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Dermbits

SCC June 2023

What is the best sunscreen to prevent skin cancer?

I love questions about sunscreen because I did one of the FDA studies along with Dr. Regal looking at high SPF sunscreen. And really, my advice for the best sunscreen is something that is a well known name brand, because those companies, those products go through much more rigorous testing. And then I also encourage my patients to use the highest SPF possible, because in that study, what we found is you were ten times more likely to get a sunburn on an SPF split face study on the SPF 50 side than you were with SPF 100. The reality is our patients, the general public, they don't apply enough sunscreen, and they often don't reapply so that higher SPF provides a greater level of safety. But at the end of the day, the best sunscreen is the one that you're going to actually use. And.

What are high risk features of cSCC?

What are high risk features for cutaneous squamous cell? Well, it really depends upon who you ask. There's, of course, the four from Brigham and women's. Is it large? Is it down to the fat? Is there perineural invasion, or is it poorly differentiated? But there's other important ones, such as immunosuppression, that they seem to have forgotten. That matters to me. And then also think about other pathologic features as well as clinical features, such as it's growing quite fast, or I care about whether or not there's nerve involvement. It's not always easy to find perineural invasion, but if you tap in the area and they're having some sort of sensation, then you know that guess what? The nerve is likely to be involved as well. So there are lots of high risk features. Years and years of experience really help us identify which features matter for us and for each patient. Thank.

Is SCC more deadly than melanoma?

You'll hear lots of talks about how deadly melanoma is, and it's true. But due to the sheer number of cutaneous squamous cell, there's actually more deaths from squamous cell than melanoma here in the US. It's a serious problem. And anybody who says they haven't seen a metastasis or a death from squamous cell, I think those patients, patients are following up somewhere else.

How do I order the 40-GEP test?

You. Ordering the 40 Gep test is actually quite easy. There's a simple order form. Oftentimes I'll get it from the rep, and when I get a new medical assistant, I'll pull down the folder and hand it to them and ask them to order the test. Usually they'll come back ten minutes later and we'll say, oh, I figured out how to order the test. And actually there's a portal, so it's even easier. So it is quite easy, and I encourage you all to give it a try.

Should I consider the 40-GEP test in lower risk patients?

You. The 40 GEP test is not just for horendomas or very, very high risk tumors. You also have to think about tumors that are perhaps, maybe not as high risk as we understand our staging systems over and under stages. And so it would be great if we could test every single squamous cell, but of course, that's not very feasible. So instead, I want you to consider those that have other high risk features, such as it was growing very fast or it was very large. If we think about, for example, the Brigham and women's criteria, there is published evidence or published data to show that even tumors that are t one, in other words, those that don't have the four factors found in the Brigham and women's criteria, the test, the 40 GEP, is able to identify three quarters of those patients that go on to have a metastasis. So it's not a needle in a haystack. It really helps identify even patients that are lower risk within the high risk cohort who is actually, it helps stratify those patients as well.

Which patients should be considered for the 40-GEP test?

You. The patients you should consider to utilize the 40 GEP are cutaneous squamous cell carcinoma with one or more high risk features. Now, what are those high risk features? There's a variety of them, and it was purposeful in this way because you and I may have a different opinion of what is high risk. I may think that perineural and agent is very important, but others may think actually, immunosuppression is what matters. So I would consider the utilization of this test for a broad group of squamous cell carcinoma patients.

How has the 40-GEP test been used by my colleagues?

You. What's great is that we have published one year data as to how you and all our colleagues are utilizing the 40 GEP. And I'll tell you, you've done a very good job with it. For the most part, the tumors that have been tested all have two or three or four high risk features. And as you get higher, such as 8910 different risk features, the number of tests drops dramatically because it's not going to change your management. So we've all done a very good job in selecting patients that are high risk, and we're trying to identify whether or not they're upstaged or actually lower risk patients.

Why has the 40-GEP test been validated on several data sets?

You. When it comes to geps, it's important to consistently and constantly validate the algorithms on a variety of data sets. You can't just have one because you may not be able to extrapolate it to your patient or other patients from other countries, for example. So it's always important to see multiple validation tests when it comes to geps.

How was the 40-GEP test developed?

You. The 40 GEP was developed for cutaneous squamous cell carcinoma with one or more high risk factors. How geps are developed is that you get a data set of a bunch of subjects with this tumor, in this case, squamous cell carcinoma with known outcomes, and then you evaluate the gene expression in these tumors and develop open algorithm that can help you predict or stratify the risk for these tumors.

How do GEP tests work?

You. It's in the name gene expression profile. So you take a tumor of interest, in this case, squamous cell carcinoma, and you're evaluating the genes, you're looking at the gene expression, so it's actually the rna, and you're looking at how far up and how far down that each is regulated, and also in relation to each other with that information. It goes through an algorithm which is then providing you with some sort of answer that will have a clinically actionable data point or information, and.

Incyte AD May 2023

Should you perform total body skin exams on patients to screen for skin cancer in patients using topical ruxolitinib?

You. I think you should screen patients for skin cancer if they are at high risk or of an appropriate age to be getting routine skin checks. I don't think that you need to do skin checks for every person that you prescribe. Topical rexillate nib cream for.

Is topical ruxolitinib still effective if only used once a day for atopic dermatitis?

Topical rexalitnib can still be effective if used once daily for AD. However, ideally a patient would use it twice daily to get maximal results.

Is topical ruxolitinib safe for use on the face, armpit or groin?

Topical rexalitnib is absolutely safe to use on the face, armpit or groin. It's great for these sensitive areas because it's not a steroid. So even for long term use, it's a great option for these areas.

Does topical ruxolitinib work for pruritus or pruritic disorders?

Topical rexalitinib can work for other paridic disorders and just generalized paritis. So it's not just for AD? It works great for any itchy disease.

What is the success rate of tralokinumab in patients who have failed dupilumab?

You. In my experience, patients who have failed dupliumab can definitely see results when treated with trallicinumab. So it's actually my goto. After a patient has failed dupliumab for the next line in treatment,

Does tralokinumab have a higher rate of conjunctivitis versus dupilumab?

Tralokinumab does not have a higher rate of conjunctivitis than dupliumab. However, the rate is also not zero. So it's great to try for patients who have had eye issues with dupiliumab, but just know that they might also develop conjunctivitis on traloquinumab.

Is it appropriate to reduce the frequency of tralokinumab in patients who respond to the medication?

You can consider decreasing the frequency of trollachinumab to patients who have responded well, but it's definitely not a requirement, and I oftentimes recommend to patients that they don't decrease the frequency because continuous dosing can help to decrease the number of flare ups and decrease the intensity of flare ups when they do have them.

Are there any complementary and alternative therapies which have data showing efficacy in the treatment of AD?

You. Unfortunately, we don't have a lot of studies on the use of complementary and alternative medicine for AD, but a lot of patients will anecdotally tell me that they get improvement with things like mindfulness and meditation, acupuncture, certain herbal supplements. So I think it's important to discuss with a provider who's experienced with these techniques to get a customized regimen and.

Do you recommend getting a CBC before using topical ruxolitinib in patients with a history of thrombocytopenia, anemia or neutropenia?

I think if the patients have a history of thrombocytopenia or anemia, you can consider getting a CBC prior to treating with rexalitinib cream. However, the risk of having any abnormalities related to just topical use with the JaCk inhibitor is extremely, extremely low.

What is the role of diet and environment in the pathogenesis of AD?

You. So diet and environment are important for patients with AD, especially patients who have known food sensitivities. So it's important for them to avoid foods that they know are going to trigger their disease. Things in the environment that could be important are things like temperature and humidity. So again, it's really important for AD patients to be aware of how their skin reacts to different environmental factors. It.

PrimusRX Psoriasis June 2023

What ingredients do you like to see in the products you use to treat plaque psoriasis?

You. I'm a general dermatologist and I have a busy extended patch testing clinic. As such, ingredient lists and specifically inactive ingredient lists are something I look at frequently. There are a number of ingredients common to the vehicles of topical therapies that are irritants or allergens, but one ingredient I actually do like to see in a product is diethylene glycol ether, commercially known as transcutol. Transcutol is an excipient and it enhances penetration and permeation of drug and importantly it does so with less reported irritation and allergenicity than other commonly used excipients. One topical approved for psoriasis that I use frequently, in part because it contains transcutol, is empoise the point 25% clobatazole cream. So while there are varying levels of evidence to support the use of active ingredients on the market, like a topical steroid versus a nonsteroidal, I think that to look solely at the active ingredient and to make a decision for treatment based only on that is to miss some of the story.

How important are vehicles in topical Plaque Psoriasis therapy? 

As Dr. Leon Kersick likes to say, vehicles matter. They're critically important for all topical therapy. Vehicles determine penetration, how much of the drug gets through the stratum corneum and permeation, how much of the drug stays in the skin and both of those contribute to efficacy. To that end, a topical that I frequently used because of its rationally designed vehicle which was formulated without propylene glycol and with an eye to enhanced penetration and permeation is sernivo, which is a 0.5% betamethasone dipropionate spray classified as medium potency but with data to show efficacy on par with augmented betamethasone lotion, a high potency steroid. Moving beyond efficacy, vehicles contribute to absorption and in the case of topical corticosteroids, absorption could contribute to HPA axis suppression and therefore are critical for safety. And lastly, vehicles can be an avenue for other side effects like stinging, burning, allergy, irritation and these things affect compliance. So yes, vehicles are important because they contribute to safety, efficacy and compliance and.

What common ingredients in topical therapies for plaque psoriasis may cause irritation for your patients?

You. As important to me as what's in a product is what is not in a product. An ingredient that is in many, many topicals used for psoriasis is propylene glycol, and propylene glycol is a well known irritant and allergen. In fact, the Journal of American Academy of Dermatology published a review in November 2019 of common allergens that are in topical corticosteroids, topical calcium inhibitors, and other topical immunomodulators. At least one allergen was found in 73.6% of the topical corticosteroids that they looked at. Among these allergens were things like methyl isothiozolinone, sorbitan derivatives, parabens, lanolin. But by far the most prevalent allergen found in these products was propylene glycol. 56.6% of the products reviewed in that study had propylene glycol in them, and roughly 4% of patch test patients are positive to propylene glycol, and that number is likely to be higher than 4% in patient populations with more cumulative exposure to topical corticosteroids that have used them chronically, like psoriasis and eczema patients, patients with sensitivity or allergy to propylene glycol or other common ingredients may find that psoriasis fails to improve or even worsens despite the application of a medication that typically improves such a condition. There's a fantastic list of generics in that review that do not contain propylene glycol. Again, I use empoise and sernivo because in my experience, they are by far the easiest propylene glycol free topical cord of steroids for patients to obtain. But any propylene glycol free product is less likely to cause irritation and allergy and therefore may be more likely to improve clinical outcomes.

Should we really care about systemic safety when treating Plaque Psoriasis with topical therapies? 

You, I think we should always be aware of ways to enhance patient safety. In particular, I think we might consider being even more vigilant in psoriasis patients who are already immune suppressed with a systemic biologic. In these patients, if they need adjunctive therapy with a topical, it might make sense to reach for a topical that demonstrates less systemic steroid absorption and therefore less risk for HPA axis suppression. That might be a nonsteroidal like topinoroff or reflumalast. Or it could be a topical corticosteroid that's formulated for less systemic absorption. Interestingly, a phase two study for empoise, for example, showed significantly less systemic concentration of clobatazol propionate when compared to clavatazol zero 5% cream.

How important is continuity of care for topical plaque psoriasis therapy? 

You again, as a practitioner who does a lot of patch testing, I'm coming at this from the perspective of allergic contact dermatitis and irritant contact dermatitis, and in those instances, continuity of therapy is very important. I referenced the review in another question published in the Journal of American Academy of Dermatology that showed that over 70% of topical corticosteroids contain wellknown allergens. And so if we look at that 70%, and if we know that patients might simply be getting whatever's in stock at the local pharmacy, a cream that was substituted for an ointment, one manufacturer versus another, then we should be a little concerned about patient outcomes. That lack of continuity of topical therapy could contribute to allergy and irritation, and therefore decreased patient confidence in your prescribing habits and.

How much time does your staff have to spend gaining patient access to medication for plaque psoriasis?  

You. I feel so bad for my staff that I really do all the prior authorizations myself. That's not even remotely true. I don't do any of them, but it is true that I feel bad for them because they spend a lot of time on pas, more so for biologic injectables and for the newer non steroidal topicals, and not just time spent. There's a lot of back and forth, and so there's multiple points of contact, even for one prescription for one patient, and that gets frustrating. And I do feel bad for them, and I think it's part of running a successful practice to help create a pleasant work environment. And in that case, I think it's important to consider the ways to minimize that type of busy work, obviously without compromising patient outcomes. In fact, I'll go a step further and say that I think actively limiting that type of work for your staff improves patient satisfaction during the office visit, and that in turn can improve patient compliance and patient outcomes as well. Framing that in terms of the two medications I've been talking about that I use frequently in my office, empoise and Serenebo. For these two, the prior authorization process is remarkably simple, and that adds to my desire to use them.

How do you utilize product samples in plaque psoriasis? 

You, samples are always nice, and patients always seem to appreciate them. Amazingly, I think there are a fair number of patients that see the provider and then never pick up the prescription. And in the case of patients that are so inclined, I think giving a sample and letting the patient see some improvement may increase their likelihood of actually filling the prescription. That's in the general sense, but in particular, it when you're prescribing a, a branded drug, that b has to be filled at a specialty pharmacy, I found that there can be a lot of patient pushback. Patients may be inclined reflexively to express a desire for the generic or for it to go to their local pharmacy. And so in this case, I find that samples are a very important hook. If you're serious about wanting the patient to have a branded drug because, for example, it doesn't contain propylene glycol, then I think samples are a must. All.

How do access, tolerability and efficacy improve compliance? 

You. Every practitioner learns the importance of setting expectations for clinical outcomes. Your acne is not going to get better in one week. Psoriasis is a chronic skin condition for which there is no cure. Topical amiquamod will cause a lot of irritation. In addition to setting clinical expectation like those, I find it's important for patient compliance and outcomes to set expectations for access. What does that really come down to? I like to be able to quote a price to a patient. Employees will be no more than $20. Sernivo will be no more than $20. And this is regardless of your insurance status. If I send a generic to the local pharmacy, it's hard to predict the cost. So that's the access part. Tolerability and efficacy are obviously important to patients, but maybe not so obviously. They're largely related to vehicle, though clearly not as catchy as Dr. Kersick's. Vehicles matter. I like to say that access plus vehicle equals compliance.

Which patients fit the profile for combination therapy of Biologics and topical treatment in Plaque Psoriasis?

You. I think every biologic patient fits the profile for combination therapy with a topical. Last I looked, the best data for POSI 100 scores was about 35% at twelve weeks and 50% at five years for an il 17 inhibitor. So in the short term, as patients are getting loaded onto the drug, and in the long term, as patients are getting full benefit from the drug, still at least one half of patients will not be 100% clear on a biologic. And even for those who are clear, sometimes there are intermittent environmental triggers that may result in a flare. So I routinely prescribe a topical for every psoriasis patient that I see.

How do you address compliance with your patients in topical treatment of plaque psoriasis?

You. Nobody likes surprises when it comes to medical care. Not the patient, not the practitioner. In the end, I encourage compliance by reaching for a product that is predictable. Predictable in terms of results, predictable in terms of ingredients, predictable safety and tolerability, predictable access, predictable amount of time spent by staff getting it covered for the patient.

BI Spevigo July 2023

What is Generalized Pustular Psoriasis (GPP)?

Generalized pustulous psoriasis, or GPP, is a chronic and often relapsing disease. It's a subvariant of psoriasis vulgaris, and it consists of widespread generalized pustulosis, sometimes superimposed on plaques. Sometimes it can occur on a background of erythroderma. These patients can very sick and require hospitalization, and others often will go and have a chronic relapsing, outpatient sort of presentation.

What is the clinical presentation of GPP?

The clinical presentation of GPP can be varied. There's two main presentations, one of which is plaque stage psoriasis, and then superimposed on these plaques are multiple monomorphous pustules. Additionally, other patients with GPP can have these pustules on a background of erythroderma, resulting in confluent lakes of us. And these patients oftentimes are very, very sick and require immediate attention and.

What are some of the systemic associations of acute GPP?

<p class="MsoNormal">Now, acute GPP can present with systemic manifestations. It can also be actually without systemic manifestations. But when we see GPP and systemic manifestations, we need to think very carefully, and watch for biochemical hepatitiso there's liver involvement. We could have renal involvement. Patients with generalized GPP can also have fatigue, anorexia, chills, rigors, often looking like an infection. So, we have to be suspicious when we see a patient with these systemic symptoms because those are the patients that do require immediate intervention.<o:p></o:p></p>

Who is at risk for GPP?

<p class="MsoNormal">Patients who are at risk for GPP can be really any patient, with or without psoriasis. So, interestingly, some patients will have a new onset of GPP. Classically, however, we see that it tends to be more common in women, and women of ages between 40, 50, 60. It is also more common in patients who have had plaque stage psoriasis in the past. The prevalence runs around 1 in 10,000 individuals.<o:p></o:p></p>

What are some known triggers of GPP?

<p class="MsoNormal">The triggers that are associated with GPP are varied. Some of them can be just stress, anxiety, or some that will really provoke a nuanced set of GPP. Other stressors are ones that we really want to be aware of and that's the acute or abrupt withdrawal of systemic steroids. And this can happen very commonly. Other triggers may include infections. They can also include drug reactions, so you want to think about all of those potential entities when we're looking at a patient who has suspected GPP.<o:p></o:p></p>

What is the pathophysiology of GPP?  

<p class="MsoNormal">The pathophysiology of GPP is very interesting. It does vary from plaque stage psoriasis. Now all of us are familiar now with the drivers of plaque stage psoriasis. We've learned IL-17, IL-23 can drive psoriasis. But it's a bit different in GPP. In GPP, what we see is extremely high levels of IL-36. IL-36 is an inflammatory cytokine which actually upregulates one of the innate immune response pathways, which then subsequently goes on to generate more IL-17 and IL-23. So, the target cytokine here is IL-36.<o:p></o:p></p>

How does the pathophysiology in GPP differ from plaque type psoriasis?  

<p class="MsoNormal">Now since GPP has, as its driver, IL-36, that's a little bit different than our classic plaque psoriasis. When IL-36 is overexpressed it then will bind to the IL-36 receptor, which is on the cell surface of all of our cells and as a consequence of that, they go in and activate this innate pathway which runs through NF Kappa. B. We see elevated levels of IL-36, so you think well, “So what?”, IL-36 drives neutrophil recruitment. Neutrophils come massively and infiltrate into the dermis and the epidermis resulting in pustules. And actually those pustules then go on to become confluent lakes of puss.&nbsp;<o:p></o:p></p>

When evaluating a patient with suspected GPP, what other entities does one need to exclude?

<p class="MsoNormal">When you're evaluating a patient with GPP, you have to think about other entities besides GPP. We have to think about infections, that's a common cause of pustulosis. We have to think of pustular drug eruption such as ajab. Those are also very common. Occasionally when you have this common sort of confined GPP, that is, pustules on plaques, we have to think of even folliculitis. So those are common things that should be running through your head when you see a patient who has suspected GPP. Oftentimes a biopsy is the best way to exclude these other entities. As well as a careful history. History can often direct you to the diagnosis of GPP.<o:p></o:p></p>

What are some of the common laboratory abnormalities associated with GPP?

<p class="MsoNormal">When you have a patient with GPP, especially those with systemic symptoms and those who are very systemically ill, those with fever, chills, erythroderma, we have to think of other things that can occur and make this disease worse. Comorbidities such as renal insufficiency, liver abnormalities are all associated with the GPP. Additionally, electrolytes can be very much out of whack with GPP, so we do see hypocalcemia very commonly in GPP. We also see, as sort of pathognomonic, a neutrophilia in the blood component. So when you get a CBC with the dip, you'll see an absolute neutrophilia or lymphocytosis and those are little characteristic abnormalities that should direct you more towards GPP than other potential differential diagnosis.<o:p></o:p></p>

What are treatment options for GPP?

<p class="MsoNormal">Now the treatment options for GPP have been woefully inadequate until this very past year. In the past, we've used systemic agents such as retinoids, we use cyclosporine, methotrexate. Even we've used in the recent past biologics. These do not adequately capture response with GPP. Currently we have a new agent called spesolimab or brand name Spevigo which has been very useful in treating GPP. In fact, it is fabulous in terms of its rapid response. GPP is run by IL-36. Well spesolimab targets IL-36 receptor gene antagonists and blocks the production of IL-36 which then decreases your neutrophils in the dermis, so we see a rapid clearing with this drug and this is fast going to become the treatment of choice for generalized pustulosis.&nbsp;<o:p></o:p></p>

What is the safety profile for spesolimab?

<p class="MsoNormal">The safety profile for spesolimab is actually quite excellent. There are very few things that we have to worry about. There's nothing to monitor pre-treatment other than your monitoring that you're doing for the baseline work-up. When we give spesolimab, we don't have to pretreat with Tylenol, Benadryl or anything like that. It is a very easy treatment - IV over 90 minutes. We can do it as an outpatient or an inpatient. Mainly people may complain a little bit of fatigue, nausea, sometimes a little bit of burning and stinging, but it's really a very, very safe drug and patient patients tolerate it quite well.<o:p></o:p></p>

Arcutis Zoryve July 2023

How quickly do patients experience clearance results with topical roflumilast?

You. I'm excited to say that with a once daily application, that's its formal indication and in a pretty elegant cream base, that my own experience so far has been that patients actually like to use, which is sort of a rare thing, that patients, not only will they tolerate it, not only will they sort of put up with it and adhere to it, but they'll actually tell me they like it. They like the way it feels. But we can see in the trial data in particular, dermis one and dermis two, that you can see itch relief that's clinically meaningful as early as week two, and some of the primary endpoints were early as week eight. You could really see this statistical difference from the vehicle. In my own experience, it's really as fast as a couple of weeks to see fairly dramatic change, but that continues to improve over time. So I definitely encourage people to stay with it. And I think that to see complete clearance for the majority of people might take a couple of months, especially if those plaques are thick. But they're going to be encouraged because you're going to start seeing improvement very early on. If.

How would you describe the overall tolerability of topical roflumilast? 

You. I am very tuned into my patients in terms of what they like and what they don't like to put on their skin. And I often joke that it is a very rare thing indeed for someone to call me, to seek me out, to tell me that they like something. Typically, those after hour calls are going to be that something is stinging, burning, uncomfortable. They didn't like it. They couldn't get it because of insurance issues. But it is a rare bird when someone calls and says, hey, really like this? This is really nice. And I have to say that with topical reflumolast, its formulation is such that I've had a number of patients call me and tell me they like the way it feels. Even people who are very, very sensitive, I have a lot of overlap. Patients who might have very sensitive skin, some features of atopic dermatitis, some features of psoriasis. A lot of times they have tolerability issues. This is one of the few things that I feel quite comfortable with saying, go ahead and try a small area first, of course, but in general, I've been extremely happy.

What is the long-term safety and efficacy data of topical roflumilast?

You? Well, the safety and efficacy data we have until now goes out to a year, and hopefully, as the drug is on the market, we will have it for longer. So far, it looks like a very benign drug.

How has topical roflumilast simplified the way you consult patients with plaque psoriasis? 

You. I think that for psoriasis patients who are more mild to moderate disease, I think this can be tricky, because many times, if they have a lot of body surface area, that topical medicines aren't going to be an option. Well, we're going to jump right to a systemic therapy. But for those patients that have more localized disease that really want to stay with topical options and maybe aren't eager to go to the bigger guns, the systemic agents, it's tricky. We only have a couple of things in our toolbox, and one of those is topical corticosteroids, which essentially 100% of my patients have used or are using, but they're not the panacea. And part of the problem with topical corticosteroids is that people can overuse them and damage the skin. So I'm really excited to have a once daily non steroidal agent that we can use, even in intratrogenous areas and delicate skin. And I love the fact that I can use my steroid to get things calm, use it if we have a bad flare up, but then we can use a non steroidal agent to help maintain, not only is it once daily, which makes it really nice, it's very, very nice vehicle. It's cosmetically elegant. And what I love about it is the safety profile is extremely reassuring. So what I'm hearing back from patients is that this is sort of what they've been looking for, that they have long needed something else in that toolbox so that they could not always rely on topical steroids or be told that they have to go on a systemic agent like a biologic. And arguably, this isn't maybe that many patients. There's a lot of patients who are comfortable doing both of those things, but it's a sizable group of people. And what I love is that as I get more experience with it and I get more positive feedback, well, that's a virtuous cycle. That's a positive feedback loop, because then the next patient comes in and says, is there anything else besides triumphsinolone? I can say, yes, there is. We have a couple of new things, things to try, and this is one that I really like. Why don't you see how this feels? Why don't we try this out? And I love being able to give people options, because the hardest part for me is that not everybody is the same. There is really no one size fits all. And it's very frustrating when you have one dominant drug or one class, and it's sort of, well, this is a standard of care. Yes, it is. It's a great place to start. But what about for all the people for whom it's not a good fit? And that's why I'm so grateful to have new tools.

How would you present the product profile of topical roflumilast to HCP colleagues who are reluctant due to poor prior experience with other PDE4 inhibitors?

You. This is a very interesting question, because I have to confess, full confession here is that while this product, the topical reflummalast, was being developed, I honestly wasn't very interested in it. And in part it's because we, of course, already have a topical phosphodesterase four inhibitor in dermatology. That's chrisoborol, and I think Chrisoborol is fine. It's a good medicine. It has been a nice addition for certain patients, but it's brought with it some baggage. Right? It really does. It has the issue that it hasn't been extremely powerful for most of my patients. In fact, many of my patients felt like it didn't do very much at all. And of course, we crossed that with the fact that post marketing, now obviously in the trials for chrysoborol, it wasn't a very high number of people that experienced stinging and burning. But post marketing, a lot more of my patients did report that, some to the point where they wouldn't use it anymore. Now that, again, could be my particular demographic, the people that I'm seeing and so on. But I think that was not that unique of an experience. And when I've talked to other colleagues, they haven't had the greatest experience with topical PDE four inhibitors in the past. That being said, once it came to market, and once I was able to try a sample and give it to a few patients, I've really flipped around. I've turned to 180 on this because I find that not only am I getting an efficacy that is the next level up, something that I think is much more robust and much more meaningful for patients than I had seen in the past, but I'm also seeing a tolerability that is really, really reassuring. In fact, now I feel it's one of the most tolerable things that I give out. And that says something again, because I have kind of a unique group of patients. So that's my language. I want stuff that obviously works well, but it also has to be safe and tolerable, and it's that very difficult tightrope to navigate. And I think topical reflumalast has really done a beautiful job with that so far. And of course, I'm still learning. I've only been using it for a few months, but as my experience accrues and I keep getting follow ups, it shapes you. If patients say, I didn't care for this one, that one didn't work, that one stung and burn, you sort of move away from that. If patients say, hey, I really like that one. Can I get a refill? Can you make sure I have more of it? That actually encourages you. You really do change your practice style depending on that feedback. Especially if you're in the trenches every day talking to people that have unmet needs.

When it comes to treating thicker plaques on hands and feet, why should you consider Zoryve instead of steroids?

You. So one of the nice things about our non steroidal agents, and in particular topical reflumolast, is that it's a pretty small molecule. Now, what's neat about these PDE four s is they actually have to get inside the cell. And to some degree, this can suggest that they can. Obviously, if they can penetrate into a cell, they can actually get through the skin barrier pretty well as well. And obviously, this depends a lot on the formula relation. So that is not operating true by any stretch. But the formulation here is kind of ingenious, and it's formulated in a way that really does get excellent penetration of the skin, including thicker plaques, including thicker areas like hands and feet. And it does so in a way that I think we can see the bioavailability is extremely high. So the drug can get to where it needs to, even in the presence of thick psoriatic plaques or those hands and feet. So that, to me, is a huge, huge issue, because many medicines, if they don't penetrate well, will often have to sort of pretreat. We can use a topical steroid or light therapy or something else, maybe eczema laser. You want to shrink those plaques, get them down, and then you could use something. And I do that a lot. That's what we've had to do. But it's kind of exciting and empowering that maybe for one of the first times, we can say, look, we can potentially even issue using a steroid every time to get the scaling down. And this might actually be enough by itself to do that. On the other hand, I'm more than comfortable using both. And I think that most of my patients, if not all, with psoriasis, are going to have multiple options, and they're going to use different things at different times. So while I think it could be a standalone, particularly for somebody that's maybe had an adverse experience with topical corticosteroids or soberus them in an area, I still think it's something that could be used intermittently as part of a rotational approach, as we do with many other things. Penis.

What are your thoughts on topical roflumilast as becoming standard of care and gradual shifting away from topical corticosteroids?

You. So this is a controversial question, and I think that to some degree, topical corticosteroids are going to be the anchor. They're a keystone of dermatology, and it's going to be very hard to push them out of that position for a long time. And there are a few reasons why. The first reason is that we have an unparalleled amount of experience with them. We have really more than 60 years of experience with them in the real world world. So we know a lot about them. The devil that you know versus the devil that you don't know. The second is that they are incredibly accessible. Almost everybody can afford a topical steroid. Almost every insurance plan, be it government sponsored or private insurer, is going to cover that. Or even if they can, a cash pay patient can often spend what usually amounts to less than $10 or $20 to get a fairly large quantity of topical steroid, at least ideally. Sometimes there are shenanigans that happen, but they're very accessible. And then the third piece is that I do think they can be used very, very broadly. Almost every single patient you put a topical steroid on, they are going to see some improvements. So just the fact that they are broadly applicable means that they're hard to beat. That being said, essentially 100% of my patients have been on at least one, sometimes multiple, topical corticosteroids over the months or years leading up to the time when they've seen me. And many times they're very frustrated. They've been given the same prescription over and over. Maybe they've had a side effect. Maybe they're concerned about side effects. And so I really think that if not, if, we can't bump them from the first line, and again, that may not even be appropriate. I really would like to get people thinking about the next step. So for the mildest patient who does use just a little bit of topical steroid intermittently, leave it be. I don't think I have a beef with that. That's fine, but it's for the patient that either is overusing the steroids, constantly needing them, and maybe isn't even getting to where they need to be in terms of safety. It's like if I put it on every day for two months, yes, those plaques improve, but then as soon as I stop, it's right back. So I'm basically putting on high potency topical storage continuously to an area of skin, which I think is a bad idea. So I'd like to avoid those. Or for people that have maybe had an issue and don't want to use them. And I have to respect that. I think obviously if costs were the only consideration, then the answer would be no. But I think that we're a little bit more sophisticated than that. It's not just a cost basis for how we make decisions for healthcare. It's a shared decision making process. And I have a lot of patients who are concerned about steroids. Now sometimes the answer really is a steroid. If they're using a lot of other non steroidal things and are still struggling, I say, listen, I think we need to think about incorporating those. But for a patient who's maybe mild or moderate and is responding to a non steroidal agent, I think it would be really nice for a patient who says, listen, I've had some issues or I have some concerns about steroids, I'd like to go non steroidal. And I really do think that for those patients, they potentially could use monotherapy with non steroidals. And increasingly so as we get newer and better ones. So it might not even just be one non steroidal agent. Perhaps we're going to pair it with other things, or again, this rotational therapy, maybe they'll do phototherapy for a while and then use one of these non steroidals. So we have some options for that.

How do you approach management of plaque psoriasis in challenging sensitive areas?

You. So it's true that some of these more delicate areas, like the intertrignous areas and the genital skin and facial skin, these can be tricky. And these are areas that I really like to minimize topical corticosteroid exposure. It doesn't mean I don't use them. I do. But it's one of those places where I think you can see people get in a very vicious cycle where they're needing to use an awful lot of steroids, sometimes increasing their dose for a long time in a way that I don't think is safe. And I've, over the years, inherited patients that have quite impressive stria that is now, of course, permanent or skin thinning and atrophy, where you say, boy, you really need to stop using it. Here we've seen people get folliculitis from it. We've seen fungal infections that have been inappropriately treated with steroids. So I think we have to keep an eye on that. And for some patients, it's going to be enough. But for many patients, I really like to incorporate non steroidal agents in whenever we can. And again, it doesn't mean we have to replace them completely, the steroids, but ideally we're going to minimize their use only for if the non steroidal can't manage it. But with something like topica reflumlast, I've found that actually it can. It can do a great job, especially in these more sensitive skin areas as a monotherapy. And I think that's a win win. I also like the fact that for many of my patients, they tell me I don't have to use it all the time. I can use it for a bit. When I'm better, I take a break, like. So again, they're intermittently using even this more safe category, which I really love. My goal is to be using as little medicine as possible to get people to where I want them to be, which is ideally clear or almost clear all the time, or most of the time, and feeling really good about their treatment, therapy and.

How important is inclusion of younger ages - adolescent or pediatric – when it comes to indication for plaque psoriasis treatments?

You. So my practice is about 50% pediatric, and I'm often thinking about my littler kids, my adolescents, along with those adults. And I think for me, not only is it really important to have treatments that are formally indicated for kids, because I think it really tells us that it has been studied in there, that it is safe and effective for that particular group. And we know kids are not just little adults. Sometimes they are, but in some ways they're not. And so it is nice to see things that are specifically studied. And I think the FDA has been so good about that in the last few years and increasing that to kids. You know, we need to treat kids. They really do get problems, and we can't just keep brushing it under the rug and saying, well, I guess we can try things off label in adults. It's just not ideal. So I love to see that we're now getting formal studies in kids. The other win for that situation. Not only then do we have something indicated for the appropriate age group and understand it well enough to talk to the patients and their families about it, but I think it also is incredibly reassuring for the older age groups. When I tell a patient that, hey, this has been FDA approved for the same condition in children, you often see their shoulders relax. They say, oh, cool, that's great. This tells me that not only has it been studied again, right, because we know each study opens up a potential can of worms, both safety and efficacy and all the issues that can come up, but if it's passed that test over and over and over, that reproducibility, and in a group of patients, that tends to be a little bit more sensitive and with maybe a lower threshold for getting concerned about side effects. Right. The kids, we don't have the same tolerance for letting things go awry. That can be incredibly empowering and I think very, very reassuring to all of us. I mean, when we give a patient a medicine, right, we're all on board. You know where to find me. We're responsible for this as well. So it's not just that I'm not trying to hurt people. I'm not. But I also would feel terrible if I did. Right. It's really both of those things. So I feel more empowered when we see things that are approved in younger ages. And in fact, some of our treatments, for example, in atopic dermatitis, we've seen them, adults, then adolescents, then children, and now down to babies. That is so reassuring to me. That's what I'd like to see for almost all medications that are appropriate, because then we really can feel good about using it for whom we need it. And even if we don't needed in that young group, I think it still informs us about the older age groups. So really nice and.

When augmenting oral and/or biologic therapy with a topical, what are some of the considerations you think through?

You. I would say that 100% of my patients who are on a systemic therapy, be that an oral medicine, phototherapy, or a biologic, 100% of them are also going to be on concomitant topicals. Now, my hope is they're going to be using them much less frequently to much less body surface area than they were before. But I have almost no patients who are literally perfectly clear on their system. Agent don't need anything at any point in the year. Sometimes it's just a few weeks, or maybe they're like, boy, my elbows are getting really dry in the winter. I'm going to use something. So I do. I mix and match quite a bit. And in general, we have a pretty long leash. There are not too many specific contraindications to our topicals and systemics, although some insurance companies have pushed back. Of course, if you're using a very expensive biologic agent and a very expensive topical, that can be a real issue. So we try to be cognizant of that. And if someone doesn't need a more sophisticated topical, it may be fine to use something that's inexpensive or accessible and even over the counter treatment. I'm a huge proponent for OTCs because I think that optimizing our OTC treatment can be incredibly safe and incredibly effective as part of a regimen minimizing the need for other systemics or other topical agents that are medicated and truly prescription based.

Castle SCC August 2023

What is the 40-GEP test?

<p class="MsoNormal">The 40-GEP test is a test using gene expression profiles to assess prognosis with squamous cell carcinoma. It's a new approach and the advantage is, in the past we've used clinical histologic factors to try to assess prognosis, this gives us an extra dimension using genomics to better assess prognosis.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Darrell Rigel explains that the 40-GEP test is a new approach to assess prognosis with squamous cell carcinoma. The test utilizes gene expression profiles (genomics) to provide additional information beyond traditional clinical and histologic factors. By incorporating genomics, the 40-GEP test offers an extra dimension to better evaluate the prognosis of patients with squamous cell carcinoma, potentially leading to more accurate and personalized treatment decisions.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The 40-GEP test is a test that utilizes gene expression profiles to assess prognosis in cases of squamous cell carcinoma.&nbsp;</li><li>It represents a new approach in contrast to the traditional method of using clinical and histologic factors to determine prognosis.&nbsp;</li><li>The test offers an advantage by introducing genomics as an additional dimension to improve the accuracy of prognosis assessment.&nbsp;</li><li>The term "40-GEP" refers to the specific gene expression profile that is analyzed in the test.&nbsp;</li><li>By incorporating genomic information, the 40-GEP test aims to provide a more comprehensive and precise evaluation of the prognosis for squamous cell carcinoma patients.</li></ul>

Why do we need to better assess SCC prognosis?

<p class="MsoNormal">Squamous cell carcinoma is a serious disease. Even cutaneous squamous cell carcinoma. And people do die from this disease. It's important that we can assess prognosis so that we can accurately determine what patients need further therapy along the way.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Darrell Rigel discusses the significance of better assessing the prognosis of squamous cell carcinoma (SCC), including cutaneous SCC. He emphasizes that SCC is a serious disease and can lead to fatalities. Therefore, it is crucial to have an accurate prognosis assessment to determine which patients require further therapy. Understanding the prognosis allows healthcare professionals to provide appropriate and timely treatment for those affected by SCC.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Squamous cell carcinoma (SCC) is a serious disease, including cutaneous squamous cell carcinoma, and it can lead to fatalities.&nbsp;</li><li>Accurate assessment of SCC prognosis is essential to determine the appropriate course of action for patients, including the need for further therapy. &nbsp;</li><li>Prognosis assessment helps in identifying high-risk patients who may require more intensive treatments and monitoring. &nbsp;</li><li>Early identification of patients with poor prognosis can potentially improve outcomes and increase survival rates.&nbsp;</li><li>Tailoring treatment plans based on prognosis can help avoid over-treatment in low-risk cases and provide more aggressive approaches for high-risk cases.&nbsp;</li><li>Monitoring prognosis allows healthcare professionals to make informed decisions and adjustments in treatment strategies as the disease progresses.&nbsp;</li><li>Improved prognosis assessment contributes to a more personalized and effective approach to managing SCC patients.&nbsp;</li><li>Research and advancements in prognosis assessment may lead to better understanding of SCC's behavior and potential new treatment options.&nbsp;</li><li>Overall, accurate prognosis assessment is crucial for enhancing the management and outcomes of individuals with SCC.</li></ul>

How does the 40-GEP test work?

<p class="MsoNormal">The 40-GEP test works using 40 genes, basically to assess prognosis and the degree of expression of those genes in combination with a proprietary formula, helps us better assess the prognosis in terms of whether patients will be in a low risk group, a medium risk group, or a high risk group, and therefore adjust our therapy accordingly.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Darrell Rigel explains how the 40-GEP test functions. The test involves the analysis of 40 specific genes to evaluate their expression levels. These genes are used in combination with a proprietary formula to determine a patient's prognosis. Based on the results, patients are categorized into low-risk, medium-risk, or high-risk groups. This classification helps medical professionals make more accurate assessments and tailor the appropriate treatment plan accordingly.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The 40-GEP test utilizes 40 specific genes.&nbsp;</li><li>Its primary purpose is to assess prognosis in medical cases.&nbsp;</li><li>The test evaluates the degree of gene expression in combination with a proprietary formula.&nbsp;</li><li>The evaluation helps categorize patients into different risk groups: low risk, medium risk, or high risk.&nbsp;</li><li>The results of the test allow healthcare professionals to tailor treatment plans based on the risk group the patient falls into.&nbsp;</li><li>By understanding the patient's risk level, the therapy can be adjusted accordingly to optimize treatment outcomes.</li></ul>

What SCCs are appropriate for the 40-GEP test?

<p class="MsoNormal">It's important to understand that not every squamous cell carcinoma is appropriate for this test. The data on this test was collected on advanced squamous cell carcinomas. This is not for squamous cell carcinoma in situ. It's not for early squamous cell, but it's for squamous cell that have at least one of the high risk factors, diameter, depth and other risk factors for advanced disease.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In this video, Dr. Darrell Rigel addresses the question of which squamous cell carcinomas (SCCs) are suitable for the 40-GEP test. He emphasizes that not all SCCs are appropriate for this particular test. The data used to develop the test was gathered from cases of advanced squamous cell carcinomas, specifically those that have at least one of the high-risk factors such as large diameter, significant depth, and other risk factors associated with advanced disease. The 40-GEP test is not intended for use with squamous cell carcinoma in situ or early-stage squamous cell carcinomas. Instead, it is specifically designed and validated for cases where there are indicators of advanced disease.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>SCCs (Squamous Cell Carcinomas) that are appropriate for the 40-GEP (Gene Expression Profiling) test are specific types of cases.&nbsp;</li><li>The test's data was collected on advanced squamous cell carcinomas, which means it is not suitable for squamous cell carcinoma in situ (early stage) cases.&nbsp;</li><li>It is specifically designed for squamous cell carcinomas that have at least one of the high-risk factors associated with advanced disease.&nbsp;</li><li>The high-risk factors include diameter, depth, and other risk factors that indicate the likelihood of the carcinoma being in an advanced stage.</li></ul>

How do you discuss 40-GEP test results with patients?

<p class="MsoNormal">When I get a result from the 40-GEP test, it's important that I have a frank conversation with patients. What's interesting about these results, it's fairly easy for the patient to understand because there's three levels of risk: low, mid risk, and high risk. Depending on where the patient falls, I will have that discussion with the patient and the idea behind this is using the degree of risk and prognosis, what I can do is talk to the patient about whether additional therapy is needed. Whether we need adjuvant radiation, whether we would use some cemiplimab or a PD1 or more advanced disease. But a low risk patient, I can say with pretty surety, that in fact there's no need to do advanced treatments or other things more than just following the patient close.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>Dr. Darrell Rigel discusses how he approaches the discussion of 40-GEP (Genomic Expression Profile) test results with his patients. He emphasizes the importance of having a frank conversation with the patients about their test results. The 40-GEP test results are relatively easy for patients to understand because they are categorized into three levels of risk: low risk, mid-risk, and high risk. Depending on which risk category the patient falls into, Dr. Rigel tailors his discussion accordingly. For patients with low-risk results, Dr. Rigel can confidently inform them that there is no need for advanced treatments or additional therapies beyond close monitoring. However, for patients in the mid-risk or high-risk category, he may discuss the possibility of additional therapies such as adjuvant radiation or the use of specific medications like cemiplimab, PD1 inhibitors, or other more advanced treatments. The primary goal of discussing these test results with patients is to provide them with a clear understanding of their risk level and prognosis. This information allows for informed decision-making regarding the necessity and potential benefits of further treatment options, ensuring the best possible care for each individual patient.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>40-GEP test results are easy for patients to understand as they are categorized into three levels of risk: low, mid risk, and high risk.&nbsp;</li><li>The degree of risk and prognosis are used to determine whether additional therapy is necessary, and the doctor should tailor their discussion with the patient accordingly.&nbsp;</li><li>Treatment options discussed with mid to high-risk patients may include adjuvant radiation, cemiplimab, PD1 inhibitors, or more advanced treatments.&nbsp;</li><li>For low-risk patients, the need for advanced treatments is deemed unnecessary, and close patient monitoring may suffice.</li></ul>

Is the 40-GEP test covered by Medicare?

<p class="MsoNormal">At this point there is insurance coverage in some of the cases, the different Medicare coverage carriers have different rules at this point. At some point that will be solidified. The company, however, does accept insurance, whatever the insurance payment is, and there's no additional payment for the patient. And that makes it much easier in terms of working with the patients to try to get the results of this test.<o:p></o:p></p><p class="MsoNormal">&nbsp;</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Darrell Rigel addresses the question of whether the 40-GEP test is covered by Medicare. He explains that currently, there is insurance coverage available for some cases, but the specific coverage rules may vary depending on the Medicare coverage carrier. He mentions that over time, the coverage for the 40-GEP test is expected to become more clear and standardized. Dr. Rigel also mentions that the company offering the 40-GEP test accepts insurance as a form of payment. This approach is designed to make it easier for patients to access the test results without facing financial burdens.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The 40-GEP test may be covered by Medicare, but the coverage is not consistent across all cases.&nbsp;</li><li>Different Medicare coverage carriers have varying rules regarding the 40-GEP test's insurance coverage.&nbsp;</li><li>The insurance coverage situation is expected to become more clear and standardized at some point in the future.&nbsp;</li><li>The company conducting the 40-GEP test accepts insurance as a form of payment from patients.</li></ul>

What are the traditional SCC prognostic paradigms?

<p class="MsoNormal">Typically, when we assess prognosis and squamous cell carcinoma, what's typically used is the AJCC criteria or the Boston Women and Brigham’s criteria and those basically are looking at clinical and histopathologic factors whether it’s a diameter of the lesion, whether it's the perineural invasion that's involved in a variety of other factors like that. But we're not really seeing the genomics. And that's the advantage of the 40-GEP test. It gives us additional information we can integrate into prognosis to better and more accurately assess.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Darrell Rigel discusses the traditional prognostic paradigms for squamous cell carcinoma (SCC). Currently, the two commonly used criteria are the AJCC (American Joint Committee on Cancer) criteria and the Boston Women and Brigham's criteria. These criteria rely on assessing clinical and histopathologic factors such as the diameter of the lesion and the presence of perineural invasion, among other factors. However, Dr. Rigel points out that these traditional paradigms do not take into account genomic information. This is where the 40-GEP test comes into play. The 40-GEP test provides additional genomic information, which can be integrated into the prognosis assessment to improve accuracy. By incorporating genomic data, clinicians can gain valuable insights into the underlying genetic characteristics of SCC, leading to a more comprehensive and refined prognosis for patients. This advancement in prognostic evaluation may ultimately aid in better treatment decision-making and patient outcomes.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Traditional SCC prognostic paradigms: AJCC criteria, Boston Women, and Brigham’s criteria.&nbsp;</li><li>Assessment of prognosis for squamous cell carcinoma based on clinical and histopathologic factors.&nbsp;</li><li>Factors used in traditional criteria include diameter of the lesion and perineural invasion involvement.&nbsp;</li><li>Traditional methods lack consideration of genomics in prognosis assessment.&nbsp;</li><li>The 40-GEP test provides additional genomic information for better and more accurate prognosis integration.</li></ul>

What are the trends in US incidence of SCC?

<p class="MsoNormal">In the United States, cutaneous squamous cell carcinoma incidence continues to rise, especially in the southern half of the country. And that makes it increasingly important to be able to better identify patients at highest risk for metastatic disease and for death, so we could appropriately treat them with more aggressive therapy.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>Dr. Darrell Rigel discusses the trends in the incidence of cutaneous squamous cell carcinoma (SCC) in the United States. He states that the incidence of SCC is consistently increasing, particularly in the southern half of the country. This rising trend highlights the need to improve the identification of patients who are at the highest risk of developing metastatic disease and facing death due to SCC. By identifying these high-risk patients, healthcare providers can administer more aggressive therapies to appropriately treat the condition and improve patient outcomes.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Cutaneous squamous cell carcinoma (SCC) incidence is on the rise in the United States.&nbsp;</li><li>The increase in SCC incidence is particularly notable in the southern half of the country.&nbsp;</li><li>Identifying patients at the highest risk for metastatic disease and death is becoming increasingly important.&nbsp;</li><li>The goal is to treat high-risk patients with more aggressive therapy to improve outcomes.&nbsp;</li><li>The rising trend in SCC calls for improved methods of identifying and diagnosing high-risk patients.&nbsp;</li><li>Early detection and appropriate treatment are crucial in managing SCC cases effectively.</li></ul>

Who is the ideal patient for the 40-GEP test?

<p class="MsoNormal">The ideal patient to use this test on is one who has a more advanced tumor. The idea behind this, you're trying to identify those at highest risk for metastatic disease. If you have a class 2B result, which is the highest risk, your risk of metastatic disease is on the order of 50 to 60%. So therefore, you want somebody who already has an advanced tumor to some extent, who has other risk factors for this. It's not for somebody who has a squamous cell in situ or very early squamous cell, because the data was not collected on those people. It's for somebody for more advanced disease to really do the testing on.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>Dr. Darrell Rigel explains in the video that the ideal patient for the 40-GEP test is someone who has a more advanced tumor. The main objective of this test is to identify individuals at the highest risk for metastatic disease. A class 2B result from the test indicates the highest risk, with a likelihood of 50 to 60% for metastatic disease. Therefore, the test is most appropriate for patients who already have an advanced tumor and have other risk factors associated with it. The test was not specifically designed for individuals with early-stage squamous cell carcinoma or squamous cell in situ, as the data was not collected for such cases. In summary, the 40-GEP test is recommended for patients with more advanced disease and additional risk factors for metastatic progression.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The 40-GEP test is designed for patients with a more advanced tumor.&nbsp;</li><li>The purpose of the test is to identify those at the highest risk for metastatic disease.&nbsp;</li><li>A class 2B result from the 40-GEP test indicates the highest risk, with a 50 to 60% chance of metastatic disease.&nbsp;</li><li>The ideal patient for the test is someone who already has an advanced tumor to some extent and has other risk factors for metastasis.&nbsp;</li><li>The test is not suitable for individuals with squamous cell in situ or very early squamous cell cancer, as the data for the test was not collected for such cases.&nbsp;</li><li>The focus of the 40-GEP test is on patients with more advanced disease to provide meaningful results.</li></ul>

Why doesn't SCC get the respect it should?

<p class="MsoNormal">Well I think of SCC as being almost like the Rodney Dangerfield of skin cancer, where it doesn't get any respect. And part of that is because it's in the middle, it's like the middle child. The basal cell, not as much risk, melanoma a lot more risk. But you have to realize, when you look at the data, almost as many people die in the United States from cutaneous squamous cell carcinoma as due for melanoma. Now the percentage is lower because there's so many more contagious squamous cells. But the reality is people do die from cutaneous squamous cell, and that's one of the reasons we need to better assess prognosis.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video "Why doesn't SCC get the respect it should?" Dr. Darrell Rigel discusses the lack of recognition that cutaneous squamous cell carcinoma (SCC) receives in comparison to other types of skin cancer. He likens SCC to the "Rodney Dangerfield" of skin cancer, meaning it doesn't receive the respect it deserves. The reason for this lack of recognition is that SCC falls in the middle between basal cell carcinoma (which has lower risk) and melanoma (which has a much higher risk). However, Dr. Rigel points out that the data shows almost as many people die from cutaneous squamous cell carcinoma in the United States as from melanoma. Although the percentage of SCC-related deaths may be lower due to the higher prevalence of SCC cases, the actual number of deaths is significant. This underscores the importance of better assessing the prognosis of cutaneous squamous cell carcinoma to raise awareness about its severity and address its impact on public health effectively.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>SCC (Squamous Cell Carcinoma) is often overlooked and does not receive the respect it deserves.&nbsp;</li><li>One of the reasons for SCC's lack of attention is because it falls in the middle when comparing it to other skin cancers. Basal cell carcinoma is considered less risky, while melanoma is regarded as a higher-risk skin cancer.&nbsp;</li><li>However, Dr. Rigel emphasizes the importance of recognizing that SCC is still a significant concern. In the United States, the number of deaths from cutaneous squamous cell carcinoma is almost as high as that of melanoma.&nbsp;</li><li>The lower percentage of SCC-related deaths compared to melanoma can be attributed to the higher number of SCC cases overall (more contagious squamous cells).&nbsp;</li><li>Dr. Rigel stresses the need to improve the assessment of prognosis for SCC to better understand and address its impact on public health.</li></ul>

Lilly Olumiant AA August 2023

In what ways can alopecia areata affect quality of life?

<p class="MsoNormal">Yeah, well, I think alopecia areata can affect patients’ quality of life and like myriad ways. So obviously there's a debilitating effect of the embarrassment and the anxiety associated with having the hair loss. There's also the anticipation of future hair loss, and so maybe you have your wedding coming up and you don't know if the alopecia areata is going to restart leading up to that due to the stress triggers. And so, there's all of that quality of life impairment. But there's also functional impairment, which I don't think gets enough attention. So sweat getting into your eyes from eyebrow loss and things like that. So there's just all sorts of ways that can affect quality of life.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In this video, Dr. Michael Cameron discusses the various ways in which alopecia areata can significantly impact the quality of life of patients. He highlights that alopecia areata can have a debilitating effect on a person's emotional well-being due to feelings of embarrassment and anxiety associated with hair loss. Additionally, patients often experience anticipation and stress related to the uncertainty of future hair loss, which can be particularly distressing during significant life events.&nbsp;</p><p>Furthermore, Dr. Cameron emphasizes that the functional impairment caused by alopecia areata should not be overlooked. For instance, loss of eyebrows can result in sweat getting into the eyes, causing discomfort and inconvenience. Overall, the condition affects individuals in myriad ways, and its impact extends beyond just the physical aspect of hair loss, affecting both emotional and functional aspects of the patients' quality of life.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Alopecia areata can cause a myriad of challenges and impairments to overall well-being and daily life activities.&nbsp;</li><li>Hair loss from alopecia areata can lead to feelings of embarrassment and anxiety, affecting self-esteem and confidence.&nbsp;</li><li>The anticipation of future hair loss can cause stress and uncertainty is also negatively impactful.&nbsp;</li><li>Functional impairment is often overlooked, such as sweat getting into the eyes due to eyebrow loss.&nbsp;</li><li>The emotional and psychological toll of alopecia areata can be profound and should not be underestimated.</li></ul>

Are patients with alopecia areata more likely to have other dermatologic conditions? 

<p class="MsoNormal">They are, they are. So we see a lot of comorbid, for example, atopic dermatitis with alopecia areata, that's a big one. But these autoimmune diseases tend to run in families, and so maybe the aunt has thyroid disease and then sister has atopic dermatitis. But it certainly, you know, we see a lot of eczema in the AA population.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In this video, Dr. Michael Cameron addresses the question of whether patients with alopecia areata are more likely to have other dermatologic conditions. He confirms that patients with alopecia areata indeed have a higher likelihood of experiencing other dermatologic conditions. One common comorbid condition seen with alopecia areata is atopic dermatitis. Dr. Cameron explains that autoimmune diseases, including alopecia areata, often run in families. Consequently, it's possible for family members to have different autoimmune conditions, such as thyroid disease or atopic dermatitis. Additionally, he mentions that the alopecia areata population frequently exhibits cases of eczema (atopic dermatitis). The video emphasizes the existence of these associations and suggests that understanding such connections may be helpful for clinicians in diagnosing and treating patients with alopecia areata.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Patients with alopecia areata are more likely to have other dermatologic conditions.&nbsp;</li><li>Comorbid conditions are common, with atopic dermatitis being a significant one.&nbsp;</li><li>Autoimmune diseases often run in families, suggesting a genetic link. • There may be a pattern where certain family members have different autoimmune conditions, e.g., one family member having thyroid disease and another having atopic dermatitis.&nbsp;</li><li>Among the AA (alopecia areata) population, eczema (atopic dermatitis) is frequently observed.</li></ul>

What was the ORAL Surveillance study, and how does it relate to the labeling language of Olumiant?

<p class="MsoNormal">So having a comprehensive understanding of ORAL surveillance really is critical if you're going to be a dermatology provider at this point in time, just because we're going to continue to get more and more JAK inhibitors approved. ORAL surveillance was a study for the original JAK inhibitor, tofacitinib, which was in the rheumatoid arthritis population. It was a enriched for high risk patient study, it was a safety study. Patients had to be over the age of 50, they had to have at least one cardiovascular risk factor. Every single one of these RA patients was on a methotrexate with a median dose of 17 milligrams and 60% were on chronic prednisone. That's a ton of data I just dropped, but it's important that you understand how high risk these patients are. Think about how different that type of patient is compared to your 16 year old or your 20 year old with alopecia areata, for example, that usually is quite healthy. And so because of that, we're seeing such different safety with our JAK inhibitors and dermatology than they were with tofacitinib in that RA population. But unfortunately we're still stuck with that boxed warning language from the tofacitinib study ORAL surveillance, but you need to have that contextualization to understand why you can safely use JAK inhibitors in dermatology.<o:p></o:p></p><p class="MsoNormal">&nbsp;</p>

<h6>Summary&nbsp;</h6><p>In this video, Dr. Michael Cameron discusses the ORAL Surveillance study and its relevance to the labeling language of the drug Olumiant (baricitinib), particularly in dermatology practice.&nbsp;</p><p>The ORAL Surveillance study was conducted to evaluate the safety of the JAK inhibitor tofacitinib in the rheumatoid arthritis (RA) population. The study specifically targeted high-risk patients, who were over the age of 50 and had at least one cardiovascular risk factor. All the RA patients in the study were also on methotrexate, with a median dose of 17 milligrams, and 60% of them were on chronic prednisone. This means the patients in this study were at a significantly higher risk compared to younger, healthier patients typically seen in dermatology, such as those with alopecia areata.&nbsp;</p><p>Dr. Cameron emphasizes the importance of understanding the context and differences in patient populations when considering the safety of JAK inhibitors in dermatology. While the ORAL Surveillance study provided crucial safety data for tofacitinib in RA patients, the risks and safety profile may differ in dermatology patients who do not share the same high-risk characteristics.&nbsp;</p><p>Despite this difference in patient populations, the labeling language of Olumiant, which is based on the ORAL Surveillance study, includes a boxed warning. Dr. Cameron points out that dermatology providers should be aware of the ORAL Surveillance study's context and the higher-risk profile of the RA patients involved. By understanding these distinctions, healthcare professionals can confidently and safely use JAK inhibitors in dermatology patients, even if the boxed warning is still present in the drug's labeling language.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The ORAL Surveillance study focused on the JAK inhibitor tofacitinib in the rheumatoid arthritis (RA) population.&nbsp;</li><li>The study included high-risk patients who were over 50 years old and had at least one cardiovascular risk factor.&nbsp;</li><li>All RA patients in the study were on methotrexate with a median dose of 17 milligrams, and 60% were on chronic prednisone.&nbsp;</li><li>The patient population in the study was markedly different from younger and healthier patients with conditions like alopecia areata.&nbsp;</li><li>The safety profile of JAK inhibitors in dermatology is different from that observed in the RA population in the ORAL Surveillance study.&nbsp;</li><li>Despite the differences in safety, the boxed warning language from the ORAL Surveillance study still applies to JAK inhibitors.&nbsp;</li><li>Contextual understanding is necessary to ensure the safe use of JAK inhibitors in dermatology.  </li></ul>

Which patients are eligible for treatment with baricitinib and are there any notable exclusion criteria?

<p class="MsoNormal">So it's really up to the provider when you look at the label for baricitinib. And so it's defined as severe alopecia areata, but there are no, you know, body surface area involvement requirements or anything like that. So the provider and the patient decide, you know, what is severe alopecia areata and what requires it. And then in terms of, you know, contraindications, you don't want to use baricitinib with other systemic immunosuppressants like methotrexate, prednisone and azathioprine and things of that nature.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Michael Cameron discusses the eligibility criteria for treatment with baricitinib and highlights some notable exclusion criteria. According to the label for baricitinib, it is defined as a treatment option for severe alopecia areata. However, there are no specific requirements regarding body surface area involvement. The decision of what constitutes severe alopecia areata and necessitates treatment with baricitinib is left to the provider and the patient to determine.&nbsp;</p><p>In terms of exclusion criteria, it is not recommended to use baricitinib in combination with other systemic immunosuppressants such as methotrexate, prednisone, and azathioprine. This indicates that patients who are already taking these medications should not be considered for baricitinib treatment due to potential adverse effects or interactions.&nbsp;</p><p>In summary, patients eligible for baricitinib treatment are those with severe alopecia areata, as determined by the provider and the patient, and who are not already taking an immunosuppressant.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>There are no specific body surface area involvement requirements for eligibility.&nbsp;</li><li>The decision on whether a case of alopecia areata is considered severe and requires baricitinib treatment is made jointly by the healthcare provider and the patient.&nbsp;</li><li>Baricitinib should not be used in combination with other systemic immunosuppressants such as methotrexate, prednisone, and azathioprine.&nbsp;</li><li>Contraindications include concurrent use of baricitinib with certain medications that have immunosuppressive properties.</li></ul>

How soon can patients start seeing results on baricitinib?

<p class="MsoNormal">I think this kind of shows you that alopecia areata is actually multiple diseases or different endotypes because we see a few different response kind of patterns. For my patients, and I have a lot of them on baricitinib, I've had patients have regrowth as early as week four and I've had other patients take nine months. And so I think there's about three different response curves. And so you want to counsel your patients that it could take up to nine months to see a response, but that you can see it as early as four weeks.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Michael Cameron discusses the response patterns of patients with alopecia areata to the medication baricitinib. He points out that alopecia areata is composed of multiple diseases or different endotypes, leading to various response curves. Based on his experience with patients on baricitinib, he has observed a few different response patterns.&nbsp;</p><p>According to Dr. Cameron, some patients may experience regrowth of hair as early as four weeks after starting treatment with baricitinib. However, he also notes that other patients may take up to nine months to see noticeable results. Therefore, he advises healthcare professionals to counsel their patients that it is possible to see a response within four weeks, but it could also take as long as nine months for the medication to show its effects on hair regrowth in cases of alopecia areata.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Alopecia areata is a condition with multiple diseases or different endotypes, leading to varying response patterns in patients.&nbsp;</li><li>Patients on baricitinib may experience different response curves.&nbsp;</li><li>Some patients may start seeing regrowth as early as four weeks after starting treatment, where others may take as long as nine months to see results.&nbsp;</li><li>Healthcare professionals should counsel patients that the time to see a response can vary.</li></ul>

What is the mechanism of action of baricitinib?

<p class="MsoNormal">So like a lot of our inflammatory skin diseases, there's a variety of cytokines that play a really important role in targeting the hair follicle as in auto antigen and then causing inflammation around the hair follicle. And so these cytokines depend on the JAK-STAT pathway to transmit their message to the nucleus. And so baricitinib is a small molecule, no different than aspirin or tylenol, and so it diffuses through the cell membrane of these inflammatory cells and blocks signaling of these inflammatory cytokines and thereby does not allow those cytokines to send their message to the nucleus. And so it halts all of that pro inflammatory pathways.<o:p></o:p></p>

How does the mechanism of action of baricitinib differ from topical JAK inhibitors?

<p class="MsoNormal">Well, the MOA itself is actually the same, really, when you look at a topical JAK inhibitor, but the delivery is what is critical here. And so, you know, I've tried topical JAK inhibitors off label for mild alopecia areata and I've had no success. And so you know I don't think we've unfortunately been able to develop a topical formulation that can effectively get the JAK inhibitor to the hair follicle consistently. And so what's great about Olumiant is because baricitinib is an oral delivery, you know, you are able to kind of get the JAK inhibitor to the hair follicle where the disease is happening.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In this video, Dr. Michael Cameron explains the difference between the mechanism of action (MOA) of baricitinib and topical JAK (Janus kinase) inhibitors. He mentions that the MOA of both baricitinib and topical JAK inhibitors is essentially the same. However, the critical difference lies in their delivery methods.&nbsp;</p><p>According to Dr. Cameron, he has personally tried using topical JAK inhibitors off-label for mild alopecia areata, but without success. The challenge with topical JAK inhibitors is developing a formulation that can consistently and effectively deliver the JAK inhibitor to the hair follicles where the disease occurs.&nbsp;</p><p>On the other hand, the advantage of Olumiant (baricitinib) is that it is administered orally, allowing the JAK inhibitor to be delivered systemically. This enables it to reach the hair follicles where the disease is happening, potentially making it a more effective treatment for conditions like alopecia areata.&nbsp;</p><p>In summary, the key difference between baricitinib and topical JAK inhibitors lies in their delivery methods, with baricitinib being an oral treatment that can reach the affected hair follicles more effectively.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The mechanism of action (MOA) of baricitinib and topical JAK inhibitors is the same, but the critical difference lies in the delivery method.&nbsp;</li><li>Baricitinib is advantageous because it is delivered orally, allowing the JAK inhibitor to reach the hair follicles where the disease is occurring.&nbsp;</li><li>Developing a topical formulation that effectively delivers the JAK inhibitor to the hair follicle has been challenging, thus an advantage of baricitinib is that it is administered orally.</li></ul>

Can baricitinib be used in combination with other biologics, JAK inhibitors, or immunosuppressants?

<p class="MsoNormal">It really should not. And so if you look at the label and the data for that matter, it's quite clear that you really should not use other immunosuppressants while using baricitinib for alopecia areata.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Michael Cameron addresses the question of whether baricitinib can be used in combination with other biologics, JAK inhibitors, or immunosuppressants for the treatment of alopecia areata. According to Dr. Cameron, it is not recommended to use other immunosuppressants alongside baricitinib for alopecia areata. The label and data for baricitinib indicate that it should be used as a standalone treatment and should not be combined with other immunosuppressant medications.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Baricitinib should not be used in combination with other immunosuppressants for alopecia areata.&nbsp;</li><li>The label and data clearly indicate that using baricitinib alongside other immunosuppressants is not recommended.&nbsp;</li><li>The video emphasizes the importance of avoiding the simultaneous use of other immunosuppressants with baricitinib for this condition.</li></ul>

What is the recommended dosing regimen for baricitinib? 

<p class="MsoNormal">So for the majority of your patients, if you read the label, it says to start with two milligrams. Now if they have total or almost complete scalp hair loss or eyebrow or eyelash involvement, the label does say you can start with four milligrams and then once you achieve a response, you should consider going down to two milligrams.<o:p></o:p></p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Michael Cameron discusses the recommended dosing regimen for baricitinib. He mentions that for most patients, the initial dosage should be two milligrams. However, if the patient has total or almost complete scalp hair loss or hair loss that involves the eyebrows or eyelashes, the label suggests starting with four milligrams. Once a response is achieved, it is advisable to consider reducing the dosage back to two milligrams.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The majority of patients should start with two milligrams according to the label.&nbsp;</li><li>If patients have total or almost complete scalp hair loss or eyebrow or eyelash involvement, they can start with four milligrams.&nbsp;</li><li>After achieving a response, consider reducing the dosage back to two milligrams.  </li></ul>

Is there any long-term safety data available for baricitinib?

<p>There is. And, so, baricitinib has been out for many years in rheumatoid arthritis. But now we're getting several years of data back for baricitinib in alopecia areata. And if you look at the data, we're really not seeing any of those safety signals that they saw with tofacitinib and RA for the oral surveillance study. And so we don't see any signal for malignancy or any clustering of organ systems for malignancy like lymphoma or lung cancers. We're not seeing cardiac events or blood clots or any really increased risk for serious infections, even shingles, which is the thing most known for JAK inhibitors. The rate is almost numerically equivalent to placebo. It's just slightly higher. And so we're seeing a really, really clean safety profile for baricitinib and alopecia areata.&nbsp;</p>

<h6>Summary&nbsp;</h6><p>Dr. Michael Cameron discusses the long-term safety data available for baricitinib, a drug used in the treatment of rheumatoid arthritis and alopecia areata. The drug has been in use for many years for rheumatoid arthritis, and now several years of data are available for its use in alopecia areata. Comparing the safety data with that of another drug, tofacitinib, used in rheumatoid arthritis, there are no significant safety signals seen for baricitinib.&nbsp;</p><p>The safety signals observed with tofacitinib in a study for rheumatoid arthritis included issues like malignancy, clustering of organ systems for malignancy (lymphoma or lung cancers), cardiac events, blood clots, and an increased risk of serious infections, including shingles. However, in the case of baricitinib used for alopecia areata, there are no such signals. The safety profile for baricitinib in alopecia areata is described as "really, really clean" by Dr. Cameron.&nbsp;</p><p>Overall, the data indicates that baricitinib appears to be safe for long-term use in treating alopecia areata, with no significant safety concerns observed in the studied period.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Baricitinib has been used for many years in rheumatoid arthritis.&nbsp;</li><li>There is now data available for baricitinib use in alopecia areata.&nbsp;</li><li>The safety signals observed with tofacitinib use in rheumatoid arthritis are not seen with baricitinib in alopecia areata.&nbsp;</li><li>No signal for malignancy or clustering of organ systems for malignancy (e.g., lymphoma or lung cancers) is observed.&nbsp;</li><li>There are no significant cardiac events or blood clot risks associated with baricitinib use.&nbsp;</li><li>There is no increased risk for serious infections, including shingles, with baricitinib use.&nbsp;</li><li>The rate of adverse events with baricitinib is almost numerically equivalent to placebo, with only a slight increase observed.&nbsp;</li><li>Baricitinib shows a very clean safety profile in alopecia areata.</li></ul>

Incyte AD August 2023

How can I identify patients who would benefit from ruxolitinib cream?

<p>A common question I get is who's the right patient when it comes to ruxolitinib cream? Well, there's a couple of things you're looking for in a lot of this is based on the FDA indication and exactly the way that the trials were designed. So you're looking for that patient who's mild to moderate and typically you can have a body surfacing area of involvement somewhere between 3 and 20% and that simply just comes from the actual trials themselves. In the real world, patient times are often coming in, having used topical corticosteroids or topical calcineurin inhibitors, and depending on insurance approval, that may be something that you're looking for too. But really you're thinking about that patient that isn't getting control through their normal therapies, and really is looking forward not only to lesional control, but also control their itch as well.</p>

<h6>Summary&nbsp;</h6><p>Dr Raj Chovatiya addresses the question of how to identify a patient who would benefit from ruxolitinib cream. He explains that the right patients for this treatment are those with mild to moderate symptoms and a body surface area of involvement between 3% and 20%. These criteria are based on the FDA indication and clinical trial design.</p><p>In real-world scenarios, patients seeking ruxolitinib cream often have already tried topical corticosteroids or topical calcineurin inhibitors, and a key factor to consider is if patients have not experienced adequate control of their symptoms with these other therapies. The ideal candidate for ruxolitinib cream is someone who desires not only lesional control but also itch control.&nbsp;</p><p>Overall, identifying patients who would benefit from ruxolitinib cream involves assessing the severity of their condition, the affected body surface area, and the inadequacy of previous treatments in controlling their symptoms.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The key question is: "Who is the right patient for ruxolitinib cream?"&nbsp;</li><li>The ideal patient profile includes those with mild to moderate symptoms</li><li>Patients typically have a body surface area of involvement between 3% and 20%&nbsp;</li><li>Patient candidates have often already tried topical corticosteroids or topical calcineurin inhibitors&nbsp;</li><li>The target patient is someone who hasn't achieved sufficient control with other therapies</li><li>The desired outcome is not only lesional control, but also itch relief</li></ul>

What makes a sunscreen well formulated from both a clinician and patient perspective?

How do ingredients beyond UV filters, like antioxidants or moisturizers, enhance photoprotection?

How do you identify sunscreens that offer reliable broad-spectrum protection beyond SPF ratings?

What makes a sunscreen particularly effective for pigment protection or visible-light defense?

What is Helioplex technology, and how does it improve stability and UV coverage?

Why does a higher SPF still matter in real-world use?

What is your take on the role of antioxidants in photoprotection?

What are your go-to strategies for improving sunscreen adherence in daily life?

Are there any patient groups you feel are undercounseled when it comes to the risks of photodamage?

Which common medications increase photosensitivity, and how should this shape your counseling?

How do you approach treating acne without compromising the skin barrier, especially in patients with sensitive skin?

Why is salicylic acid a useful ingredient in acne cleansers, and how can formulation approaches improve its delivery?

What role does the skin barrier play in acne pathophysiology, and how should it influence treatment selection?

Are there specific ingredients or technologies that help balance acne treatment with barrier preservation?

What are hydrophobically modified polymers, and what role do they play in cleanser tolerability?

What role do hydrocolloidal patches play in an acne routine, and when do you typically recommend them?

What’s the clinical significance of using 2% salicylic acid in combination with polymeric cleansing technology?

How can dermatologists help patients pair prescription acne medications with over-the-counter products that protect the skin barrier?

What role does patient education play in making sure over-the-counter products support rather than interfere with prescription therapies?

What is the "retinol sandwich" method for managing acne?

What are the practical advantages of prescribing the 350 mg packet of tirbanibulin over the 250 mg?

In terms of a clearance timeline, what expectations should clinicians set with themselves and with patients starting tirbanibulin, especially when comparing it with therapies like 5-FU?

How do you counsel patients and colleagues about the timeline of response, given that visible skin reaction may not appear immediately?

When might you choose tirbanibulin over 5-FU for AK field therapy?