More Answers for Tough Questions

Welcome to season two, "Derms on Drugs" a video podcast brought to you by scholars in medicine, the best educational platform in dermatology and provided to no cost to medical providers. And by the way, if you haven't checked out, scholars in medicine already, they just did a big revamp of the platform, new AI, new layout, the whole thing. It is incredible content now even easier to use. So, "Derms on Drugs" is where cutting edge derm meets hidermis comedy. I'm Matt Zyres from Docs Dermatology and each week I'm going with a residency buddies Dr. Laura Ferris from the University of North Carolina and Dr. Kim Patton from the University of Pittsburgh. And we use our 60 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be on the cutting edge of derm and you'll probably have some fun listening. New episodes drop every Friday in scholars in medicine, Apple Podcasts, Spotify and other major podcast platforms. And a reminder that this is a video podcast and the video component has some of the key figures and tables from the articles that we talk about. So this week we got another one of our patented six pack episodes where we talk about what's been the newest, coolest stuff we've seen in the literature. Let's kick it off Dr. Ferris. What do you got? All right. So, I have a research letter from JAMA Dermatology. "Demo Discosis." I never think I say that right. I say it Dermatocosis. Dermatocosis. That's how we're going to say it. And Ivermectin associated Mazzotti like reactions after hematopoetic stem cell transplant. There's old Mazzotti reactions. I know. I had never heard of a Mazzotti reaction. So I figured I'd learn something about that and how to say Demo Decosis. All right. So, um, okay. So this is from the NIH group, Strong at All, Isaac Brownel, who's one of those people that like every time I talk to him, I'm like, "Wow, I didn't know how dumb I really was until I got into a conversation with Isaac Brownel." So I thought it'd be kind of an interesting paper. So they looked at 307 Allogenea, comatopoetic stem cell transplant patients who had been seen within 100 days of transplant. And it turned out that 17 of them, which is about 5.5 percent, were diagnosed with D Medex by Dermatology. So they presented a median of 32 days after with air thematous parietic folliculacentric papules and papula postules of the face neck, trunk, sparing the periocular skin and hairbearing scalp. Okay. So why does this matter? I mean, when you see this sick person, you just had a hematopoetic stem cell transplant and you have this really just dramatic facial eruption. Probably what the team is thinking is acute GVHD. And so one, like I thought if there's nothing else to take away, if you think you're seeing acute GVHD and a hematopoetic stem cell transplant patient, because I've got these facial papules, think could it be D Medex and do a prep? Okay. So what is the Mizzotti reaction? It is an acute inflammatory response when you kill lots of parasites like helmets of famously onco-surcheysis. They get Ivermectin, our diethyl carbamazine. And then they get this like bad paritis edema blah, blah, blah. That we think is due to and sometimes like hypotension, GI, diarrhea, all this stuff. That's really true. It's like that Yarex, herchzymer thing that you hear about was syphilis being treated. So you release all these antigens, you get this massive systemic inflammation. So it turns out that this Mizzotti-like reaction can happen when you give Ivermectin to patients who have bad diemodex and are profoundly immunocompromised. So I thought that that was sort of interesting. You know, it was about, so there were more people at D Medex, but it was about a quarter of them that got this dramatic flare from the Ivermectin. So and some of them actually needed like systemic steroids to get it back into control, somewhere managed with topicals alone. And so, you know, I guess like my, so it was like, there weren't any like really bad outcomes that came. It wasn't like like a like nobody had to go to the ICU, nobody had anaphylaxis. But you know, when weird things happen in stem cell transplant patients, you know, people get worried about it. And I think like the big take home to me was if you're thinking acute GVHD and it's mostly facial, look for deemodex and then if you treat them and they get this reaction, remember that that might be what's going on. This has apparently actually been described for like patients being treated for scabies with Ivermectin too. First I can say, Ferris, thank you. Unlike Patton, you regularly bring articles that I get something useful out of. Now here's what I got useful out of this. So oral Ivermectin combined with oral metronite is all 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 papula pus to the rosacea are actually deemodex even if you get a negative deemodex 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 some of a kind of gun you 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 I this this helps explain something that I see you not infrequently in regular people. And you would expect that this mizadi reaction would be less common in people on immunosuppression since it's an immune, you know, that immunologic response. So I thought it was super cool. This was really good. Thank you. Yeah. How does interesting paper. So that's good. And if we save one person from being treated for GVHD when they really have deemodex, it will be worth it. It's true. Pat, you got anything you want to add? No, loved it. Cool. Cool case reports. Pictures really impressive. They they have that before and then after. And it's it's an impressive response. Yeah. Yeah. I agree. All right, Pat. What do you got? My another useless paper apparently. So sorry, Matt. My first six back is from November 20, 25 edition of clinical and experimental dermatology and is titled comparative effectiveness and safety of a patissetinib, abercetinib and dipillumab and treatment resistant purigo, perigo, nodularis. By the mere boss at all, it was a retrospective multi cohort study from 2024 to 2025. Patients had to have failed to prior systemic therapies had to have 20 lesions and were excluded if they had a topic, derm or any sort of a topic, diathesis, which is weird because they say that in the paper. And then there's a graph. And it's said that two of the patients in the dupe group had asthma. So they they didn't really do that. I don't know. What's going on there? All patients had biopsies confirming PN. In the final analysis, 12 patients prescribed dupe eight prescribed abro 200 milligrams eight prescribed UPA 30 milligrams. And they were they were pretty different populations. Dupe patients were older. They had a longer disease duration. Those two things I think would have an effect on efficacy. Figure one shows a little line graph of the primary endpoint of PP and RS so that peak paritis numerical rating scale and all the medications worked. Jack's being faster and more effective. Although I don't think statistically so more effective. They were statistically, I think faster. Figure three shows decreases in nodulal counts in all groups. But again, the jack's being more effective. Like it's six months, 11% of dupe patients had a 50% decrease in the number of nodules versus 100% of the abro and who patented to 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 PP on RS and the nodule count secondary endpoints were patient reported outcomes. Patients and all groups reported improvements with more rapid responses in the jack groups compared to the dupe 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 its reductions 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 paragonal nodulaleros compared to dupe, but I think different baseline characteristics make this hard to interpret. Yeah, I don't know. I always have that thing about a weird thing about paragonal nodulaleros. When when dupe came out without approval, I was kind of, I was almost a little bit puzzled like paragonal nodulaleros is a topic term. So of course this medication is going to work. Like I still to this day like diagnosing paragonal nodulaleros, 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 atopic dermatitis, you now have like 10 drugs, both topical and systemic. I mean, for me, pyrogynousularis is a topic term. So, you know, now we say like, Jack's probably in the patients who are not responding to, you know, right now if you just say pyrogynousularis, you got Dupi, you got Nemo. If you say they have atopic dermatitis, which again, I don't think that's fraud, I don't think you're making it up. I think pyrogynousularis is really just a manifestation of atopic dermatitis. Diagnosing with that, and then you have now Jack's, and we have evidence that they may even be quicker and maybe more effective. - So, I, number one would agree with you completely. I think that PN is a type of, we shouldn't think of it as a subtype of atopic dermatitis. We agree with you completely. On, however, I will say there are lots of Iitch experts who completely disagree and lots of atopic dermat experts who completely disagree, but none of them live in the real world. And I think that in the real world, yes, I think 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 gonna call it that. I'm gonna call it PN, no AD, so that I limit your therapeutic options. - Yeah, that makes sense. - Doesn't make any sense. - I think they're two different diseases, sorry, that doctor. - You know, for high, I think that there is this type two immunity cycle, and I think there's the nerve part, and I think there's 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 eggs, you don't know which one it is. In my mind, that's the chicken first, but that's another one. - Well, where did the chicken come from? - God. - That's right, it had to be, I think it was the egg before the chicken, 'cause what had to happen was a non-chicken had got a germline mutation, and then laid an egg that the first chicken came out of. - Okay, so we're not gonna do that. 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've, but they're doing the same thing. Like I think it's the same cycle, but I think it's like which chicken is which? - So I agree with, if so fair as I was agree with what you just said, and whenever I say that, I think it's a subtype of AD, like 'cause I define AD as inadequate barrier function to protect your skin from non-specific environmental insults. So I think there, when I say, I think if you look at like the pygo lesion itself, you're going to find barrier deficiency, and I think there are some pygo patients who if you look at non-leasional skin do not have any barrier deficiency, and that is a difference from atopic germ patients. And that's why I, like, I'm not like, like I get the, yeah, they might be different diseases. They are different disease in some people. There's some people who have both, there's some people who most have one, most have 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. 'Cause they have more therapeutic options. - Yeah, and I think they're even in the like, the genome-wide association studies, like there's a lot of overlap between P 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 P and patients. But you know, genes are disease. And if there's overlap, then like, it's kind of the same thing. - I think it's all a spectrum, and I am definitely like a lump or not a splitter. So I'm fine. Every time I treat a P and patient now, I'm gonna be thinking, which came first, the chicken or the egg? - Exactly. - That's all I'm gonna be thinking about now. - Glad I could make you think. - All right, so my first one was a premalast in Japanese patients with pomegranate pustulosis. They randomized phase three trial. Basic takeaway, a premalast worked really well for pomegranate pustulosis. The clinically useful takeaway is this tells us that ruck that reflumalast will work even better in pomegranate pustulosis and be much cheaper. So we can't go any episodes without talking about or a reflumalast. And so my main takeaway from this was pomegranate pustulosis patients, if I can't get them on a good biologic or if the biologic doesn't work well enough, if the biology didn't work well enough, then I'll add on the reflumalast. If I can't get them on the biologic, I will just give them oral reflumalast. It also suggests that topical reflumalast 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 gonna talk about it. That's it. - Yep, I like it. - I like it. Next one was probably a little more controversial slash interesting. This one was a randomized double-bone physical 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, there's a lot of pressure to publish and I just don't know the like of this. But so this article. - I pronounce it Iran. That's as political as I'm gonna get on that one. - Oh, Iran. Not so Iran is not correct Iran. - That's like cracker pronunciation. I ran, I ran. - Yeah. - Exactly. - Right, it's your Ohio root showing through it. Not sophisticated places like North Carolina and tons of things. - So that's it. - All right, so this study was intranasal corticosteroids. They promised a new approach for adults with chronic etiopathic erdecaria linked to arrow allergens double-blind randomized clinical trial. So basically a fairly small number of patients here. So 29 and 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 erdecaria activity score went down by like five-ish points. The people who didn't get it, their score went down by like two-ish points. And it was a difference. And like what I think is going on here, 'cause right, you don't really get systemic steroid levels from intranasal uidesinitis. So this was intranasal uidesin. I basically, the over-the-counter stuff, just two squirts a day and each not one squirt twice a day and each nostril. What I can, I ask a couple of my allergies buddies about this and they were like, that sounds like baloney, but it's a randomized trial. So like, hmm, like mechanistically, if anything is happening, it's that you've got mass cells in your nose. And whenever the mass cells get activated by the arrow allergens, they're releasing, not just histamine, but also some cytokines. And that might make your mass cells more responsive to whatever it is, the autoimmune process that is driving your urinary carrier. So the efficacy, nowhere near good enough to be like, hey, this is what you do, but where this could be useful is somebody who's on Zolaer or Dupy or Hapsado and does better, but not like, oh, I still get some hives, 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 anti histamine? Hey, go get some over the counter generic steroid noisel spray, use that twice a day. Let's see if you get better. There's been a study that shows it helps. So it, that's just something to have in your therapeutic toolbox of tricks for people who have an inadequate response to systemic drugs for C.I.U. 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 gonna be like, oh, it didn't work at all. I'm still terrible. We're here, tithing it. No, it's gonna be something like, I'm a lot better, but I'm not 100% tried the nasal spray on top of that, make some sense. That was kind of the takeaway of it. Any thoughts from either of you guys on this one? Did they look at nasal symptoms correlating with improvement of the hives or now? Okay. No, they didn't, 'cause 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 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 protest. Or nasal polyposis or anything else like that, right? So that's those people would have tons of lymphoid tissue in their nasal passages. Maybe they would benefit differently. But yeah, it's just right. We'll see. Right, it's cheap and easy. That's what I'm always looking for cheap and easy. Kind of like whenever I'm dating. Exactly. All right. - All right, we gotta cut, we gotta, no, I probably will, maybe we'll cut that part out. (laughing) - Let's leave it in there. - I'll leave it in, all right. Next article, Ferris, what do you got? - Okay, I have from the J-E-A-D-V infection risk in atopic dermatitis patients treated with biologics and Jack inhibitors, biode 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. Trax adolescents and adults monitor 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 Jack. So all these patients were, like they were pre-screened with thing like for hep B, hep C, HIV. And then if they were on a Jack inhibitor for latent TB2. So like you did have a little pre-screening for infection. And the other thing that was interesting 'cause they treat differently than we do, the Dutch. What they did is if they were persistently controlled, apparently they taper the biologic dose and they've got a standardized protocol, which they didn't share. And for Jack inhibitors, they're like, you're well controlled. We're gonna 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 would do pill you map and longer term follow up. So 16, 73 treatment events, 30, like 3,300 patient years. And then the next most common was you've had a sit-knob, 242 treatment events, 279 patient years. Then Trail, Trail, a kidney map, then a person, then a barricade. And they ended up with, 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 did they find over this, the infection, the crude infection incidents was 19.6 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 Jack inhibitors had a herpes incident rate of about 13.6 to 20 per 100 patient years for biologics that was only about three per 100 patient years. So I thought that was interesting. And then if they looked overall, if they used dupellumab as the reference, and then 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. Trailo had a similar, it was about hazard ratio of about 1.4, but it's 95% confidence interval overlapped, it was like one to two. 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. Yes, and the other things that I kind of took away from it, 'cause this is an important issue, 'cause the other big ones are the skin, it's bacterial skin and it's off tissue infections, that the biologics are so dupe and trailo, we have pretty good data that they significantly reduce the risk of those compared to placebo. And whenever you look at the numbers for them versus Jacks, it was also a big difference. So the incidents with dupe of impotago was 7.7 per event, it's 1,000 patient years, whereas with you Pat, it said in a bit was 60.9. So like eight times more likely to get impotago and it was similar for the other bacterial skin infections, then looked like they really had enough data to draw much of an answer for Abro or Barry. But so yeah, Jacks, 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. - 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 viral skin infections in about 2.4. So for fungal skin infections. So people who have a history of skin infections are likely, you're sometimes I'm like, oh, but will you get treated and you'll be better, but they actually were at higher risk of subsequent infections after starting treatment as well. - Interesting. - So yeah, I think just something to think about. So I like the fact that it was a prospective, have you noticed that we have done no trinetics papers? There's a whole episode that could change, but I don't think it well. 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. - Yeah, I do think of a history of staff infections as a, if I've got somebody who for whatever reason, I'm like a biologic or jack, like I have no reason to pick one versus the other and somebody, history of staff infections definitely makes me go biologic. 'Cause we've got 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 jacks increase the disease just as much but do not decrease the risk of skin infections. It's more to do with restoration of cutaneous in natumune function, which is interesting. - 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 exomella, skin infection must go biologic first. - Yeah, and biologic specifically in IL-13 blocker. We don't have any data to show that the same goes for IL-31 blockade. It's specifically IL-13 blockade. - Yeah, so that's your DEP or yeah, okay. All right, Pat, what do you got? - All right, my second six pack paper was from November, 2025 edition of Derm Surgery titled Superficial Radiation Therapy versus Mose Micrographic Surgery, a systematic review and meta-analysis. First author was Jay Patel. We covered Superficial Radiation Therapy for Skin Cancer Priests podcast. One of the papers we did was a deltty panel which didn't contain a radiation oncologist and contain the sentence. Authors concluded IGSRT. So that's image guided Superficial Radiation Therapy outperforms Mose Micrographic Surgery for non-melodomal skin cancer based on statistically significant superior two-year recurrence probability, which could possibly complicate our counseling like NMSC patients. I'm gonna send you to Mose, which is not the best option based on this delfeed 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 delfeed panel paper. So I thought I'd be able to use this paper to reassure myself that Mose indeed remains the gold standard. And I could discourage patients from seeking offices that offer a general cure, but this paper actually excluded image guided Superficial Radiation. - Oh, I know. And it only looked, so I should have picked a new paper, but by then it was too late and podcasts was coming up. So yeah, this only looked at Superficial Radiation Therapy. - Do you know if there's any data confirming, 'cause 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 meaning, focal clinical benefit. Is there any data that says that the image guidedness makes Superficial Radiation Therapy have better cure rates? - I didn't look into that. I mean, I've talked to the radiation oncologists and they're like image guided skin care, 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 being 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 really wasn't sort of this new image guided versus mose, but oh, well, in any event, the authors performed a literature search came up with 26 studies, nine for superficial radiation therapy, 17 for mose, 7800 patients about treated with superficial radiation therapy, about 10,000 patients treated with mose. Meeting, median time follow up was a little over 50 months in each group, recurrence rates, 1.9 for mose, 6.3 for superficial radiation therapy subgroup analysis. So that was just a 12% statistically significant lower recurrence rate for mose. I'm pretty sure the senior author is a mose surgeon. So definitely potential for some bias. Her name was Dr. Frank E. Smith. I think that's a Rochester. I think most 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 moses 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 come up with a way to better counsel patients. But 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 squames on his face. And I said, go get mose. So I would because I do want to leave that because whenever we did the image guided super radiation therapy, kind of the takeaway is it does work pretty well. It's pretty good. I mean, it's like 90 some percent. It's not like it's horse. It's just 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 by-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 moses 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. Yeah, even the high political because the recurrence is is good for superficial radiation therapy, but it's it's higher. I mean, technically speaking, it is higher and like recurrent basal on the tip of the nose. Now instead of a by-lobe flap, you've gone to a paramedian forehead flap. So I think like I would still counsel the patients on that like, yeah, get why you may not want to have whatever, but you know, you're you're that one patient where that your, you know, your forehead's down on your nose now. You're like, why did I just not get the mose the first time? I mean, because I've seen, I've seen like people do surgery, just wide local oxygen on the cheek and that's that's not unreasonable, right? For a little teeny basal. Yeah, they recurve. Like I've seen those recurrent. The patients are like, should I have gotten mose? Maybe the first time around instead of this wide local oxygen and you're kind of like, yeah, I mean, probably. So I don't know. So and just as I did a AI deep search while we were talking and essentially there is no head to head comparison of image guided supersuridiation therapy versus traditional. If you're a historical controls, it IG SRT has better numbers, but completely non comparable. Like so there is no data really saying that IG SRT is better than SRT. We don't have data on that. And like really what you should do is get a randomized control trial of IG SRT versus mose if you want to be able to make the claim. I mean, that would be the ideal. Yep, agree completely. So nothing. And they're randomized studies of mose, right? Like there is an ongoing and rolling randomized mose versus wide local oxygen for melanoma. There is an enrolling. It's on clinical trials. But it is an enrolling, interleational, semiflamedverse randomized versus mose for squamous cell, low risk squamous cell carcinoma. 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. Okay. All right, 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, multionstitutional, retrospective study of 121 patients. So these were people with reels melanosis and like in Plano, like in Plana's pigmentosis. And so reels melanosis is kind of a diagnosis that a lot of us probably don't use real frequently. It's basically the hyperpigmentation in somebody, facial hyperpigmentation in somebody who has kind of color. And when you don't know what's causing it. So people talk about, well, it could be from drugs. It could be autoimmune. It could be pigment contact dermat. 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 in the pictures, if you look at the video podcast, right, 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 like in Plano's 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 carotenicides and shedding carotenicides. And this is by definition dermal melanocyte doses. 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 key lightest. So specifically, this was a topic key lightest. So key lightest people with a topic dermatitis. So this was adjuvant lip gauze, wet dressing, restores lip barrier function and improves a topic key lightest. So basically what they did was have people with a topic dermatitis and key lightest, either do standard therapy, which was triumson alone to their lips and parol areas twice a day. And petroleum jelly, he has needed or they would have them put wet gauze on their lips. So they, and they wedded 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 triumson alone on. Do that twice a day instead of using just triumson alone on dry skin. And it worked much better. And that shouldn't surprise us. Because we have data for years that wet, you know, wet wraps, followed by steroid or dramatically more effective than topical steroid by itself. So this doesn't surprise me that it worked better. But these are incredibly pain and these are painful patients. Key lightest is difficult to deal with. And so anything that's new, I'm like, "Ooh, great." Okay, so put a damp washcloth on your lips twice a day. Put a damp washcloth on your lips for 20 minutes. And then put your, what I'm probably not going to use triumson alone. I'm probably going to do either obstalura or vatama or zoree. 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 five minutes or 10 minutes is still going to help. So just useful and something now that's nice to, you know, if somebody would be 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. Which is a saline though. I mean, you can buy normal saline at the drug store, right? It's not like you'd have to make it at home. So I would tell them to do it with saline. 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. That's a reasonable take. I will allow it. Thank you. The other thing you could do is add a couple drops of apple cider vinegar to it to restore the skin's acid mantle. That's the homemade stuff. That's some salt and vinegar. Put it on your lips. - Just eat pickles. - Oh, right. (laughing) - The question about the real melanosis. I always thought, like, reals is like pigmented contact urn. 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 isotretinone, they didn't really go into that. Is my concept of reals melanosis being pigmented contact urn? Is that incorrect? - So that's generally why I have some experience seeing these patients, that they would get sent to me for patch testing. - Yeah. - I gen, 'cause if they would as well, 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 reals 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 itching rash, the patch test is irrelevant. Now that's why I think of it, I don't know that everybody thinks of it that way. But I think of reals as hyperpigmentation without itch or dermatitis. - 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. - So if I've only seen that like once or twice and in that I'm like slam dunky, 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. - Like, maylar lateral cheek, that kind of like hyperpigment. Yeah. - Yeah, now it could be the whole face and the whole thing, but it was more like photo exposed areas and just was normal looking hyperpigmentation. Like no real surface. - So it's seen like, kind of mentioned too that like you can use isotretinoin for like, erothema, dyschromium perstands. I guess I don't ever think about that. - No, I don't. - I can think about a couple like, tough cases and now I'm like, maybe I should try that. - And yeah, what's the other thing that I thought was interesting was the duration. Mean duration of isotretinoin was almost seven months for reels and nine months for LPP. Now they did say like 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 that five months, it may be a longer course than what we think of for acne. - You and C, we have them on 120 milligrams a day of isotretinoin from day two. - 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 no way they're taking that dose. - You've got Steve Feldman right down the road. You guys should have Steve Feldman do a study on it. - We don't need Steve Feldman. We can do our own studies for UNC. - We probably won't wait. - Yeah. - 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 trannix amic acid like a half a pill once a day, probably give that three to six months, and if they're not getting better significantly, then add the isotretinoin on to the trannix amic acid. 'Cause we did just do that paper a few episodes ago about that seem to help with acne as well. Adding trannix amic acid isotretinoin. So there's precedent for combining those two drugs. - All right, well, I wanna thank everybody for joining us this week. Hope you'll last once or twice. Hope you learned a few things, but mostly hope you're planning to join us next week. And until then, I'm Matt Zyrus. I'm Tim Patton. - I'm Laura Ferris and we are Derms on Drugs.