A (4:20)

So let me ask you my first question when I was looking at this.

B (4:24)

Yeah.

A (4:24)

The one that made me question the whole thing was the psychotic disorders. So I think of everything else in there as something where like bad stuff's happening to you. You get things anxious, depressed, insomnia, eating disorder, whatever. But like psychotic is your brain's messed up. Like you've, you've got, you know, that's genetic, it's whatever. So that one made me question the whole thing a little bit.

B (4:56)

So 1. Matt, if you look at the percent risk, it's low, right? So it's 0.4 in the AA group versus 0.1 in the non AA group versus things like, you know, anxiety which is like 10 and 3%. So 1. This isn't like a. Even though the risk ratio, the ratio is high, the absolute numbers relatively low. The thing I would say is that I think how do you get diagnosed with the psychotic disorder? It's usually you have an episode. And you know, we do know that people can have, you know, stressors contribute to that. Right. So you can have underlying disorder but you might be well controlled. But when you have an acute stressor and things like alopecia areata can be that, that was kind of my interpretation that it throws people over the edge. Right. So personality disorder should be not, I mean it should be part of your personality. Right. It should not be related to things like aa. But you know, in my view like where, when do you present and get a diagnosis of these things? It's when it's exacerbated enough that you have to hit them medical system.

A (6:02)

So Dr. Senna, in your experience. Right. We also talk some about the psyche, the, the immunologic effects of stress and psych disorders and whatever and we're all comfortable with the idea that like psychologic stress can cause telogen effluvium. But do you think there's any two wayness here that like people or it's the susceptibility to anxiety and depression makes you more likely to get alopecia areata or is it, you know, do you think this is pretty consistent with your experience though that people like get AA and it makes them anxious and depressed?

C (6:40)

Yeah. So I think it's a bit of a double edged sword. Sword. Right. Because at the one hand you don't want people who get AA to be thinking oh crud, this is something I did, this is my fault. Because we know that even if stress does cause an exacerbation or, or contribute somehow to onset of disease, it's not the whole story. We know that there's more to that. Right. But I think probably the most telling examples that I see of telogen effluvium like triggers leading to exacerbations of disease is in my patients who sometimes are on JAK inhibitors have completely regrown. They'll have, you know, God forbid, loss of a loved one or something major that happens. Right. Not the day to day stress that we all experience but something really bad that happens and they'll go through a flare. Now they won't lose all their hair, but they'll develop patches and it's come to the point where we actually screen them and the vast majority of people will have had some trigger. It's either weight loss, the common ones are weight loss, adjustment in their thyroid, medication, significant stressor, those are probably the top three. Or stopping a hormone medication, stopping hrt, stopping a birth control hormone, eluding IUD or birth control pill. And it's like I would say 90% of my exacerbations have a telogen effluvium trigger.

B (8:03)

I have a question about this for you too. So we did some of the early JAK inhibitor AA studies and so when you have patients in a clinical trial, you really get to know them a little better than you do when you just have a patient who's in your clinic for 15 or 30 minutes.

A (8:18)

That's just you, Faris. I don't talk to the clinical trial patients either.

B (8:22)

Okay, you don't, but I do. One of the things that really struck me was the number of people who had a severely traumatic event prior to developing aa. Like, oh, I was fine, and then it was like horrible things like the death of a child or the death of a spouse, and something that was very unexpected, and then they developed aa. So I, I agree with you. I think that there is this, you know, important psychiatric component to it.

C (8:54)

Have you seen that? Not everyone, but there are definitely a subset of patients, right? Just like ATP can contribute to aa, there are a subset of patients who I think are a bit more subject to this. What I, what I think is neuroinflammatory process that contributes to their AA pathogenesis.

B (9:15)

Yes, no, I agree. And so, yes, I think it's interesting. So, you know, it is like the chicken and the egg question, right? So are you also capturing things? But, you know, they did try to control for that by not having. For people who did not have any of these diagnoses prior to their diagnosis of aa. So, you know, the, the interesting little statistical thing that I thought was interesting because I'm always like, what's the, you know, what's the risk ratio? What's the hazard ratio? But basically, risk ratio is excess burden overall. So more people with AA will end up with these diagnoses. Hazard ratio also controls for, like, the time to event. So, you know, and so what they. The hazard ratio being elevated suggests that there's more of it, but it's also more likely to occur sooner. So. And that was the elevated hazard ratio sort of takes that into account as well. So I thought that that was interesting. The other interesting things that they did was, you know, it's like, okay, well, this, this whole. The study ran over Covid, and so they actually compared like, pre and post Covid, and so the risk did go up far higher, higher after Covid for particularly anxiety, insomnia, eating disorders, self harm, and suicide. So is that just Covid effect? It may be, but I thought that.

C (10:36)

Was interesting that they comment there too. Laura. Like, one thing that I was kind of thinking about is, you know, we got our first FDA approval for baricitinib in July 2022. I think they looked at the data from, like March 2020 to January 2020. Five, is that right?

B (10:54)

Yeah.

C (10:54)

And. And so, like, you would think maybe, oh, their anxiety might go down. Of course, we don't know severity of these cases. We don't know, you know, anything like that. But you'd almost think, well, now at least there's an option. But maybe it's sort of, you know, patients aren't aware if they're newly diagnosed. It's hard to know. But I did think that was interesting too.

B (11:11)

Yeah. That the treatment landscape, like, changed so dramatically in the. Yeah.

A (11:18)

Brought something that I hadn't thought about before, that since this is basically an unselected population of alopecia areata patients, this. The vast majority of them are going to be fairly mild. And so these psychiatric stuff is for people who, you know, four times more likely to be anxious or depressed. The majority of them were mild alopecia areata, not, you know, salt 70.

C (11:43)

It's the unpredictability of this disease that absolutely and understandably. Right. Really can mess with people because they don't know. And there's no test that we can do to promise them one way or the other. If they're just gonna have, you know, couple patches that'll spontaneously regrow and never be an issue again or patchy persistence disease or lose everything. They don't know why it came about. They don't know, you know, what caused it. And, you know, sometimes those. Those types of alopecia areata can be even harder to camouflage or deal with in. In some cases.

A (12:15)

So do you have a number you give people? So say somebody comes in with one pat, you know, we need one spot or a couple. They're like injection done.

C (12:25)

Yeah.

A (12:26)

But they're like, well, what are the chances all my hair is going to fall out? What do you. The number I give people is probably one in probably 90% chance you're going to be fine. I'm making that up completely. Is there any data. Is there a number you give people?

C (12:41)

I mean, the range really varies depending on what study you look at, but it's somewhere around 10% up to as high as 30%, which I think is a high estimation. I think it's probably somewhere in the 10 to 15% range. Okay, you're right.

B (12:58)

You're right. Sometimes you just make stuff up. And you're actually right.

A (13:04)

That's right.

C (13:04)

You take.

D (13:06)

That's right.

A (13:06)

You take enough shots, eventually you make one. That's right.

D (13:11)

Mary and I had a question.

C (13:12)

Please.

D (13:15)

You said you screen pretty much all your AA patients. Right. With. With those psychiatric questions. Do you have a Like, system in place where, hey, look, the rate of psychiatric disease is so high, I really want you to see somebody or do you discuss it and then they say, I'm going to be okay. I know that I'm in good hands in your care. Like, how many patients do you actually sort of say, hey, go. Go see a psychiatric professional about this? Because, I mean, it's no surprise that there were higher rates of psychiatric disease. But it's like, what do I. What am I going to do with these patients? I mean, I'm. I'm probably, like, terrible at saying, here's what you should do, and you should talk to somebody about this. You just kind of make a note of it and then I don't know the next step.

C (14:01)

Yeah, I think it's an excellent question. Interestingly enough, patients are pretty insightful. And those who, who I am, like, this person needs help, are usually already seeing someone or have already started medication. Now, you know, we're in this sort of, you know, environment where PCPs are prescribing antidepressants and anxiolytics and things like that. So a lot of patients, by the time they come to me anyway. Right. Have already had access to some of these people. We do also have a social worker here at Leahy who we work with. So when we do group sessions, she comes and gives a presentation, gives out her information in case people want to contact her. And oftentimes, you know, I probably refer maybe a handful of patients to her in the four years I've been here. So it's not really common. I think the question comes up most commonly and again, understandably with the adolescent population. Right. The kids who all of a sudden lost their hair are like, floundering, don't know where to go. And those are sometimes the hardest patients to find the right care for because it's the particular age group. And you want someone, too, who understands alopecia. So I'll usually connect them first with, like, NAF and some patient support groups and things like that. But that's one that I often have a hard time finding access for. Right. Someone I direct go to.

A (15:21)

And just the other thing I would say is of interest, as somebody who has seen many therapists over the years, you now can almost always find virtual therapists who take your insurance. So if somebody has insurance, even if it's terrible insurance. Yep, there will be therapists like that. Most of the therapists I've seen in the last five years, I've never met face to face. Then all of the visits virtually and it's been covered by insurance now are my, my workplace has a high deductible plan, so I'm still paying basically, you know, the full price, but at least it's going towards my deductible now.

C (15:59)

Yeah, that's a great point. I have referred a couple recently to, to those online things. I don't know how they've worked out. Seeing them back soon to I could probably find out. But yeah, they were another great option. Yeah.

B (16:12)

And I would just sometimes like papers like this are helpful for me to say to patients who are struggling. Like, you know, this isn't just you. Like this isn't you. Like this is part of your disease. And I think sometimes patients need to hear that, like you're not, you know, how could we expect you to deal with this? You're not just somebody who's not coping well. This is part of your disease. And you know, if you had high blood pressure as part of your disease, I'd send you to somebody. So why would I not send you to somebody? Sometimes that's helpful.

C (16:41)

I think that and just a quick thing too, like you don't have to do like a had seven and some depression scale and this and that like on our intake form in the front page for every hair loss patient. How much is your hair loss bothering you? Like your score, you know, with the happy face all the way to the sad face. Right. And they circle it. And so you know, if you're walking into a room that's like a 9 hour 10 or if it's a room that's a 2. Right. And that's really helpful because it helps you kind of gauge where you're going. And sometimes patients will be reluctant, they feel embarrassed admitting how much their hair loss is bothering them. But by writing it down and just circling a number, you kind of have a, have an opportunity to just open the conversation if you choose to.

A (17:21)

And so far says you first. I love that and I hope that on your likert scale the unhappy face is somebody is a happy face that's got no hair. And the happy face is one that's got like hair drawn on.

C (17:33)

But we need to update it. Yeah, that's a good idea.

A (17:38)

But Ferris, you know, as you know, I like to take everything to an extreme. So what I will do in what I do reasonably frequently is say to people, you know, anybody who had any normal person who has what you have would be really psychologically like just depressed and anxious. If you don't need to see a therapist, there is something wrong with You. That's the. That's, you know, I. I don't say I don't bring that out often, but I have brought that out whenever I'm really having trouble.

B (18:10)

It's an extreme way to handle that situation. Yeah.

D (18:15)

They had one disease and now they have two.

B (18:18)

Right? Exactly.

D (18:20)

Strong work, Matt.

C (18:21)

All right, let's say to like, for women, too. This is tricky, right? Because, like, if you think about it, I'm really dating myself here. But like, back in the day, right? Like Michael Jordan, bald, hot. Right. Like Vin Diesel, bald and handsome. Right. Tyson Beckford, good looking. Bruce Willis. Right. Old school Bruce Willis, handsome. Right. Heartthrob. You can't think of a single bald woman like that. Right. There is zero cultural acceptance for women to have hair loss. And the other kicker is not always, but often women are wearing their hair longer. So even when they start regrowing on a JAK inhibitor, they're not taking off that wig for years because they don't look like themselves. Right. If the hair is growing a centimeter a month, it's taken years. By the time they feel like they can go out and about and have their identity back. So while it can affect everybody, we have to treat everyone the same and think about everyone the same. For women, I do think there's sort of this disproportionate, Disproportionate, you know, effect when it comes to these psychosocial comorbidities.

A (19:27)

Some of my men with totalis or universalis on Jax who are happiest, got their eyebrows and eyelashes back, but not their scalp hair.

C (19:36)

Yep.

A (19:37)

And they're like, this is. I was hoping I was wor. Like, I didn't want to have to start getting a haircut, buying shampoo again, but I look really weird with no eyebrows or eyelashes.

C (19:46)

Yeah, it's been.

A (19:47)

Yeah, it's been interesting because that is kind of the opposite direction. Because eyebrows and eyelashes, it is socially acceptable for women to, you know, use an eyebrow pencil and use false eyelashes. Men are not going to do that. And so eyebrows and eyelashes, I think, are more impactful for men, not just because they care less about their scalp, but also because they don't have a way to cover it up. Whereas women do have a way to cover up eyebrow and eyelashes.

C (20:15)

Totally agree. Yeah.

A (20:16)

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

D (20:18)

All right, my deep dive is from July 2025 edition of Acta Dermatovineologica Alopecia Areata Impact on Patients, Quality of Life and Disease Perception, a survey based study by Vestergaard Et al is written by like a bunch of Vikings. Senior author was Mork, a name that up until I read this paper was exclusively associated with an alien played by Robin Williams, as the title states. What's that?

A (20:45)

And Mindy. It was Mindy.

D (20:48)

Yeah. Nanu. Nanu. All right. As the title states. It was a survey conducted in Norway and Denmark. Why leave Sweden out? It's right between the two. Subjects were recruited from social media sites surveyed on an objective measure of disease, the SALT score, as well as two questionnaires that measured how their disease impacted their life, the DL QI and the PUSH D scores. And patients were also asked to subjectively rank their AA as mild, moderate and severe. Over 300 respondents. 94% of the respondents were female, which, you know, that may skew the results that we've already discussed because it may have a larger effect in females. Over half of the respondents perceived their AA to be severe. The younger patients had higher percentages of severe disease perception compared to patients older than 60. Younger patients tended to have worse DLQIA and push D and salt scores. So that all seems to track overall objective severity scores. 15% mild, 29% moderate and 56% severe. And that's just them answering the question. Mild, moderate, severe. It doesn't have anything to tie to any of the other scores. When you left out patients with alopecia universalis and totalis, the percentages were 25 mild, 38 moderate and 37% severe. Figure 2 was pretty interesting when focusing in on the patients who perceive their disease as severe. So for like DLQI, you could have a DLQI of 5 or less and still perceive your disease to be severe. You could have scored less than 20 on the push D score. Lower scores being better still perceived your disease to be severe. And the salt score was kind of crazy. You could have a salt score of less than 24. Like you could have a salt of 5 and still perceive your disease to be severe. So I think the paper how.

A (22:32)

How strong of a. I mean I assume there was some level of correlation between SALT scores and perceived perceived disease severity. Did they report that of like how is, you know, is it a correlation coefficient? So as I think of it, Correlation coefficient of 0 is no correlation. Correlation Correlation of 1 is perfectly correlated. Did they say like they did those.

D (22:56)

Calculations for DLQI and also for the PUSH D and the correlation was pretty poor. Like DOQI was terrible and it was the correlation of DLQI versus SALT and there was a very poor correlation.

A (23:12)

But was DLQI was closely associated with perceived disease severity. I'M sure it was stronger than salt.

D (23:20)

It depended, right? So like if you had, if your perception of disease was mild, then the likelihood that you had a SALT score or I'm sorry, a DLQI of greater than 10 was like zero. Like none of those patients did. Like, if you had mild disease, 100% of the patients had like a DLQI of 5 or less or something that's like the top bar. But as you got down, so, so in other words, I think everyone agrees this is mild. I'm fine. But what people don't agree on is I have really, really severe disease. And you would objectively look at them and say you have a salt of five. But some patients will still say, well, I still have severe disease. And same with, you know, they would do the DLQI and the PUSH D questionnaire and actually have pretty good scores, but they would still be calling their disease severe. So I think with the, the, the argument that the paper was making, and I think successfully, DLQI pushed E. SALT may not be the best way to evaluate severity disease in AA patients. But what is also probably true, and I think this is where it gets tricky, is that patients with mild aa, objectively mild AA may be overestimating how bad their AA is, which, like that feels like really mean to say like that they're the ones with the disease. So how could I say, you have one little spot like, this isn't that bad. In the discussion, the authors mentioned that a DLQI score of greater than 10 is required by the Danish AA guidelines to initiate systemic treatment and. Right. I mean, I wouldn't say that that makes any sense, right, that you're, you're probably not treating patients who like, may actually have severe disease because the DLQI is just not capturing severity. It seems that DLQI is just a poor measure of AA severity. But it also, this data raises some important questions, especially those severe patients. How do providers draw the line on offering more aggressive therapy? Is it solely based on how severe patients perceive their DS to be disease to be? If a patient with objectively mild disease rates their disease as severe, are they a reasonable candidate for LIT flow? This paper was funded by Pfizer and some of the authors were employees of Pfizer. So, you know, I think it deserves a little bit of scrutiny.

A (25:34)

But Pfizer has that thing that they leave back of the office that says, you know, it's got the normal, like less than 20 mile, 20 to 50 moderate, 50 to 95 severe, 95 very severe, but you can upgrade by 1 if they have significant that was my paper, Matt.

C (25:53)

You better not be making fun of it.

A (25:54)

I'm not.

C (25:57)

No. But here's the thing, though. You don't know. Like, they didn't ask. Do they have eyebrow. Eyebrow eyelash involvement. To your point, they didn't ask. Where is this patch? Is it right here in the front of your head, or is it someplace you can camouflage it? Are they responding to treatments or not? And, Yeah, I think 5%. I mean, that's not someone that you're going to put on a jack inhibitor. But listen, if Suddenly you had 30% of your hair on your head gone, that's actually a lot of hair gone, you know, and if your eyebrows. So maybe, you know, maybe you try some initial treatments, but if they're not responding, that could be a reason. If they're not. You know, in the clinical trials, we used a salt of 50 or more, so basically 50% or more scalp hair loss. But. And so a lot of payers are saying, well, that's what you need to show in order to get this person treatment. But if they're not responding to treatments and they're going from 30 to 40 and no eyebrows and not wanting to go to work, you know, I think we. You know, the point is we have to. We really do have to think about that. And the other thing is, the DLQI is horrible for aa. I mean, it's asking, like, how itchy, sore, painful, or stinging has your scalp been? How much does your hair loss, you know, affect what clothes you pick out? Right. There are much better measures. And we saw it in the clinical trials, right. With JAK inhibitors, people would have full regrowth of fear. You would see it on their face. They'd be like, yes, they had their life back. And the DLQI would not budge. So it's just not a good measure of this at all. So these really didn't surprise me.

B (27:37)

Some physician objective measure. And the reason is, like, think about. Not aa, but, like, think about the patients who come in to see you for hair loss. And you're like, I cannot see anything that would look like. Like you have a full, thick head of hair.

C (27:54)

More hair than I do.

B (27:55)

Yeah, yeah. Which frequently, you're no Tim Patton.

A (27:59)

You're a matt zir.

B (28:01)

Yeah, yeah. I mean, so, you know, I feel like it is unethical for me to treat those people, right? To be like, here's what y'. All, oh, I'll do this. And I can, you know, and if I don't, like, do a cash hair loss. But what.

A (28:17)

What do you mean, unethical to treat them.

B (28:19)

It's something aggressive. So let's say that I had a fancy hair clinic and I could offer them PRP for $2,000 out of pocket. Okay. Is that right to do? I don't think it is. I think there's some, you know, it's in a, in a sense like a form of body dysmorphic disorder. I mean, I've had people come in and they are like, okay, in tears over hair that I've never had that thick in my entire life. And like, you know, they want to see what medications they can get and they want to get a panel of blood work and they want to go see somebody for prp. I'm like, I can't in good conscious say, that's a good idea.

A (28:55)

Huh. That's fair. She. I think you just coined a new disease. HDD Hair dysmorphic disorder.

C (29:02)

Disorder.

B (29:03)

Okay, but it's a thing, right? Marianne, would you agree?

C (29:06)

The hair loss patient with no hair loss? Yeah, it certainly is. And, you know, you just got to be real with people. I have to say, and like I said, like, 98, 99% of my patients are hair loss. Those patients are few and far between.

B (29:19)

Yes, they really are.

C (29:22)

Most people have real hair loss. I mean, even if it's like mild female pattern or mild, you know, male, there's hair loss there that you can do something about. But thankfully, those patients are few and far between. Yeah.

B (29:35)

Now, I agree they're few and far between. But, you know, it's also think about bio. Like, we have so many biologics for psoriasis. We all have the patient who has 1% BSA and they're like, I just would like to be on one of those Skyrizi. Like, I think Skyrizi is a great drug, but I'm not going to give it to somebody with 1% BSA who's tried nothing. It's just not the right thing to do. And I do think we need to have some input.

A (29:59)

I'm bringing it back out. Again, my desires measure of if a drug should be covered is we, you can either go on the drug or we will write you a check for half of the cost of the drug for a year. Right. So for that 1% BSA person, you can either have Skyrizi or we'll give you a check for 20 grand. And if they say, I would rather have the Skyrizi, then they get it.

B (30:26)

Really? But what if they say, I'll take the money because I'm going to go in and Be like, okay.

D (30:34)

This is a hypothetical situation.

A (30:37)

All right.

D (30:38)

Yeah.

A (30:39)

Anything else weird or interesting come out of yours?

D (30:43)

I mean, probably, but that. That. That's all I. That's what jumped out at me. There was. There was like. Like a ton of different numbers. I'm like, I could talk about this for 20 minutes, but that's what jumped out at me is the severe disease that objectively have mild. And that's a tricky situation for us as practitioners. I think.

A (30:59)

Think the. The other thing I wanted to talk about from it a little bit was it did show that the. The younger somebody was, the more severe they perceive their disease or the. Or the. Or the worse it affected. Like, is it. I feel like younger people did. It affects them more than older people, which would make some sense, I guess, but it did it am I.

D (31:21)

They also had higher salt score. Like, they had higher salt scores. So the fact that they perceive their. That kind of map. They scored higher on dlq. I know that could be a perception thing too, but.

A (31:34)

Okay.

D (31:34)

Yeah.

A (31:34)

I mean, doctor said what I think.

C (31:37)

Like, the longer someone's been living with something, like, I've always been amazed. And that's another reason why in some of the, you know, phase three clinical trials, these jacket nippers, not much moved, because at baseline, you ask them the glqi, and they're like, yeah, I'm coping all right. Like, I've been dealing with this forever, and, like, let's see how this goes. This would be great. And so it's low to start. You don't get movement on it, right. And it kind of stays put. And so I think the longer people have dealt with it, even really severe alopecia areata, the more adjusted they get to it somehow, whereas it, you know, so it has something to do, I think, with duration of disease, too, that if you. And also, like, listen, you know, if you're a teenager, you're in your 20s, you're in your 30s, you know, you're trying to meet a life partner, you're trying to go out and have fun. You're trying, you know, you're just coming into your own. Right. You're dealing with this. It's a lot different than if you are, say, more settled. Now, that's not to say that everyone who's older is settled. That's because sometimes, complete opposite. But in general, you know, like, people sort of are, at bare minimum. Right. More comfortable in their own skin.

B (32:45)

Right.

C (32:45)

Than you are when you're younger, you have some life experience and you're. I think that all Contributes.

A (32:50)

Okay, all right, let's, let's, let's jump onto mine here. So this was quality of life in patients with scarring and non scarring alopecia. Exploratory cross sectional study. 510 patients split roughly 50, 50 between scarring and non scarring. 75% female, 25% male, 46 years old on average hair loss duration. The mean was six years. 42% of the patients had alopecia areata, 21% had FFA, 16% had LPP. About 10% had androgenics, some telogen effluvium, a little folliculase decalvans thrown in. And the interesting takeaway, quality of life was worse with non scarring alopecia, primarily AA compared to scarring alopecia and more anxiety and depression with the non scarring. But right. As you would have expected on dlqi, which we all agree is not the best measure for, for hair loss, the people with scarring alopecia, the, the one thing that they had a higher score on was symptoms. But everything else, so, meaning you know, pain, burning, blah, blah, blah, everything else to people with non scarring had higher scores. And it's, you know, I think, Marianne, you said this earlier. It's, it's the unpredictability, I think that makes this make sense because.

C (34:20)

Right.

A (34:21)

You would assume that somebody who's got hair loss and their head hurts and you're saying, oh, and it's never going to grow back. Like they should have more anxiety and depression than somebody who, it doesn't hurt. And you're like, hey, we get it to grow back. But it's, I mean, is this your experience that.

C (34:40)

Not at all. I mean I definitely think the AA patients, especially the ones that are actively progressing or kind of persistent, severe, they definitely carry a lot of anxiety and worry and all of that. But my scarring alopecia patients really do too because they, they don't know what's going to end. No one's studying their disease that well and there's no FDA approved treatments and they kind of feel like left hanging out in the wind like. But the one thing, and I might be wrong because it was just like, you know, yesterday I looked at the papers, but I thought the AA group here was younger too. And that was, I was going to say that 10 years or something.

B (35:20)

Yeah.

C (35:21)

And that was one thing that jumped out to me that like that might have played a role as well. Again.

A (35:27)

Yeah, that, that's so you, you don't feel like there's a Huge difference. Like it, it. Everybody hates it. Your scarring and the non scarring. It's not like the. Yeah.

C (35:39)

And my new young FFA patients are absolutely devastated. If I compare a brand new, you know, girl, a woman in her 30s with mild FFA and a new diagnosis to the same age kind of demographic coming in with a patch of aa, the FFA wins every time when it comes to, you know, concern and worry and, you know, all of that.

A (36:06)

Okay, so let's. I, I kind of want to open up a little bit more now to some general AA questions I've got. So, you know, one of the interesting questions, you know, when you're seeing somebody with AA that's bad enough to warrant a jack, do you have any rhyme or reason for why you would pick one over the other? Right. Or is it basically which one's easier for insurance to get on? We don't have comparative trials. Their data is close enough that I'm not comfortable saying one's better than the other. Do you have any rhyme or reason for picking one of the three over the others?

C (36:44)

Yeah. So the first thing is, you know, you might think a little bit about side effect profile. If someone, like crazy, if someone has, you know, crazy familial hypercholesterolemia, maybe you're leaning more towards, you know, ritle sitinib over barisitinib or duroxalitinib because it tends to not elevate lipids as much because it doesn't target JAK2 as much. If someone has baseline, like inflammatory bowel disease, hypersensitivity, urticaria, you know, You know, any GI sort of distress at baseline, I'm probably going to shy away from let fallo simply because you get 10% of the patients in clinical trials having diarrhea, and then you have about 4 to 5% having, you know, like, hypersensitivity reactions, urticaria, stuff like that. So those are some initial thoughts I have. Other than that, you know, I think baricitinib is really great. They've done a very good job at showing their safety profile not just across AA patients and their large, you know, clinical trials, but. But also we have data from the rheumatoid arthritis population. Right. We have data from COVID We have all this data globally. So there's a lot of safety. So for patients who tend to be more tentative or worried, I'll usually start there. I also like that you have a two and a four that you can kind of titrate up, titrate down. If people don't want to be on the full dose long term sometimes though. More recently I've had patients who say have had a partial response or haven't done well with baricitinib or Litfullo. I think there is something about the bid dosing with Duruxolitinib and tofacitinib that some patients just need the dose pushed a little bit more. And I think, you know, being able to do that with Xeljanz or with Luxelvi can be helpful in some cases.

A (38:41)

All right, next is how long. So we've talked about a few articles over the last year and basically my takeaway has been you give somebody six months if they're not showing really good regrowth and progressively getting better, six months is probably a reasonable cutoff for like let's switch to a different drug. Is that, do you have a, like how, how do you decide when to switch in somebody who's not a home run?

C (39:11)

Yeah. So it really depends highly on baseline severity. If someone has complete scalp hair loss at baseline, I'm giving them a year. I'm giving them at least nine months.

A (39:23)

Before you would, before you 100%.

C (39:27)

You switch sooner and it's not the new med, it's longer time on a jack usually. So hopefully under review at the JAT we have a multi site study that we did. Hundreds of patients looking at Jackie switching and all of them had to be on the original Jackie for at least six months or more. And we break it down by how long they were on the original Jackie. But you got to give people time to be able to respond, especially if they're severe, if they're less severe, if they're more like a 50 salt, then yeah, by six months I'm like hoping to see something. I still might give them up to nine months but usually by then I'm hoping to see a little bit more.

B (40:09)

Okay, anybody you'd say, you know, we're going to give you a year. Do you ever like looking at some of the data? It seems like maybe out to a year you can start to see, you know, some regrowth. But I feel hard pressed to ever say this is worth continuing. Greater than a year.

C (40:25)

Yeah, greater than a year is tricky unless they really start showing some movement at like month nine or something. Month.

D (40:30)

Okay.

C (40:31)

Otherwise it's, it's tricky. It's, it's unlikely it's going to do much.

D (40:35)

Do you ever think of maybe goosing the effect a little bit with corticosteroids? Maybe six months, just some pulse, dexamethasone or a little bit of prednisone?

C (40:46)

Yep. I'll often, you know, give people who are like kind of moving but need a little push, always with minoxidil, obviously low dose oral minoxidil and then sometimes with like, you know, weekend pulses of dexamethasone or pred.

A (41:02)

So do you, so that's interesting, the minoxidil I've seen, you know, Brett King has published a couple of things about this and I've always been like, nah, I don't know, like, doesn't make sense to me. But I don't know, like, do you, do you do that in most of your AA patients when you start a jack, do you put them on oral medication?

C (41:21)

Unless they're sort of reluctant to take an oral medication to begin with and I'm not going to try to push them onto. But yes, almost always. And you know, back in the day when people had, you know, severe AA and happened to be on minoxidil for their hypertension, they regrew hair just on a, just on minoxidil rather. So, you know, it's not everybody. But I did have a patient of my own who had severe aa. She was allergic to steroids. It couldn't do steroids. I said, this is a Hail Mary but I'll give you Minoxidil. And she fully regrew the all of of her hair, which I was like, what is now it's an n of 1. But yeah, benefit to adding minoxidil when.

A (41:58)

You'Re doing it with a jack. What's your dose? Do you start at 2.5? Do you go to 5? What do you do?

C (42:03)

2.5 is the average starting dose in guys, I'll push it. And women, you know, you can go up to 5. I usually hover around 2.5 because when the hair hopefully starts coming in, then the facial hair becomes an issue for the women.

A (42:16)

Okay. Do you ever do. There's been a couple of reports now of clobatazole under a skit, under a swim cap to get to jump start it and then which you know is safer than do you would assume safer than doing like, you know, IMK or dex pulses, which I, I always thought, well yeah, but then once the hair grows a little, then the clobazole is not going to get to the scalp. But if they're starting on a jack, maybe it can jump start a bit.

C (42:44)

You know, I don't routinely do that. I wouldn't fault anyone who tried it. But like, I just feel like that Makes the patient so miserable. Usually if they're thinking about starting a track, their life is like, oh, like the last thing they want to do is be slobbering clobatas all on their head and going to bed with a swim cap. I mean, talk about really feeling like I've really hit a low point here, you know, So I try to think of the practical implications of it I'm telling people to do as well.

A (43:12)

Fair, fair. Patent fairs. You got any other burning AA questions?

D (43:17)

There was a paper, I think it was in one of our six packs, where it looked at basically patients who had been on multiple jacks, like tried multiple jacks.

C (43:26)

Just.

D (43:27)

It was not many patients, seven patients. But I think the, the last jack before they got the hair growth was a patacitinib more than it was any of the other jacks can. Do you have any feel of a patacitinib? And do you think that, you know, I kind of looked at that and said, well, maybe patacitinib is the most effective thing. Like, people went on a pat sit and after failing two or three and bang, all sudden they had the hair growth.

C (43:57)

Rate is like fleeting or just has completed phase three trials. Think a lot of people have a lot of hope in that. I mean, you know, I wonder sometimes how many of these patients have, you know, might be having ATP too. And so the JAK one really helps with that as well. The dosing on a patacitinib could also be a little bit better, depending on which dose they're treating with. Right. And then, you know, the other thing that I'm starting to toy with a little bit that can help some patients again, if there's some background AT B is like also combining with dupilumab with a jack.

B (44:32)

Do you think that works? I mean, obviously there was some early reports on that. And then it's like, ah, we have JAK inhibitors. But do you still do that?

C (44:41)

Now in my experience, like Emma Gutman's group, she's like, if the IGE, you know, baseline is over 200 or higher or and they have a history of ATP or family history of ATP, they regrow. That unfortunately has not been my experience. The times that I use it's patients I think it works best in, and it's amazing are people who have active moderate to severe atopic dermatitis, in my experience, and they regrow like crazy.

B (45:10)

And you don't combine it with a JACK inhibitor. You just do that and then we let them go. Okay, yeah.

A (45:16)

That is so fascinating. To me, because I think of AA as like, H1, TH1, and so Dupy should make it worse.

D (45:26)

Right?

C (45:26)

But you. If you have a heavy TH2 skewing with allergy and all this, and animal models, they've shown, you have a huge depletion in your Tregs, which we know is the case in AA, your Tregs also start acting like Th2 cells and drive the inflammation. So I think what happens is if you're really severe and you bring down that TH2, your tregs come back up and you have more homeostasis and your hair regrows. Whereas if you are. You're, like, kind of teetering. You're like, maybe you're a little genetically predisposed to getting aa. You haven't gotten it yet. You're. You know, your atopic dermatitis is mild, your T regs are more or less normal. And then someone gives you dupy, and you get rid of that TH2, and now you're like, TH1. You develop AA on dupilumab. So I think it's all where the patient's at when they start.

A (46:27)

Thank you. That's the first time anybody has explained that in a way that I buy.

C (46:31)

There's a commentary we did years ago in Jad on it. It's like, dupilia Mab, like friend or foe or something, you know? What are these?

A (46:39)

Okay. All right.

D (46:41)

Sherry Varghese, who I know is one of our loyal listeners, He. He actually sent me a photo within the last two weeks of a young atopic girl, alopecia areata. Brother was on doopie. She started doopie and has, like, a full head of hair. It's. It was impressive.

C (46:57)

It's amazing when it works. Yep.

A (47:00)

All right, Patton, let's. Let's do some trivia. So, Dr. Senna, the. The rule is you gotta let Pat finish reading the question, and then you shout out the answer as quick as you can.

C (47:12)

I'm gonna stink at this. I can tell you right now. You know what?

D (47:16)

This is the lamest category I've ever. We've had a few hair people on, so I have. I kind of exhausted my hair. Cool trivia. So I just. I just went really lame. So these are words. The answers are words that are spelled using the letters in alopecia areata.

C (47:35)

Oh, my gosh.

B (47:36)

Okay.

A (47:36)

All. All of the letters are these.

D (47:39)

No, no, no. They're. The words are made of letters. No, it's not all the letters.

A (47:44)

Okay?

D (47:45)

Like, if the answer was par, that would be the answer. Okay, got it.

C (47:51)

Is that one of them.

B (47:52)

That would be too easy.

D (47:54)

Okay, here we go. It's the only country that falls into this category.

B (48:01)

Peru.

D (48:02)

No, no, there's no you shoot.

C (48:06)

I was gonna say.

D (48:11)

I'll give clues in a little bit. So we don't like running.

C (48:13)

The only country is that.

D (48:14)

Dinner time.

C (48:16)

I'm gonna stick it.

D (48:17)

Yes. There's actually two, but if you go by this strict, you can only use like, L once. There's only one. It starts with a C.

A (48:31)

Now I can't even think of any countries to start with the letter.

C (48:33)

Cuba. Canada. Cuba.

D (48:40)

China. Second letter is R.

C (48:44)

Croatia.

D (48:46)

That's it.

A (48:48)

That's it.

C (48:51)

There we go. I only needed 85 clues to get it. All right, go me.

A (48:55)

That's pretty good.

D (48:57)

Oh, that was good. After two letters. That's very impressive.

A (49:01)

If this was Wheel of Fortune, you just won the jackpot pot.

C (49:05)

So what do I win, guys?

B (49:07)

Oh, nothing.

D (49:09)

Are undying admiration. That's right. She's worth more than any money amount. Yeah. This adjective could be used to describe the group of muscles that are strengthened by push ups and bench presses.

A (49:21)

Pecs.

D (49:23)

Pectoral.

A (49:24)

Pectoral.

D (49:25)

Pectoral.

B (49:25)

Yeah.

D (49:26)

Very good. Wow. All right, third and final. Oh, this is terrible. The number one hit song Mac the Knife was adapted from the opening song of a German musical whose name, when translated into English, means the three penny Blank.

C (49:46)

The three penny.

B (49:47)

What are we trying to figure out? What word goes in blank?

D (49:51)

Yes.

C (49:51)

A three penny blank.

B (49:53)

The three penny.

A (49:56)

Alpaca.

B (50:02)

That was like too many levels of bread.

C (50:07)

No.

D (50:11)

If it's a treat. If it's a musical, like, if it's a musical. If it's something on stage and people are singing, you could call it a microphone.

C (50:23)

A musical like people are on stage and singing. It's a musical.

D (50:31)

Like Carmen would be a more famous example.

B (50:33)

Opera.

C (50:34)

Oh.

D (50:36)

Oh.

B (50:36)

All right. That was good.

C (50:42)

That was so lame. There's so many A's there. Like string.

D (50:48)

Yeah, it's tough.

B (50:49)

All right, well, that was good. We each got one. Matt got the fewest clues, Marianne got the second fewest and I needed the most clues. So that's how we would. I would structure the winning on this one.

A (51:00)

Yeah.

D (51:01)

So, but like, points. Matt would win.

B (51:04)

Yeah.

D (51:05)

Because he had zero clues. But we don't do that. We don't play that way.

B (51:08)

We're all winners.

C (51:09)

We're all winners. That's what's so great about this. We all get a trophy.

B (51:12)

Exactly.

A (51:17)

Dr. Senna, thank you for coming on. This was so much fun. And I now feel much better about dealing with AA patients, so really appreciate you, and I really appreciate all of our listeners for tuning in. I hope you laughed once or twice, hope you learned a thing or two. But mostly I'm hoping that you're planning to join us again next week. And until then, I'm Matt Zyrus.

D (51:39)

I'm Tim Patton.

B (51:40)

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