When Psoriasis Pretends to Be Eczema (And Other Problems)

Summary

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Podcast Summary: Derms on Drugs – “When Psoriasis Pretends to Be Eczema (And Other Problems)”

Host: Scholars in Medicine
Panel: Dr. Matt Zirwas, Dr. Laura Ferris, Dr. Tim Patton
Date: June 12, 2026
Episode Theme:
This episode dives into recent advances and curiosities in dermatology, covering scabies treatment strategies, nodal staging in high-risk cutaneous squamous cell carcinoma, the overlap (and confusion) between psoriasis and eczema, breakthroughs in lichen sclerosus therapy, skin manifestations of vasculitis, and pearls for treating rare inflammatory dermatoses. As always, the presenters keep a lively, collegial tone with personal anecdotes and practical clinician tips.

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Key Discussion Points & Insights

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1. Crusted (Norwegian) Scabies: Best Treatment Strategies

[01:07–10:14]
Presenter: Dr. Laura Ferris (B), w/ commentary from Dr. Matt Zirwas (A) and Dr. Tim Patton (C)

• Overview:
  A large French RCT (“Gale Crusted Study”) investigated high-dose versus standard-dose oral ivermectin, both with 5% permethrin cream and adjunctive emollients/keratolytics.

• Major Insights:

  • Higher 400 mcg/kg ivermectin dose was NOT superior to standard 200 mcg/kg dose for crusted scabies cure rates (82% vs. 75%).
  • No major safety differences; adverse events mostly limited to eczema/irritation.
  • Standard regimen: Oral ivermectin days 0, 7, 14; permethrin cream days 0, 7; plus emollients and keratolytics.
  • Visual Recognition Pearl: Crusted scabies presents as “gray powdery hyperkeratosis and nothing else looks like it.”

    “If it looks like a gray, powdery hyperkeratosis like you’ve never seen before, think about crusted scabies.” (B) [06:39]

• Practical Pearls:

  • Dosing conversions for ivermectin:

    "200 micrograms per kilogram translates into 1 milligram per 10 pounds...so the 400 is 2 milligrams per 10 pounds for all us Americans." (A) [02:37]

  • Formaldehyde allergy warning: Permethrin contains 0.1% formaldehyde—worsening after treatment may mean concurrent formaldehyde contact allergy. [07:34]
  • Many clinicians treat for “overkill” (4 weeks), though the RCT shows that may not be necessary.

Notable Quote:

“Crusted scabies...super contagious. You touch them and you are likely to get it.” (B) [07:24]

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2. Pearls & Pitfalls in Scabies and Head Lice

[09:01–13:14]

• Product pearls:

  • Permethrin is ovicidal (kills mites/eggs); ivermectin is not—hence never do only a single ivermectin dose.
  • Alternative treatments (spinosad, malathion) discussed for head lice; ivermectin works for lice too (if kids can swallow pills!).

• Memorable Moments:

  • Personal stories: Dr. Zirwas mistook his daughter’s head lice for psoriasis, only realizing when bugs literally “fell on her textbook.” [11:43]
  • Dr. Ferris’s late-night scramble for lice medication at Rite Aid after an unexpected diagnosis. [12:34]

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3. Nodal Staging in High-Risk Cutaneous Squamous Cell Carcinoma

[13:21–20:09]
Presenter: Dr. Tim Patton (C)

• Study Overview:
  A multicenter study compared sensitivity of physical exam, high-resolution ultrasound, and contrast-enhanced CT to detect nodal metastases in advanced cutaneous SCC.

• Key Findings:

  • Physical exam misses most nodal metastases—picked up 1/12 in this study.
  • Ultrasound and CT were comparable (US: 64% sensitivity; CT: 55%), but both missed most nodes in immunosuppressed patients (20% and 17%, respectively).
  • Sensitivity approached 100% for immunocompetent but dropped drastically in immunosuppressed patients.
  • Implication:
    • “In immunosuppressed patients, cutaneous squamous cell carcinoma is a bad, bad cancer” — imaging often fails, so close clinical follow-up is needed. (C) [18:14]
    • Ultrasound has advantages (cost, no radiation, immediate biopsy), but is more operator dependent.

Notable Quote:

“So for all the emphasis—physical exam is so important, blah blah blah—not for nodal involvement with cutaneous squamous cell.” (C) [17:03]

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4. Psoriasis-Eczema Overlap: Four Clinical Types & How to Treat

[20:34–27:22]
Presenter: Dr. Matt Zirwas (A), w/ discussion

• Background:
  Increase in reports of patients manifesting both psoriasis and eczema, or shifting from one to the other with biologic therapy.

• Key Clinical Types:

  1. Coexistent Disease: Both classic psoriasis and classic eczema in same patient.
  2. Overlap Lesions: Individual lesions ambiguous—can’t tell if eczema or psoriasis.
  3. Psoriasis patients on biologic (IL-17) who develop eczematous lesions.
  4. Eczema patients on dupilumab who develop psoriasiform lesions.

• Treatment Takeaways:

  • JAK inhibitors work best for overlap/coexistent cases.

    “In contrast, JAK inhibitors always worked...you want to put these people straight on a JAK inhibitor.” (A) [22:59]

  • If IL-17–treated psoriasis patients develop eczematous eruptions: switch to IL-23 or JAK inhibitor.
  • If dupilumab–treated eczema patients develop psoriasis: can consider IL-23, IL-13 inhibitor, or JAK inhibitor.

• Conceptual Insight:

  • These are not on a spectrum—psoriasis and eczema have “totally different cytokine pathways.” (A) [21:25]
  • Some patients have genetic predisposition to both.

Notable Quote:

“If they’ve got both diseases at baseline, then you want to go JAK inhibitor.” (A) [24:55]

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5. Ruxolitinib Cream for Lichen Sclerosus

[27:27–32:08]
Presenter: Dr. Laura Ferris (B)

• Study Summary:
  Phase 2 RCT (Goldstein et al., J Am Acad Derm): Ruxolitinib cream vs. vehicle in women with biopsy-confirmed anogenital lichen sclerosus.

• Outcomes:

  • Primary endpoint (4-point itch reduction) NOT met (ruxolitinib 35.7% vs. vehicle 40%).
  • However, significant improvement seen in clinical signs like whitening, hemorrhage, fissuring.
  • Most patients had prior clobetasol, but ruxolitinib seemed less effective for itch or symptomatic relief, but better for visible skin changes.

• Safety:

  • One patient developed a BCC at an application site.

• Clinical Reflections:

  • Ruxolitinib may be a maintenance/adjunct option, especially for disease progression/structural change, not symptom relief.

    “If you can actually halt disease progression, could something help to maintain it?” (B) [31:19]

  • Assessment of physical findings was unfamiliar and challenging to standardize.

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6. Skin Manifestations of Systemic Vasculitis

[33:17–39:38]
Presenter: Dr. Tim Patton (C), w/ group

• Major Report:
  Large international cross-sectional study (Micheladi et al., Int J Dermatol) of over 4,000 patients with systemic vasculitis—described frequency and patterns of skin findings.

• Key Findings:

  • IgA vasculitis: Skin lesions present in nearly all cases.
  • In ANCA-associated vasculitides (GPA, EGPA, MPA): Skin involvement in 20–40%.
  • Biopsy sensitivity: When done, up to 75% positive (varies by vasculitis type), but not universally reliable.
  • Odds ratios: Skin involvement associated with more severe systemic disease in GPA, EGPA; opposite in PAN.

• Clinical Pearls:

  • Negative or equivocal biopsy should not rule out systemic vasculitis. Don’t be falsely reassured.
  • Biopsy “medium-aged” lesions, or more than one, for best yield.
  • Techniques: Consider telescoping biopsies or wedge for deeper vessel involvement.

Notable Quote:

“If you have a high enough suspicion, don’t let a negative or sort of hedgy biopsy discourage you from working them up for systemic disease.” (C) [38:12]

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7. Case Pearls: Linear Psoriasiform Dermatoses & Sotyktu (Deucravacitinib)

[39:38–43:16]
Presenter: Dr. Matt Zirwas (A) & group

• ILVEN (Inflammatory Linear Verrucous Epidermal Nevus):

  • Two case reports: Taspinrova (Tapinarof) used with decent, if moderate, clinical effect.
  • Personal success with Sotyktu ("melted the whole thing away").

    “Once I actually pulled the paper and looked at the pictures...it worked. And so this will probably be now my...if I see another case of Ilvin I’ll probably call it linear psoriasis and try treating them with Vitama.” (A) [40:01]

• Emerging Drugs Discussion:

  • Sotyktu (deucravacitinib): Panelists universally impressed by efficacy.
  • Icoctide, Sunolocumab and other new “tick” inhibitors discussed re: their potential in practice and trials.

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Memorable Quotes

• On dosing confusion:

  “Whoever came up with [the 200 mcg/kg ivermectin dose] is just sadistic and hates US dermatology residents.” (A) [02:37]

• On clinical practice:

  “If you treat people with permethrin and they get worse, permethrin is like the one product that has actual formaldehyde in it… you may have concurrent formaldehyde contact dermatitis on top of the scabies.” (A) [07:34]

• On physical exam for nodal disease:

  “For all the emphasis, physical exam is so important, blah blah blah. Not for nodal involvement with cutaneous squamous cell.” (C) [17:03]

• On therapy for psoriasis/eczema overlap:

  “JAK inhibitors always worked…put these people straight on a JAK inhibitor.” (A) [22:59]

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Timestamps for Key Segments

• Scabies dosing & pearls: [01:07–10:14]
• Head lice stories & alternative treatments: [11:43–13:14]
• High-risk SCC nodal staging: [13:21–20:09]
• Psoriasis/eczema overlap—definitions and treatments: [20:34–27:22]
• Ruxolitinib cream for lichen sclerosus: [27:27–32:08]
• Vasculitis skin findings & biopsy advice: [33:17–39:38]
• ILVEN treatment & new psoriasis drugs: [39:38–43:16]

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Overall Tone & Closing Thoughts

The “Derms on Drugs” team delivers up-to-the-minute clinical pearls, plenty of laughs, and practical wisdom applicable for everyday dermatology practice. They challenge dogma (dosing, physical exam utility, one-size-fits-all therapies), share hard-won lessons, and highlight where evidence is changing fast.
Quote to remember:

“Hope you laughed once or twice. Hope you learned a few things, but mostly I hope you're planning to join us again next week.” – Matt Zirwas [43:32]

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Transcript

[A]

Welcome to season three of Derms on Drugs, the video podcast brought to you by Scholars in Medicine, the best educational platform in dermatology and provided at no cost to medical providers. Terms on drugs is where cutting edge derm is hit or miss comedy. I'm Dr. Matt Zyrus from Docs Dermatology and each week I'm joined by my residency buddies, Dr. Laura Fares from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. And we use our 70 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be in a Kennedy term and you actually have some fun listening. New episodes drop every Friday on Scholars of Medicine, Apple Podcasts and other major podcasts, College of Medicine, other major podcast platforms, and I highly recommend that you download the Scholars in Medicine app to access the full podcast video archive. Explore the latest Durham educational content out there. We're talking real pharma, independent coverage, all of dermatology, supported by an amazing AI clinical consultant called Ask Simon. And this week we've got another one of our patented six pack episodes. And let's go ahead and get into it. Dr. Farris, what do you got?

[B]

Okay, so I have a paper from the New England Journal of Medicine. I would say it's not the most earth shattering paper, but anytime dermatology makes the New England Journal, you got to know about it. Okay, so this is combined oral ivermectin and 5% permethrin cream to treat severe scabies. This was done in France. Senior author is Olivier Chidal who I, I remember war canceling on scabies. He's like the world's expert in scabies. Okay, so what do we mean by severe scabies? It's what we would call crusted scabies. Or back when we were less politically correct, when we all trained, we called it Norwegian scabies, but now we like the Norwegian so we'll call it crusted scabies. Okay, so this was a study called the Gale crusted study. And so the question was, does higher dose ivermectin make a difference when you are treating patients with crusted scabies? So scabies, it was a blinded, randomized, head to head trial. And, and they had to have, you know, crusted scabies confirmed with dermoscopy or parasitology. I think you should have to have parasitology. If you don't see a mite on crusted scabies. It is not crusted. Scabies, but they were randomized one to one to either ivermectin, 400 micrograms per kilogram or 200 micrograms per kilogram. And that was taken on days 0, 7, and 14.

[A]

Wait, can I first. Wait, I need to interrupt for just a second before I forget. So for all of our listeners out there, if you've never heard this, because we always talk about scabies dose and being 200 micrograms per kilogram. Whoever came up with that is just sadistic and hates United States dermatology residents. Because 200 micrograms per kilogram translates into 1 milligram per 10 pounds. So, like, that's. So the 400 is 2 milligrams per 10 pounds for all of us Americans out there. All right, don't. Don't cave and start going to the metric system just yet.

[B]

I know this always throws me. I need to remember that I told the residents.

[C]

Yeah, I told the residents, take their weight in pounds and chop off the last number. That's your ivermectin dose.

[A]

There you go.

[B]

Okay. There you go. That'll be the most useful thing that everybody gets out of this.

[A]

Well, now we got to double it. Now it's going to be.

[C]

We don't. Oh, spoiler alert.

[B]

Spoiler alert. All right, I'm just going to stop. Yeah. So everybody got. Also. Also 5% permethrin cream days 0 and 7, and then they got emollients, and then like a keratolytic, like 5% salicylic acid for, like, when. Where they had the crusting. Okay. Primary endpoint cured. Cured. Which is something Matt doesn't think we do very often.

[A]

It's an infectious disease.

[C]

Okay, fine.

[B]

They had to have no mites or might products on dermoscopy or scrapings on days 18 and 21, and no active clinical lesions on day 28. Okay, so it's like. It's like whatever. Might and clinical cure.

[C]

So I like the idea, by the way.

[B]

32. What's up?

[C]

I like the idea of some. Somebody with crusted scabies. And you're going with your dermatoscope, like, up real close to them. Like, all these mites are jumping on you. Like, I would not use a dermatoscope to diagnose crusted scabies. No, you want to stay as. You want to stay far away from these people.

[A]

The other thing I want to know is what the hell is going on in France.

[B]

Yeah, because you know how many people were in this study? 132. That's right. It's nuts. Like, maybe they all. You know, last week we did the study on, you know, the infection in the bath houses. I don't know what they're doing in France.

[A]

I don't know. Yeah, yeah. Be careful. Yeah, be careful.

[B]

Okay. Median age 67, but like, a third of them were over 80, and about 60% of them were in the hospital. So this is like, you know, kind of the people who you think about getting crusted scabies. And so what was the cure rate? In the high dose group, it was 75%, and in the standard dose group, it was 82%. Totally, like, odds ratio, 0.64. Confidence interval crosses 1. No superiority.

[A]

Wow.

[B]

And then, you know, when they, like, no matter how they tried to cut the data, there was really nothing there that, like, there was no way to show that the higher dose mattered and safety was fine, like we know it is for both of these drugs. AES were like eczema and skin irritation, which was equal among both groups. So, you know, clinically, just because it is crusted scabies does not mean that you need to go to the higher dose. Combine ivermectin and permethrin, use amaliance, and, you know, the Cure rate's about 80%, which is not a full cure. That's still, you know, that means 20% of the people are still going to have some scabies. So I thought that was kind of interesting, a. I mean, good for them for making the New England Journal of Medicine. But I was a little surprised that that was a New England Journal paper. But it was a pretty large study, and if nothing else, maybe, like, it will remind the people who read the New England Journal, which is generally not dermatologists, but people who see hospitalized patients. Like, what to look for to think about crusted scabies. Now, unfortunately, what they did not have in here was a picture of crusted scabies. For people who have not seen it, like, it has such a distinctive look. If it looks like a gray, powdery hyperkeratosis like you've never seen before, think about crusted scabies. I feel like when I've seen it with residents for the first time, they generally don't get the diagnosis. I would say it's like a gray powdery hyperkeratosis and nothing else looks like it. What would you guys say?

[A]

Yeah, I would. Yeah. Yeah. I've got some pictures in my, like, collection. When I'm scrolling through. Oh, yeah. Oh, I remember that. It's like A very distinct yes.

[B]

Yeah. Or go like, Google a couple pictures. You'll see it and then you'll never miss it. And you do not want to miss it because it is so contagious. And you touch them and you are likely to get it.

[A]

And I've got a couple other scabies pearls for people. Number one, if you treat people with permethrin and they get worse, permethrin is like the one product that has actual formaldehyde in it, so it has 0.1% formaldehyde. So if you give them permethrin and they get worse, you. You may have concurrent formaldehyde contact dermatitis on top of the scabies. Number two. And I'm curious what you guys do. When I treat scabies, I always do weekly for four weeks because I'm like, why the hell not? Like, I would want to be treated out the wazoo if it was me. So I do permethrin and ivermectin every week for four weeks, which is probably massive overkill. What do you.

[B]

Like? That's more than what they did in this study.

[A]

Yes. And they. Only 20 of people didn't get cured.

[B]

I know. No, it. But you're right, it probably is not. And I think that there's a lot of re. Infestation. Right. So people who get crested scabies, generally, you know, they're. They're not like.

[A]

Yeah.

[B]

You know, they're generally have, you know, challenged psychosocial challenges.

[A]

They're not going home and doing all the laundry in the house.

[B]

Yeah.

[A]

It was kind of the. The takeaway there.

[B]

Yes.

[A]

Surprising results.

[C]

I like alternating, like, oral ivermectin, topical marathrin, then oral ivermectin, then topical permethrin.

[A]

Huh. Any. Any theory or reason for that or just easier for people?

[C]

No.

[B]

Make it harder on the patient.

[C]

It's not, though, because you're only. Do like, the permethrin is hard. I think head to toe is difficult. But a fair number of patients with scabies, it took a long time to get there and they're miserable and they're like, I have to get rid of this. Like, can I do both? And I'm like, well, if you're going to do that, just alternate. And then, you know, I'm saving half the. Half the money.

[A]

Saving eight.

[C]

Yep. It adds up.

[B]

This is a cheap thing. Cheap thing to treat. Yeah. And then just, you know, the pearl is that the ivermectin kills the mites but not the eggs, whereas the Permethrin is. Kills both the eg in the mites, so that's why you never do one dose of ivermectin.

[A]

It is one of the interesting things that whenever they've studied, if you use permethrin correctly, like if you get it in every crack and crevice in the whole thing, it works. It is. It is more effective than ivermectin.

[B]

Yep. Yeah, it's the ovicidal.

[A]

Yes.

[B]

You know, activity.

[A]

Have either of you ever used those other ones? What the hell are they called?

[C]

Oh, yeah. That new. No, because it's, like, too expensive and no insurance would cover it.

[B]

Yeah.

[A]

There's the malathion. One that has been around. That was the one that would catch on fire. You had to be worried.

[B]

Oh, well, that's for head lice.

[C]

That's for head lies.

[B]

Yeah. So malathione should do a head lice episode. Mouth ion is approved for the treatment of head lice. It. I think it is highly effective.

[A]

Have I told you guys my head lice story?

[B]

Hear it.

[A]

So Margaret goes away for the summer, does overseas things, comes home a few weeks later, she's like, oh, my scalp's itchy. And I look, she's got red, scaly, whatever. I'm like, oh, you got psoriasis. Okay, well, here's some clobazole. Month later, she's like, oh, my scalp's so, so itchy, dad didn't get any better. And I'm like, huh? Okay, what are the huh? Now she's got what looks like some nail psoriasis. And I'm like, son of a. We're gonna have to put you on, like, biologic or something. But here, use this shamp addition. So now, another month later, she goes like, oh, did. My scalp is still so itchy. And now my tailbone really hurts. And I'm like, oh, my God, you've got psoriatic Arthur. I'm making her an appointment with the rheumatologist. Then she's in school, and she's like, you know, reading her textbook. And like, a bug falls on the book. And she's like, wow, this school is so gross. Like, almost have fallen off the ceiling. And then she looks down again, and two more fall onto her textbook. And she's like, oh. And so she goes down to the nurse, and the nurse is like, this is the worst case of lice I have seen in, like, years.

[C]

Nice.

[A]

Yeah. Yeah, that's it. And I wonder why my kids believe the tick tock skinfluencers more Than they believe me.

[C]

Yeah. Hard to imagine.

[A]

Hard to imagine.

[B]

My life story is I was out for dinner with Robin Garris, who is a pediatric dermatologist who trained with us. And she's looking at me and says, I won't say my daughter's name, but do you think she's. She's really scratching her head. I was like, oh, she twirls her hair. She said, do you think she could have head lice? I was like, no. So then we go to Baskin Robbins, because those are always really, really well lit. And we look, and she's got, like, floor. All my kids have flora and head lice.

[C]

Yeah.

[B]

My husband's out of town.

[C]

Their vanilla cones became chocolate chip.

[B]

Exactly, exactly.

[C]

Those aren't chips.

[B]

Right. The Rite Aid is about to close across the street. We, like, run over there, try. I'm like, could you please? And so I got them, like, they had, like, one box of malathione in stock. And so I'm, like, trying to treat everybody for head lice. It's fun. It's fun.

[C]

Yeah.

[A]

Nice. You can also use ivermectin for head lice. That's another.

[B]

You can. Actually, there was another study, it may have even been, like, in the New England Journal, too, that showed that ivermectin is effective, and I would say a heck of a lot easier, except kids aren't good at swallowing pills.

[C]

That newest treatment is spinosad.

[A]

Spinosad. I knew it's, like, made of Kitosam,

[B]

I think, but that's also headlights. Yeah.

[A]

Yeah. Okay. All right. All right, Patton, what do you got?

[C]

April Jamaderm, Diagnostic Modalities and Nodal Staging in High Risk Cutaneous Squamous Cell Carcinoma by Ferrandez, Pulido et al. So, like, 10 years ago, I was minding my own business, and Kristen Bybee, one of the residents, was like, we should do a transplant clinic. And I'm like, I'll precept one of those, because, like, skin cancer, I can do that. And then, like, cutaneous squamous cell carcinoma in those patients is just absolutely horrific. I mean, it is worse than melanoma. It is a really, really difficult disease to treat. I had no idea that that. That could be that difficult to manage. There's all sorts of questions. What do you do? Who gets adjuvant therapy? Who gets imaged? Should sentinel node be done? Do we change immunosuppressive? Like, it's a lot. So this was a study that wanted to address one of those questions, and they Did a prospective study. Like that's what we need. It was the Lacunas study, which stands for something I didn't write down. Its goal was to compare physical exam versus CT versus ultrasound to detect nodal metastases and advanced cutaneous squamous cell carcinoma performed in Spain. 13 centers. 2022, 2025 patients with advanced cutaneous SEC. So this was like Brigham and Young 2B 3 women's. Bring them in. Bring. I always do.

[A]

This was the more they did this one in the Mormon section of France.

[C]

Why? I mean it's a, it's a. It's as bad as pruritus. I can. I always say bring them in young. Bring them in. Women's. Thank you. They were like two B3 Brigham and women. And there were some two A's thrown in there, but they had to have something in additional to just being a 2A. Like they had to be immunosuppressed or something along those lines.

[A]

Well, they're all immunosuppressed. Isn't this a transplant thing?

[C]

It wasn't. It was advanced cutaneous squamous cell carcinoma. Close to half. Like 40% of the patients I think were immunosuppressed.

[A]

What does 2. What's 2B mean? I have no idea.

[C]

Like vaguely there's risk. There's four risk factors greater than 2cm, poor differentiation, pa, neural invasion, and some like invasion past fat or something along those lines. So basically there's these four risk factors. And so if you have zero risk factors, you're stage like one. If you have one risk factor, you're two A. If you have two to three, you're two B. And if you have greater than three, you're three.

[A]

Okay.

[C]

They found that that discriminated a little bit better compared to the AJCC 8 staging. Like, like that's a cutaneous gram cell carcinoma is very, very complicated. Suffice to say these were advanced patients and the patient said, or the study said all patients are going to undergo a clinical exam. So you examine their lymph nodes. You did a high resolution ultrasound in the lymph node, the draining lymph node area and a contrast enhanced ct. It was like around this time of surgery, plus or minus one month on the surgery. And then the patients were followed up for three months. So lots of numbers. Weirdo statistical terms like a McNeamer Mid P test.

[B]

Like what?

[C]

Anyways, 150 patients included in the study, 12 patients eventually developed lymph node metastases. Physical exam picked up one of These mets. So for all the emphasis, physical exam so important, blah, blah, blah. Not for nodal involvement with cutaneous squamous cell. Now, like, bulky nodal disease was excluded for obvious reasons. So if they don't have bulky nodal disease and you do a physical exam and you're like, well, that's good enough. You don't have any. Like, don't do that. Ultrasound and CT were actually comparable. It's, it's interesting because there was like a, a review maybe 20, 25, and CT was deemed the better test for picking up nodal disease. But in this study, the ultrasound and the CT were comparable. CT picked up six true positives, ultrasound picked up seven. There were some good. There were some false positives that both the tests picked up, but the sensitivity was pretty good. It was like 64% for the ultrasound, 55% for the CT. The huge difference was in immunocompetent versus immunosuppressed patients. So in immunocompetent patients, sensitivity was 100%. For both modalities, they picked it up. I mean, they also picked up things that weren't. But, you know, so what, you picked up the cancer. For immunosuppressed patients, sensitivity was 20% for ultrasound, 17% for CT. So the immunosuppressed patients, a fair number of them, the only reason they found out that they had nodal disease is that within that three month period, the patients were like, my neck's swollen. Like, a study did not pick it up.

[A]

Wow.

[C]

So if you were implement theory, they

[B]

could have not had it. Detectable disease.

[C]

Yeah, but like in three months, right?

[A]

Three months.

[B]

That's not that. I mean, bad cancer grows in three months.

[C]

That's the, that's the point. Like in immunosuppressed patients, cutaneous squamous cell carcinoma is a bad, bad cancer. Where you did an ultrasound in a CT and it was like, there's nothing. And then the patients came back and was like, this thing is growing in my neck. So.

[B]

Okay, I thought you were saying it was.

[A]

Yeah, yeah.

[C]

If you were to implement ultrasound CT at baseline to lymph node positivity and immunosuppressed patients is just not a great test. So you just counsel those patients, like lymph node exam, and when you start to feel something, come back. But ultrasound and CT were comparable at baseline. And given the fact that ultrasound is like, less expensive and you're not subjecting patients to any sort of radiation therapy, and a lot of times in the ultrasound clinic, they're like, okay, well, if you can see a node, let's do the ultrasound guided lymph node sampling right then and there kind of an argument to be made for ultrasound. I'm sure there are patients like experts in cutaneous gram cell carcinoma that know way more than I do about it and are like, actually, that's really dumb.

[B]

But with this study prospect, probably more subjective, right? Like user dependent. That's been the argument in melanoma that, you know, it's more subjective being able to identify metastases with Right.

[C]

In the high resolution ultrasound. I don't think that's like your everyday run of the mill ultrasound. Like that is a, a different modality than what is used most of the time. So definitely yes. And this was all. And I think the Europeans are just more ultrasound savvy compared to Americans. So a lot of caveats there. But I thought it was a night. Like, these are the prospective studies we need because we sit around in tumor boards and we're like, yeah, I mean, sentinel. No. Okay, radiation. Why not? I mean, we, we don't. There. You can't point to a lot of prospective studies that's like, hey, this helps guide us, telling us exactly what to do. So studies like this are nice. It was a good study.

[A]

Okay. Do they use ultrasound in the er like all the time? So I've started watching the pit and it's like they're just ultrasounding everybody.

[C]

If it's on tv, I don't know how you would argue that that isn't in real life.

[A]

Must be. It must be what's really happening.

[B]

Probably knows more about ultrasound in the ED than any of us do. So better research than our opinions, I'm sure.

[A]

All right, let's move on to mine. So my, I, I got two articles, but they were very closely related. So we're getting a lot more in the literature now about psoriasis, eczema, overlap. And, and like people going from, you go on a biologic and you get the other one and the blah, blah, blah. And some people like to say, well, it's, it's, it's just one spectrum of disease. And you're. And I'm like, you're an idiot. That is the dumbest thing I've ever heard. Because if it was one spectrum of dis, it would mean there was one cytokine pathway. And it was like, if it was too low, you got this and if it was too high, you got that. It's two totally different cytokine pathways. Okay, now here's what they found though, so they. They broke it into four different types. And. And so first, the main clinical takeaway was with, with this. JAK inhibitors work great. Like, you should put these people on JAK inhibitors, period. Like, that's for all of them. Well, one group. There's one group that you should put on IL23s, but other than that, everybody else should get a JAK inhibitor. So they have four different types. Number one, there's coexistent disease. So coexistent means you have both classic psoriasis lesions and classic atopic dermatitis lesions. Those people get the psoriasis first, and then they get the ectopic dermatitis as a separate disease. And so they'll have both, you know, extensor elbow and flexor elbow both. And those people genetically have both the genetic predisposition to psoriasis and the genetic predisposition to atopic dermatitis disease. Number two is overlap. So coexistent means you have classic of both. Overlap means the individual lesions. Like you're looking, those are the people that you're looking at. And I can't tell if this is eczema, psoriasis. I cannot tell what they found with those people. And this was probably the most interesting thing to me in the whole paper was that the biologics really did not work. So in the overlapping people, they put so five out of seven people did well on io23. They put a couple of people on io4s and io17s did not do well. And then in the other paper, they gave the treatment summary again. So when they put these people on biologics, psoriasis, biologics, 18 people ad biologics, quote, were often inadequate. In contrast, JAK inhibitors always worked. And so I've always with these people, been like, take a guess. Like, if they're itchier, try doopie. If they're not so itchy, try a psoriasis, try an IL23. And their takeaway was basically like, no, it's very unlikely to work. You want to put these people straight on a JAK inhibitor. And then the other two types, so and those people as well have genetic predisposition, both diseases. And then the two other types, the people who get you have psoriasis, you put them on an IL17 and they go on to get eczematous lesions. Them, you can switch them over N23, and the examinous lesions will go away and the psoriasis will do great. And then you got the people who are on dupy and they get A psoriatic lesion with. They get psoriatic disease. And whenever you see those people, you can actually switch them to aisle 23, Ill 13 only inhibitor. So they had a number of those patients that they put on Trelo and they actually did well also. And so it's, it's reasonable with those people to just get them off the IL17, get them off the IL4, and they should do well. But the. If they've got both diseases at baseline, then you want to go JAK inhibitor. And so that was. Pathophysiologically, I think we. This was actually really useful because it did show that there is this group genetically that is predisposed to both. Both diseases. And it can be. They actually have both and it can be an overlap where they just look the same.

[B]

And some of them like flip flop from one to the other. But that there's people who, like, I don't know.

[A]

They didn't, in this. They didn't talk about that.

[B]

There's a JEADV paper where they talked about that.

[A]

Yes. About the cytokine, sort of the flipping.

[B]

Yeah.

[A]

I'm not convinced that I, like, like, if, if the drug flips you, then, you know, I don't know if I really count that as flipping. Like, I don't, I don't. I see people more like, when I hear flipping, I want it to be like, I got psoriasis this week. Next week I got atopic derm. Then I got, you know, that I'm not convinced exists.

[B]

But having. I mean, but have you seen people. I've seen them. Not a lot, but where you're like, it kind of looks like atopic derm. You put them on dupy and then they're like, bam, it's psoriasis. And then you put them on an aisle 17 and be like, bam. They're back to what really looks like atopic derm. I have had a couple of those people, and it's like they just polarize one way to the other. And this study looked at that a little bit like the people who flip from one to the other. Maybe we'll go over that in another one. But I think aisle 17s tended to drive the flipping from what looked like psoriasis to atopic. More than 23s did. And then dupilumab drove it more the other way. But it's also probably that was the vast majority of biologics that were used to treat.

[A]

I have not, I have not seen any of those people. But I could believe that. I could believe that would exist. I could believe that that would exist.

[C]

This, this is four types. Like do they have a. I'm looking through the paper. I don't see like a table. Like what are the four types?

[A]

So it's in the. It's not. You're probably looking at the one that was like from Korea or Japan or somewhere. There was. The other one was from Italy. The one that's in Italy has the four types.

[C]

That's what I'm looking at.

[A]

The dermatitis, psoriasis, overlap. So table number one is psoriasis, eczema, coexisting phenotype. That's on page two. Okay.

[C]

Each table is a separate phenotype.

[A]

Yes, each table is a separate phenotype.

[C]

Oh, got it. Okay.

[A]

But so bears, like I, I can buy that existing and the, the, the. Yeah. And the answer would be put them on a jack, right? Yeah, that, that would be.

[B]

Or, or a methotrexate. Like when I've had a couple of those people, they do. Well, they do better on non biologics. So a jack or a methotrexate.

[A]

Okay.

[C]

Okay, cool.

[A]

All right, that's it. Let's, let's move on. Ferris, what do you got?

[B]

Okay, so this is efficacy and safety of ruxolitinib cream and patients with lichen sclerosis. Results from a phase two randomized double blind vehicle controlled study, Goldstein et al, which was just recently published in the jad. Okay, so lichen sclerosis, tough condition. So it is kind of nice that there are now some clinical trials for things other than clobatazole because, you know, it is hard to tell. Patients stay on clobazole forever. So this was only in women. Double blind. 11 sites, 61 women, they had to biopsy, confirm anal genital lichen sclerosis. They had to have a BSA of less than or equal to 10% IGA of 2 or more. And then they had to have itching. So they had to have baseline itching NRS of 4 or more. They did stop all their other treatments and then they were randomized to vehicle or ruxolitinib. And then everyone rolled for up to, for 12 weeks and then everyone rolled over up to 24 weeks to an open label extension. So what's interesting is they made their primary endpoint because this is I think a big obviously thing for patients. Itch. They're like, what proportion of patients have a four point improvement on itch? NRS at week 12. And it missed its primary endpoint. It did not. They did not See a significant difference in itch. It was like 35.7% in the rucks group and 40% in the vehicle hit that four point improvement. So no like pain, time to itch. Nothing, nothing, did nothing. So you're like, okay, well whatever. It's like a moisturizer. They also did look at like clinical signs. So they used. There are two different measurements. One's called the clinical lichen sclerosis score and then the other is like the LSCA Lichens sclerosis clinical assessment that looks at both symptoms and signs. And what they saw actually was that when you looked at the change in the signs there was a significant difference. So you know, when they looked at things like, you know, petechi are hemorrhaging and whitening and changes in architecture, Roxib did work better and it was statistically significant. And so, you know, there was not like it wasn't power to look at this. So but it was for both of them. So I thought that that was interesting. There were like, the, the adverse event stuff was actually kind of interesting too because obviously like what we worry about are squamous cell carcinomas in patients with lichen sclerosis. There was one patient who developed a vulvar basal cell carcinoma at an application site. So I thought that was kind of crazy. So, you know, small study, did not meet its end point. But, you know, maybe this could work. And I also thought it was interesting because they looked at, you know, at not just symptoms but it's signs. So if you look at the signs I looked at, it was petechiae and ecclesiastic whitening, fissures and then structural changes primarily. So maybe this does have potential. The question is, if it doesn't help the itch, how meaningful is that? But again, you know, maybe there are like, you know, again, this is another disease where you're not going to just have one treatment, clobatazole. It's great that it works, but it's not an everyday, forever treatment. You know, if you can actually halt disease progression, could something help to, you know, maintain it? So I thought this was promising. Maybe we'll see more in bigger studies.

[A]

It's a. So I, I was an investigator in this trial. I had a bunch of patients, they had all been on clobazole before. And like when I'm doing a trial, I'm sure you do the same thing, Ferris. I'll always be like, so, like, what do you, you know, I don't know if you're in placebo or the real thing. But you think this is better or worse, and especially once you get into the open label, you think this is better or worse than what you've been on before. They universally were like, this is working, but I think the CL is always better.

[B]

Okay.

[A]

That was what I, I heard from everybody. So I do, I do think it works, but I don't think it works great. Which was, which was surprising. If you had asked me ahead of time, I would have said, I think it'll work for the itch and the burning more so than the, you know, structural changes and visible signs, but the opposite result of what I was expected.

[B]

Yeah. Did you think you could see changes in people clinically or. Hard to say.

[A]

Yes, I thought. I thought I could. I thought I could. The assessments were difficult to do just because you're not used to like, looking for petechiei and looking for cigarette paper wrinkling. And is it a grade 2 cigarette paper wrinkling or a great, you know. So the assessments were kind of difficult, but I did think I saw people get better.

[B]

Yeah.

[C]

And we just had, we had the lichen sclerosis physician on a few weeks ago, and she says like, clobetazole and it's lifelong, but she did say she tapers it out towards like once they kind of get a decent response. Right. She's not using it every day.

[B]

Yeah, no, and I do that too. I'll tell them, like I always tell them, don't go, like, you cannot go below once a week with your clobatas. All like you do need to.

[C]

So maybe something, something else to use on those days.

[B]

Yeah.

[C]

Or maybe it would decrease. Maybe the long term exposure to combat is all. I don't know.

[B]

Yeah, but interesting.

[A]

All right, cool. Patton, what do you got?

[C]

All right, second six pack. International Journal Dermatology, May 2026. Cutaneous manifestations of vasculitis. A cross sectional analysis from an international cohort by Micheladi et al. I kind of thought this would be a paper that like, took patients with aculitis, skin, vasculitis, and would give us clues, like what findings make us worry about what systemic disease. But it was like totally the opposite. And I should have picked a different paper. But I finally got to this while I was watching hockey last night. And I wasn't about to go find another paper because I was watching hockey. This paper looked at patients with systemic vasculitis and asked, what are the skin findings? So big study, lots of patients, over 4,000 from some sort of multinational collaborative. Vasculitis thing. Skin lesions are very common in IgA, almost like 100. Close to 100% of patients with IgA have skin lesions. Cryoglobulinia, it's also pretty common. Around 90%. Bachettes and polioritis in the dosa have skin involvement in around 60% of patients. But SHET sets, that's mostly in the mouth and genital, not really cutaneous per se. MPA, GPA, EGPA, the Inca vasculitides. They have skin lesions in 20, 30, and 40% of cases, respectively. How often is definitive vasculitis seen on biopsy? That was kind of a hard number to come up because not everybody was biopsied, but in the patients that were, when a biopsy is done, it's like upwards of 75% for most types of vasculitis. Biopsy. Less often useful for Bachettes, Takayasu, and giant cell arteritis, which makes sense. Table 2. It was a short paper.

[B]

It was a letter.

[C]

It was a short paper. Table 2 had odds ratio of severe systemic disease based on the presence of skin lesions. That odds ratio was high for GPA and egpa, and it was lower for pan. So, like, more severe GPA and EGPA if you had skin lesions, less severe polioritis nodosa if you had skin lesions. I don't know if this changes anything from a clinical standpoint. Vasculitis like that, like, scares me. I've missed a couple cases of systemic vasculitis because vasculitis wasn't present on the biopsy. So I was, you know that 75% is in Wagner's and things like that. So I guess that was a little reassuring. But if you suspect vasculitis and the skin biopsy doesn't show it, that should not let you stop. That should not stop you from thinking, okay, this isn't vasculitis because it's not always there. Maybe that's the point. I don't know. What did you guys think?

[B]

Yeah.

[A]

Yeah. I. I've missed some vasculitis cases because of that. And it's. I. I feel like we talk a lot more about systemic vasculitis than you actually see. Like, I can. Maybe you've seen more being at the universe. You know, I've been doing dermatitis for 20 years, so. But you just don't see that much of it.

[B]

No.

[C]

And. And I mean, leukocytoclastic vasculitis without systemic involvement. I want to say that's the. That's the vast majority of what we see, I mean like the vast, vast majority of what we see, or drug induced vasculitis where they don't have systemic disease. This paper, like didn't even have that as a category. Like lcv. Cutaneous only was not even a category they looked at because I think they wanted to start off like systemic vasculitis and working backwards to the skin. So, yeah, like there were a thousand patients with Wegner's. I mean, I've seen like four cases of Wegner's that I diagnosed from the skin, two of which I missed because one I thought was pg and there were a bunch of other people in the department that had seen the patient, diagnosed them with PG and it turned out to be Wegner's. Sorry, we don't say that anymore. Granulomatous polyangiitis. And, and the other patient had like what we were just basically calling superficial pyodermatous pyoderma gangrenosum that turned out to have GPA. So like 1,000 patients with GPA. I just like, it seems way that's a bigger number than I would have ever suspected. If you had 4,000 total overall.

[B]

Yeah, I mean, I guess the take home points from, I mean your experience too is if it is, if it looks like pg, do consider, you know, vasculitis. And then what would you say, I think like for pearls of biopsying vasculitis sounds like you miss it because it depends what you biopsy. Right. Like you want to biopsy more established lesions. You don't want the newest lesion if you suspect vasculitis. Right.

[C]

Well, you kind of want in between.

[B]

Because you want in between. You don't want it to be all decimated and burned out. But you don't want the newest. I don't know, I, I think or like pick a couple. A couple lesions. Like, I think there is a little bit to the timing and lesion selection for vasculitis.

[C]

I agree. You know, there's a lot of hedging by pathology on vasculitis. Like not definitive vasculitis, but suggestive of. And then you're like, okay, well, I don't know. Is that terribly helpful?

[A]

Yeah.

[C]

So suspicion of systemic vasculitis. If you have a high enough suspicion, don't let a negative or sort of hedgy biopsy discourage you from working them up for systemic disease.

[B]

And maybe I'll do two biopsies. Every time I think it might be. I'm hedging on vascular.

[C]

Yeah, it's not a bad idea just

[B]

to get more lesions in different stages. Yeah.

[A]

The other thing I have done here is telescoping biopsies where, like, you do a six and then you put that in the jar and then you do a four into the hole, the six to get deep enough or doing like a little wedge biopsy where you do a little, you know, a thin ellipse. But that way you can get like a longer section that the pathologist can get a better, you know, you have a higher chance of getting it. Yeah.

[B]

Telescoping biopsies. I'm not sure I know why, but I guess because they can't orient it. But yeah, yeah, yeah, yeah.

[C]

That's especially true for pan. I think pan, like, don't, don't do a little 5 millimeter punch. If you think it's pan, wedge it. Like, go down deep.

[A]

Yes.

[B]

Yeah.

[A]

If, like, it's the only time I've ever done that. I. It's like somebody with. It's like horrendous. I don't know if this is PG or some horrible systemic vasculitis. And like, I'm going to send in big chunks to try and find out. Like, it's not like lcv. You, like. It's got to be kind of a scary patient.

[C]

Yeah. Yeah.

[A]

All right. My last one again, kind of a cute one. So Ilvin, inflammatory linear verrucous epidermal nevus, which, I don't know what you guys think about this, but I always assume that these are kind of a Blasko's line following somatic mutation.

[B]

Yeah, they're like a mosaic type thing

[A]

and that you got the psoriasis mutation there. Yeah, Like, I, I think of it as a somebody who, thank God you didn't have it your whole body or you'd be covered in psoriasis. But it's always been super hard to treat. And so this was Tapinrov. So good old Vitama in two cases of Ilvin. Now, once I actually pulled the paper and looked at the pictures, which we'll put in the video, it was like, ah, I get like, okay, it worked. But it wasn't like, oh, that was great. But like, it, it, it worked. It worked. And so this will probably be now my. You know, if I see another case of Ilvin, I'll probably call it linear psoriasis and try treating them with Fatama.

[B]

Because it's just one time I had a great response in Elvin. It was the same thing. Like, I was like, oh, we're going to Call this linear psoriasis. Like a biopsy. Psoriasiform. I tried like every biologic, every topical methotrexate and then finally I was like, I'm just going to do so Tic two. I mean, it melted the whole thing away. I was pretty impressed.

[C]

I have three patients on Sotiktu and I am absolutely like blown away how good they responded. So tick to like they did get killed in the market. It's a really, really good drug.

[A]

They were, they were just, they never communicated well. Like, okay, assess people for tb. Doesn't mean you have to do a tb. Like, do you have a cough? Do you work in a prison? Like, that's, that's good enough. But they were, they were. I don't know who was advising them. I don't know what their deal was. Hopefully Takeda will do a better job of communicating the actual risk profile because that's an even better drug than so Tick two.

[B]

Yeah, we should have three new Tick two, potentially three new Tick two inhibitors that are seem like they are better relative to ducravacit Nibs. So it'll be interesting.

[A]

Have you guys seen any or had anybody tell you they've been using. I could put icotide.

[B]

I, I did the trials in it. I have not actually had anybody on it. I don't have anyone on it clinically yet.

[A]

Did you. What was your take from the trials? Do you think it's.

[B]

I thought it was pretty good. Yeah, we got good. Yeah, good responses. You know, it's, you know, I could go like, do patients really want pills? Do they really want, like, do they really not want shots? I don't know that they do, but I will say I had some excellent responses. And again, I don't know who was on what dose, but I think it is impressive if you want a biologic and the patient really doesn't want a shot. I think it's a good option. And now what was interesting to me in like the trials was I thought, oh, this is going to work in like puma, plantar disease or whatever. And it really wasn't that great. So I'm very curious to see the PSA data.

[A]

Yeah, yeah. Because right there's that theory that like, oh, since it's a smaller peptide, it penetrates better into stuff and the blah, blah, blah.

[B]

Right.

[A]

And then it's not derived from a camel, is it? That's not the one that came from a camel.

[B]

No, that's Sona Locomab.

[A]

Sonalikumab. Okay.

[C]

Yeah, that was hs, right? Is Sonalikumab being actually studied in psoriasis.

[B]

Studied in. Sorry. Yes. Psoriasis or psoriatic arthritis, as well as hs. I think that primarily psoriatic arthritis, but there's some psoriasis data for it, too.

[A]

Okay. All right. Well, that's it. I want to thank everybody for joining us this week. Hope you laughed once or twice. Hope you learned a few things, but mostly I hope you're planning to join us again next week. Until then, I'm Matt Zyrus.

[C]

I'm Tim Patton.

[B]

And I'm Laura Ferris. And we are germs on drug.