokines. And that might make your mast cells more responsive to whatever it is, you know, the autoimmune process that is driving your urticaria. So the efficacy nowhere near good enough to be like, hey, this is what you do. But, but where this could be useful is somebody who's on zolaire or doopie or rhapsodo and like, does better, but not like, oh, I still get some hives, you know, like, so like I'm a lot better. But like, is there anything else we could do? And you've already got them on four times the antihistamine. Hey, go get some over the counter generic steroid nasal spray. Use that twice a day. Let's see if you get better. There's been a study that shows it helps. So it, it, that's, it's just a something to have in your therapeutic toolbox of tricks for people who have an inadequate response to systemic drugs for ciu. Now in theory, in this study, people had to have a positive prick test. But this is such a cheap, harmless thing. And it's not like they did it in people with a positive prick test versus not a positive prick test. Or maybe it works in everybody. So it's a cheap, easy enough thing that in a patient who's not responding well enough. And again, it's not going to be like, oh, it didn't work at all. I'm still terrible. Oh, here, Ty the. No, it's going to be somebody's like, I'm a lot better, but I'm not 100. Tried the nasal spray on top of that. Makes some sense. That's. That was kind of the takeaway of it. Any thoughts from either of you guys on, on this one, did they look.

C (19:08)

At nasal symptoms correlating with improvement of the hives or. No. Okay.

A (19:14)

No, they didn't. Because from what I could tell, it didn't even require that you had any nasal symptoms. Like the most common allergen that they found was dust mite, which Right. You don't really think of as a rhinitis kind of thing anyways. So they didn't talk really about rhinitis symptoms, just that people had a positive.

B (19:34)

Prick test or nasal polyposis or anything else like that. Right. So that's Those people would have tons of lymphoid tissue in their nasal.

C (19:43)

Yeah.

B (19:43)

Passages. Maybe they would benefit differently. But. Yeah, it's just. Who knows? We'll see, right?

A (19:49)

It's cheap and easy. That's what I'm always looking for. Cheap and easy. Kind of like whenever I'm dating.

B (19:56)

Exactly.

A (19:59)

All right, we gotta cut. We gotta. Now I probably was. Maybe we'll cut that part out.

B (20:05)

Let's leave it in.

A (20:06)

Yeah, we'll leave it in. All right, next article. Fares. What do you got?

B (20:11)

Okay, I have from the J eadv infection risk and atopic dermatitis patients treated with biologics and JAK inhibitors. Bio day results. Okay, what's, you know, this is basically looking at infection risk. And so this is a prospective, multi center Dutch registry. So this isn't like a, you know, retrospective study. This is actually like a prospective registry. So it is not a randomized study, but it's also not retrospective. So it's kind of between those things. Tracks adolescents and adults, moderate to severe AD who are either treated with biologics or jacks. And they looked at patients 12 and older who'd had at least one treatment episode with a biologic or a JAK. So all these patients were p. Like they were prescreened with thing like for hep B, hep C, hiv, and then if they were on a JACK inhibitor for latent TB too. So like you did have a little prescreening for infection. And the other thing that was interesting because they treat differently than we do, the Dutch, what they did is if they were persistently controlled, apparently they tapered the biologic dose and they've got a standardized protocol which they didn't share. And for JAK inhibitors, they're like, you're well controlled. We're going to now dose reduce you to the lowest labeled dose. So I thought that that was kind of interesting. But patients were then evaluated, followed, they did have standardized follow up, like baseline week four, eight, and then every three to six months after. So what did they find? First of all, more treatment events with dupilumab and longer term Follow up. So 100 like 16, 73 treatment events, 30 like 3300 patient years. And then the next most common was upadacitinib. 242 treatment events, 279 patient years, then Trelo kinumab, then abrasit nib, then baricitinib. And they ended up with, you know, if you kind of lumped everybody together, they had 4,000 ish patient years of follow up on biologics and no, sorry. They had 1886 biologic treatment episodes and 480 jack episodes and about over twice as much like patient years with biologics versus Jack. Okay, so what, so what did they find over this? The infection, the crude infection incidents was 19.6 per per 100 patient years overall. But when you break it down, for Jacks it was 58 to 66 per 100 patient years. For biologics it was 14 to 22 per 100 patient years. So that was a significant difference. Yeah. And the biggest thing that really stood out was herpes infection. And JAK inhibitors had a herpes incident rate of about 13.6 to 20 per hundred patient years. For biologics it was only about 3 per 100 patient years. So I thought that was interesting. And then if they looked overall, if they used dupilumab as the reference and then they looked, they looked at the three Jacks separately. If they looked at the hazard ratio for infection, it was really about four for all of them. They did not differ. Treo had a similar, was about, has a ratio of about 1.4, but it's 95% confidence interval overlapped. It was like 1 to 2, so it was pretty similar. So I thought that that was interesting. There were truly in this prospective non randomized registry more infections and the herpes was like significantly different. So I thought that that was interesting.

A (24:25)

Yes. And the other things that I kind of took away from it because this is an important issue, because the other big one are the skin and soft tissue bacterial skin and soft tissue infections that the biologics are. So Dupy and Trelo, we have pretty good data that they significantly reduce the risk of those compared to placebo. And whenever you look at the numbers, right, for them versus Jax, it was also a big difference. Right. So the incidence with doopie of impetigo was 7.7 per events per thousand patient years, whereas with upadacitinib it was 60.9. So like, like eight times more likely to get impetigo. And it was similar for the other bacterial skin infections. Doesn't look like they really had enough data to draw much of a answer for Abro or Barry, but. So yeah, I think, you know, Jax, I think definitely increased the risk of herpes stuff. And I think that they also do not decrease the risk of bacterial infections the way that biologics do.

B (25:48)

Yes. And then the other thing was, I thought that was interesting was that if you had a history of skin infections, particularly viral or fungal skin infections, then your risk of having A future skin infection was higher. A hazard ratio of like 1.9 for back for viral skin infections at about 2.4. So, you know, for fungals, for prior fungal skin infections. So, you know, people who have a history of skin infections are likely, you know, sometimes I'm like, oh, but, well, you'll get treated and you'll be better. But they actually were at higher risk of subsequent infections after starting treatment as well. So, yeah, I think just something to, you know, think about. So, you know, I like the fact that it was a big A prospective. Have you noticed that we have done no trinetics papers this whole episode? That could change, but I don't think it will. So this is truly like a prospective study. So I just think it's something for us to be. To keep in mind and think about.

A (26:53)

Yeah, I do think of a history of staph infections as a. If I've got somebody who, for whatever reason, I'm like biologic or jack, like I have no reason to pick one versus the other in somebody. History of staph infections definitely makes me go biologic because we've got good, good data that they reduce the risk of skin infections by about 50% compared to placebo. And that's not just due to the disease improving because jaks increase the disease just as much but do not decrease the risk of skin infections. It's more to do with restoration of cutaneous innate immune function, which is interesting.

B (27:35)

Yeah. Yeah, I think that's a great take home. If nothing else is. If they've got that history of skin infection, it is a reason to sort of. Even though we want to get people better quickly because bad eczema makes your skin infection risk up. Go biologic first.

A (27:50)

Yep. And biologic specifically an IL13 blocker. We don't have any. We don't have any data to show that. The Same goes for IL31 blockade. It's specifically IL13 blockade.

C (28:00)

Yeah.

B (28:00)

So that's your DB or. Yeah. Okay.

A (28:02)

Yep. All right, Pat, what do you got?

C (28:05)

All right. My second six pack paper was from November 2025 edition of DERM Surgery titled Superficial Radiation Therapy vs. Mohs Micrographic Surgery a systematic review and meta analysis. First author was Jay Patel. We covered superficial radiation therapy for skin cancer. Previous podcasts. One of the papers we did was a Delphi panel which didn't contain a radiation oncologist and contain the sentence authors concluded igsrt. So that's image guided. Superficial radiation therapy outperforms Mohs micrographic surgery for non melanoma skin cancer based on statistically significant superior two year recurrence probability which could possibly complicate our counseling like NMSE patients. I'm going to send you to Mohs, which is not the best option based on this deli panel of experts. Not that that ever came up, but still, I just thought it was a pretty bold statement to throw in the middle of that Delphi panel paper. So I thought I'd be able to use this paper to reassure myself that Mohs indeed remains the gold standard and I could discourage patients from seeking offices that offer general cure. But this paper actually excluded image guided superficial radiation. Oh, I know. And it only looked so I should have picked the new paper but by then it was too late and podcast was coming up. So yeah, this only looked at superficial radiation therapy.

A (29:28)

Do you know if there's any data confirming because. Because the other thing we kind of decided on the superficial radiation therapy episode was that the image guidedness was more or less just to allow you to bill more. It didn't seem to add any clinic meaningful clinical benefit. Is there any data that says that the image guidedness make superficial radiation therapy have better cure rates?

C (29:52)

I didn't look into that. I mean I've talked to the radiation oncologists and they're like image guided skin cancer therapy like on the skin makes no sense whatsoever. Like they, they would never even think to do that. So just from, you know, people that use superficial radiation therapy, they use actually electron beam way more frequently, which technically is a little bit different. But that's just in as I would put in a paper, personal communication. Yeah, so. Right. So it really wasn't sort of this new image guided versus Mohs, but oh well. In any event, the authors performed a literature search, came up with 26 studies. 9 for superficial radiation therapy, 17 for Mohs. 7,800 patients about treated with superficial radiation therapy, about 10,000 patients treated with Mohs. Median time follow up was a little over 50 months in each group. Recurrence rates 1.9 for Mohs, 6.3 for superficial radiation therapy subgroup analysis. So that was just a 12% statistically significant lower recurrence rate for Mohs. I'm pretty sure the senior author is a Mohs surgeon, so definitely potential for some bias. Her name was Dr. Frankie Smith. I think that's at Rochester. I think Mohs surgery is the gold standard. And if patients ask about radiation therapy, I actually am going to say well there was just this paper that came out looking at thousands of patients and Mohs is better. I won't say that okay. They didn't take that image guided thing into effect, but that's all. I was hoping that the image guided stuff, we would have more data, maybe more head to head and, you know, come up with a way to better counsel patients. But I, like, I just don't even mention radiation therapy. I had one patient within the last six months that said he saw this radiation therapy and he wanted to do it and he had two screams on his face. And I said, go get Moses.

A (31:48)

So I, I would because, and I do want to leave that because whenever we did the image guided superficial radiation therapy, kind of the takeaway is it does work pretty well.

C (31:57)

It's pretty good. I mean, it's like 90 some percent. It's not like it's horrible, it's just.

A (32:02)

It should be like, if you've got a little tiny basal cell in the tip of your nose and it's going to save you from having a bi lobe flap or a paramedian forehead flap, then it makes sense if you've got like an easy, you know, one on your forehead or your cheek that MOHS is going to, you know, be one stage and give you it. Like, it doesn't make any sense in those settings. It's very specific where it really may, or like right on your eyelid margin, maybe it makes some sense there. But then you're going to want to use shielding of your eye. So you wouldn't want to send him to, you'd want to send him to a real radiation oncologist for that.

C (32:36)

Yeah. And even because the recurrence is good for superficial radiation therapy, but it's higher. I mean, technically speaking, it is higher. And recurrent basil on the tip of the nose. Now instead of a bi lobe flap, you've gone to a paramedian forehead flap. So I think I would still counsel the patients on that. I get why you may not want to have whatever. But you know, you're, you're that one patient where that you're, you're, you know, your forehead's down on your nose. Now you're like, why did I just not get the Mohs the first time? I mean, because I've seen, I've seen like people do surgery. Just wide local excision on the cheek. And that's, that's not unreasonable. Right. For a little teeny basil. Yeah, like they recurve. Like, I've seen those recur and the patients are like, should I have gotten Mohs maybe the first time around instead of this wide local excision. And you're kind of like yeah, I mean, probably so. I don't know.

A (33:38)

So and just as I did an AI deep search while we were talking and essentially there is no head to head comparison of image guided superficial radiation therapy versus traditional. If you use historical controls, IGSRT has better numbers but completely non comparable. Like so there is no data really saying that IGSRT is better than srt.

B (34:08)

We don't have data on that. And like really what you should do is get a randomized control trial of IG, SRT, SRT vs Mohs if you want to be able to make the claim. I mean that would be the ideal.

A (34:21)

Yep, agree completely. So nothing.

B (34:25)

And there are randomized studies of mohs, right? Like there is an ongoing enrolling, randomized MOHS versus wide local excision for melanoma. There is an enrolling, it's on ClinicalTrials.gov but it is an enrolling intralesional simiplumab versus randomized versus Mohs for squamous cell low risk squamous cell carcinomas. So you can do randomized, you know, they're not blinded, but surgical trials. So it's expensive, it takes time, but it's the right trial design.

A (34:59)

Okay, all right, let's, let's move on to my last couple. So the first one again, just looking for therapeutic answers to pain in the butt situations. So treatment of acquired dermal macular hyperpigmentation with oral isotretinoin. Multi institutional retrospective study of 121 patients. So these were people with reels melanosis and lichen plano. Lichen planus pigmentosis. And so reals melanosis is kind of a diagnosis that a lot of us probably don't use real frequently. It's basically though hyperpigmentation in somebody, facial hyperpigmentation in somebody who has skin of color. And when you don't know what's causing it. So people talk about it could be from drugs, it could be autoimmune, it could be pigmented contact derm, it could be lots of things. But the patients I've seen who I think fit this diagnosis, I don't know why you're getting facial hyperpigmentation and I don't know what to do for you. And so this was super useful. And the pictures in, if you look at the video podcast gives you an example of kind of what this looks like. And it worked pretty well. Like it improved the severity in the majority of patients who had either reels melanosis or lichen planus pigmentosis. Hard. Don't know why. Right so we think of retinoids as helping with hyperpigmentation via epidermal things, of helping with the melanin transfer to the keratinocytes and shedding keratinocytes. And these are, by definition, dermal melanocytosis. So hard for me to explain why it works, but at least, you know, I have this now as a therapeutic option for somebody with facial hyperpigmentation. When I'm like, I don't really know why you got this. Just kind of useful. The other one was another pain painful patient type. So cheilitis. So specifically, this was atopic cheilitis. So cheilitis would be with atopic dermatitis. So this was adjuvant lip gauze. Wet dressing restores lip barrier function and improves atopic cheilitis. So basically what they did was have people with atopic dermatitis and cheilitis either do standard therapy, which was triumphant alone, to their lips and parallel areas twice a day, and petroleum jelly as needed.

C (37:35)

Or.

A (37:38)

They would have them put wet gauze on their lips. So then they wetted it with normal saline. So if you're going to do this in real life, you maybe have the patient add a little bit of salt to some water or whatever, but put wet gauze on their lips for 20 minutes, then take the gauze off, put the trimecinolone on, do that twice a day instead of using just trimecinolone on dry skin, and it worked much better. And that, you know, shouldn't surprise us because we have data for years that wet, you know, wet wraps followed by steroid are dramatically more effective than topical steroid by itself. So this doesn't surprise me that it worked better. But these are incredibly pain in the. You know, these are painful patients. Cheilitis is difficult to deal with. And so anything that's new, I'm like, ooh, you know, great. Okay, so put, you know, a damp washcloth on your. Twice a day, put a damp washcloth on your lips for 20 minutes and then, you know, put your what? I'm probably not going to use trimecinolone. I'm probably going to do, you know, either Opzelura or Vitam or Zoriv. If I can't get any of those, I'm probably going to do a TCI because I don't want to use steroids on people's lips. But giving it a, okay, put something damp on there. And if you can't do 20 minutes, probably 5 minutes or 10 minutes is still going to help. So just useful and something now that's nice to. You know, if somebody was like, hey, I heard this works, I'd have been like, okay, that sounds good. I'm going to try it. But we've actually got something in the literature now that like says this works.

B (39:13)

Sailing, though, I mean, you can buy normal saline at the drugstore, right. It's not like you'd have to make it at home. So I would tell them to do it with sailing. Like, I could imagine water versus saline is going to have a pretty decent effect on like, the barrier of the skin. Like, if you're going to bother to sit there with something on your lips, it might as well be actually the thing that they study.

A (39:36)

That's. That's a reasonable take. I'll allow it.

C (39:41)

Thank you.

A (39:43)

The other thing you could do is add a couple drops of apple cider vinegar to it to restore the skin's acid mantle. You know, that's the homemade. Homemade stuff. That's, you know, some salt and vinegar. You know, put it on your lips.

B (40:00)

Just eat pickles.

C (40:04)

Question about the real melanosis. I always thought like, reels is like pigmented contact derm. And in the paper they do say, what did they say? There was like a 78.3 positive patch test positivity in the reals patients. So what I was confused about was, so then did they counsel those patients on avoidance and then give them the isotretinoin? They didn't really go into that. Is my concept of reels melanosis being pigmented contact? Is that incorrect?

A (40:39)

So that's generally why I have some experience seeing these patients as they would get sent to me for patch testing. Yeah, I generally. Because it is way. If they had like bad itching and rash, then sure, I think it's pigment. I think it's contact dermatitis with post inflammatory hyperpigmentation. But when I think reels melanosis, I think hyperpigmentation without itching and rash. And so in those people, maybe they have a positive patch test, but if it's not like significant itch and rash, the patch test is irrelevant. Now that's how I think of it. I don't know that everybody thinks of it that way, but I think of reels as hyperpigmentation without itch or dermatitis.

C (41:20)

Right. And it's. Do you think it has a characteristic like morphology? I always think of it as like this reticular. It's almost like flat carp on the face. Like it's like a reticular sort of pattern. It's kind of distinctive, but maybe I'm wrong there too. I don't know.

A (41:36)

So if I. I've only seen that like once or twice and then that I'm like slam dunkey. Like, oh, what you got? Most of the people that I saw that I called this just had like. Usually it was temples, forehead, less on the lower cheeks, sort of more sun exposed areas.

B (41:56)

Malar lateral cheek. That kind of like hyper. Yeah, yeah.

A (42:01)

Now it could be the whole face and the whole thing, but it was more like photo exposed the areas and just was normal looking hyperpigmentation.

C (42:09)

Like.

A (42:09)

No, real interesting.

B (42:10)

They kind of mentioned too that like you can use isotretinoin for like erythema dys. Chromium perstans. I guess I don't ever think about that. I can think about a couple like tough cases and now I'm like, maybe I should try that.

C (42:24)

And yeah, the other thing that I thought was interesting was the, the duration. Mean duration of isotretinoin was almost 7 months for reels and 9 months for LPP. Now they did say like the. The most common dose prescribed was 20 milligrams. So maybe it was a function of that. But just, you know, like it's not your typical acne. You're gonna, you're gonna maybe see big differences at five months. It may be a longer course than what we think of for acne Unc.

B (42:53)

We'd have them on 120mg a day of isotretinoin from day two.

C (42:58)

Nobody else does that. There's no way that the patients are taking that dose. I mean 60 milligrams. I'm tearing people up. If I did 120 milligrams, I think you're prescribing 120. And they're like, this is crazy. I'm taking one third of the dose that was prescribed. Maybe there's no way they're taking that dose.

A (43:20)

You've got Steve Feldman right down the road. You guys should, should have Steve Feldman do a study on.

B (43:27)

We don't need Steve Feldman. We can do our own studies here at unc.

C (43:31)

Wow.

B (43:34)

Yeah.

A (43:35)

I will say what I would probably do now if I had one of these patients come in or what I will probably do is start with oral tranexamic acid like a half a pill once a day, probably give that three to six months. And if they're not like getting better significantly, then add the isotretinoin onto the tranexamic acid. Because we did just do that paper a few episodes ago about that seemed to help with acne as well, adding tranexamic acid, isotretinone. So there's precedent for combining those two drugs. All right, well, I want to thank everybody for joining us this week. Hope you laughed once or twice. Hope you learned a few things, but mostly hope you're planning to join us next week. Until then, I'm Matt Zyrus.

C (44:20)

I'm Tim Patton.

B (44:22)

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