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How long do you allow patients to use hydroquinone 4% since melasma is a chronic disease that can last for years? Do you use "drug holidays"?

You. Hydroquinone and hydroquinone holidays, as I like to call them, are important. Hydroquinone is not something you should ever tell your patient. Hey, go use it for six months to a year and come see me in a year. No, doesn't work like that. You need to use the hydroquinone in a systematic fashion with an on off regimen when needed. Twelve to 16 weeks initially. I'll have a new patient come in. They get no refills. They get pictures at baseline, pictures at follow up. They're counseled on side effects, and then we go into second line topicals after that. So hydroquinone holidays are critical, in my opinion, especially at preventing irritation and okranosis.

Is ruxolitinib cream effective in treating itch associated with atopic dermatitis?

You. Roxoladin cream is very effective for treating the itch of atobic dermatitis. More than half of the patients achieve more than four step improvement in each. When the scale goes from zero, which means no itch, to ten, which means absolutely worst each anybody can imagine. You have to have at least four step improvement in this zero to ten scale. And by week eight patients who received raxolitinib 1.5% cream, more than half the patients achieved this four point improvement. So roxalinip cream is very effective for each.

Is topical ruxolitinib cream useful for patients with moderate disease?

You. Topical raxolitinib 1.5% cream is very effective for patients with moderate atovic dermatitis. About three quarter of the patients achieved clear or almost clear status by week eight, and in fact, the moderate patients did better than patients with mild disease, according to the FDA way of looking at this. That is an artifact of the fact that FDA not only demand clear, almost clear, but also two steps, improvement and patients with mild disease when they joined the study. Two improvement means they have to be absolutely clear. And so, ironically, many people with mild disease did excellent, but if they are not absolutely clear, FDA will classify them as treatment failure. So in reality, braxolynib cream works well, extremely well, both for moderate and for mild disease. But in the clinical trial, because of the a criteria of what is considered treatment success, moderate patients actually look better in terms of outcome than mild atopic dermatitis. Patients.

How much does atopic dermatitis affect a patient’s quality of life?

You. Atopic dermatitis, especially in children, seems to affect patients quality of life even worse than psoriasis because psoriasis tend to have less problem in children with atopic dermatitis whole lot of children affected and that has tremendously negative quality of life, not only because children tend to experience bullying and other stigmatization at school. Kids can be cruel more so than grownups, but also family dynamics can be perverted with atovictomatitis. I have often seen that atobactomatitis child the parents feel so bad that oftentimes the mother pay more attention to the child with atobic dermatitis as compared to other siblings and that can create jealousy among other siblings. And also sometimes when the child has really bad atovic dermatitis, the mother tend to sleep with the child and that might actually make that husband frustrated that they no longer can spend time together in bed because the mother is spending more time with the child with bad atopic dermatitis. Now, in general, whether patient is child or adult, atopic dermatitis consistently show more problem with itching and more intense itching than other skin conditions such as psoriasis, so that also make quality of life negative impact even more intense with atopic dermatitis compared to psoriasis or other skin conditions more intense each and more generalized each.

Any tips for when patients won’t use their topicals due to burning with application?

How does treating atopic dermatitis in elderly patients differ from younger patient populations?

You. Treating etobic dermatitis in elderly is different than treating etobic dermatitis in younger patients because elderly patients tend to have drier skin. So we have to emphasize more about using moisturizers, especially recommending that they use moisturizer that lasts as long as possible, which are, in my experience, generally ointments instead of something like lotion. But the other thing that is different is among elderly patients, they tend to have more generalized itching, as opposed to younger patients who may be more localized. So there is a whole group of elderly patients with eczema, toy rash, with generalized itching that we have many, many names in terms of how we call them. The one that I generally use is eczema and paritis of the elderly. But there are many other names, such as adult onset atopic dermatitis or itchy red bump disease of the elderly. I can name at least five other ones. They do tend to have more generalized itching. So in addition to topical medication, oral medication, and also phototherapy, especially ubb phototherapy, I find that very helpful for elderly when they have more generalized itching in with their atrobic dermatitis.

How long after bathing do you recommend applying moisturizer?

You after bathing. For patients with atopic dermatitis, I personally recommend putting moisturizer as soon as they pat themselves dry with cow. And the reason is that way we are trying to trap the moisture, the water content, which went into the skin from bathing. As we know, dryness of the skin is a real problem with atopic dermatitis. So moisturizers are very important. But putting moisturizer on right after bathing. So the water that went into the skin during bathing actually get trapped into the skin. And that is like an extra help with regard to dryness of atobic dermatitis. So I recommend applying moisturizer right after they come out of the bath and pat themselves dry and then right away put on the moisturizer.

Does a patient with latent TB need treatment before using ruxolitinib cream?

You. As far as we know, and also according to the package insert, there are no specific contrary indication if somebody have latent TB. Now, of course, if somebody have latent TB, whether they take any kind of medication or not, they do have to go through the oral regimen for latent tv. But as far as the package insert and whatever we know clinically, there is nothing that states that you have to wait for that latent tv oral medication to finish before you can start raxolitinib. As far as we know, you can go ahead and start raxolidinib topical 1.5% cream while the patient is undergoing oral medication for the latent TB prophylactic treatment for tuberculosis.

What are the most common side effects of ruxolitinib cream?

You. The most common side effects were application site burning and itching for ruxolitinib 1.5% cream. But amazingly, the actual currents was less than 1% both burning and itching at the application site. And that is remarkably low for some non steroid agents because generally, non steroid agents like Tacrolimus Pimacrolimus for atopic dermatitis have much higher rate of application site burning and itching than what was recorded with raxolydinib.

Are topical JAK inhibitors, on the whole, more efficacious than superpotent topical steroids for atopic dermatitis?

We don't really know how the efficacy of vacciolitinib compare against superpodant topical steroid because we don't have head to head comparison study. But from phase two study, head to head against chime synolog, we know that raxolitinib does perform much better than chime synolog. In terms of this phase two study, percent of patients who achieve clear or almost clear, which was the main endpoint, roxalitinib was 38%. Triumphinolone was only 25%. So we have that data that raxalitinib much higher achievement rate in terms of clear or almost clear, but we just don't have head to head comparison against super potent topical steroid. And that is the kind of data that I even personally will be very interested.

Do topical JAK inhibitors and oral JAK inhibitors have similar rates of systemic adverse events?

You. Topical jack inhibitors have much, much less concerns about systemic side effects because the systemic absorption is so much less. With regard to ruxolitinib, 50 milligram oral ruxolitinib was compared directly against 1.5% topical agent used up to 90% of the body surface. And what happened was that the plasma blood level less than 100 nanometer nanomoles for the topical, which is about one six of what happened with the oral. And this is so much less than the blood level necessary to affect the blood count. So topical is so much more safer than oral in terms of systemic side effects.

When do you restart retinoids and azelaic acid after a chemical peel?

You. So restarting topicals after a chemical peel procedure is really important in terms of timing and treatment outcome, especially for your skin of color patients. Typically, if it's a retinoid, I will wait a minimum of 72 hours post peel to restart azalaic acid and sunscreen and cosmeceuticals. I'm a little bit more open to starting those sooner if the patient would really like. Honestly, it's very treatment dependent depending on your depth of your peel and how the patient is reacting. A good rule of thumb is five to seven days as a blanket rule and then adjust accordingly for dependent on the ingredient subtype.

Are JAK inhibitors (specifically tofacitinib or ruxolitinib) an effective treatment option for alopecia areata?

So jack inhibitors specifically tofacitinib, and to some extent, even ruxolitinib for alopecia areata are a challenge. They work for alopecia areata. The problem is when you stop the therapy, it tends to relapse. There's been a couple of good papers out on ruxolitinib for patients who have failed tofacitinib therapy. And we've shown that in those papers that the authors actually published, that when you go up to the ten milligram dosing, potentially even ten milligrams twice a day, you get some nice treatment outcomes. Topacitinib, on the other hand, really, the data is quite mixed. And to be very frank, in my practice, it's not consistently been a slam dunk for every alopecia areata patient.

How do you manage conjunctivitis that occurs while on dupilumab?

You. So conjunctivitis is a known comorbidity of AD patients. And really regardless of therapy. And the risk factors for conjunctivitis include history of severe atopic dermatitis or really just a past history of conjunctivitis. And in dupilumab trials, conjunctivitis occurred in about seven to 12% of patients that were treated with dupilumab, compared to about 2% on placebo. So when I think about patients who later may present with conjunctivitis, I really think about classifying them into the more mild to moderate versus a bit more severe categories. And I shall say most cases of conjunctivitis that occurred with dupilumab tend to be mild or moderate and can be managed without discontinuation of dupilumab. So for my patients, first of all, what I do is that before I start dupilumab, I have them really just go buy some artificial tears. So as they are starting the therapy, they can actually use artificial tears to make sure that their eyes are lubricated. So sort of a preventative measure. And if they do experience mild conjunctivitis, again, the use of artificial tears is really important. And I have them buy those single use twisty tops just to prevent potential for infection by using ones that may be containing large volume. In addition to that, I also recommend the use of if they have some mild conjunctivitis, antihistamine eyedrops. And some of those may include the over the counter antihistamine drops such as padaway or alloy, and if they are more severe, if they have more severe presentations of conjunctivitis, I refer them to ophthalmology immediately. But sometimes there can be a little bit of a wait between my referral and when they can actually get to see ophthalmology. So if the wait is a bit long, I oftentimes will prescribe a corticosteroid topical eyedrop. And the one that I like is called fluoromethylone or FML eyedrop. And the reason is because it has poor penetration really into the anterior chamber of the eye. As a result, it has a lower risk of cataracts or glaucoma compared to other types of eyedrops, topical cortical steroid eyedrops and then other options include cyclosporin eyedrops such as things like restasis that you can prescribe until they see ophthalmologist or tacholimus eyedrop or ointment can be super helpful as well. All.

How do you manage patients who develop candidiasis while on IL-17 inhibitors?

You. Most patients who present with oral candidiasis while on IL 17 inhibitors will have mild or moderate oral candidiasis. Most cases actually will be mild and those can be managed without discontinuing IL 17 inhibitors. So how do I manage them? When I have a patient who present with oral candidiasis, typically Lee, I use oral fluconazole because it is quicker and just easier to administer. So I use oral fluconazole either 100 milligrams or 200 milligrams, depending on the person's weight, daily for seven days. Now, I also want to let you know the recommendation by the id societies for them. If the patient presents with more mild to moderate oral candidiasis, they recommend the use of clotrimazole, troches or nystatin suspension topically. For these patients and for the more moderate or severe cases, they also recommend oral fluconazole 100 or 200 milligrams really at a dosing of about three milligrams per kilogram for seven to 14 days. Again, I personally do 100 milligrams or 200 milligrams, depending on patient's weight, daily for seven days, and I find that to be quite effective. But I know that some of my colleagues prefer using topical antifungal agents and I think those have work quite well as well, as long as you use them for about two weeks or so. Bye.

What resources exist for those new to cosmetic procedures?

If you are new to cosmetic procedures, whether it's neuromodulators or toxins or fillers, lasers, etc. There are many resources that are available for you to become quite good at using these cosmetic treatments. I think that it's a great idea to continue to participate in CME meetings such as fall and winter clinical. I also think that you can approach each individual company for training. Companies would love to train you to use their products. Now, one thing that you have to know is they can only train you to use the products on label, but in CME forms, you are going to be able to learn more advanced techniques. But I think in the very beginning, it's great to go to meetings, discuss with colleagues, et cetera, but also approach each individual company and have them set up training sessions for you so you can become an injector, learn how to use neuromodulators, learn how to use fillers, learn how to use lasers and devices. And I think this way you could be on your way to becoming a master injector and using advanced techniques for cosmetic procedures. Teachers.

How do you give folic acid with methotrexate?

You. There are two ways in which you can give folic acid for patients who are on methotrexate. I used to give 1 folic acid on the days, every day of the week, except for the day that they are getting methotrexate. And I actually have changed my practice for that over time because studies have shown that you can also do this other method where you can give five milligram of folic acid to be taken the day after they get their methotrexate. So now this is what I do, because it's a bit easier for patients just to take the five milligram of folic acid in one day of the week, and that day is a day after they take the methotrexate. And it's just a bit easier for them to number.

Which toxin is best?

One of the most common questions that patients and colleagues alike ask is which neuromodulator and toxin works best, lasts longer, etc. Well, all the data out there, all the head to head studies show that each of the four products that are currently FDA approved is very similar and onset of action. I do think, from a practical perspective, that some patients may prefer one versus another. So what I usually do is give the patients an option of different toxins that I have available and let them decide, and let them try one or the other each time they come in and pick the one that's their favorite. In my practice, I think most patients do not have a favorite, but I do think that each product has some differences, and you, as a practitioner, may be able to pick the one that's right for each and individual patient.

How effective are home phototherapy/UV units for Vitiligo?

Home phototherapy for vitiligo is something that I do find effective in my practice. I'll tell you. During the COVID pandemic, home phototherapy helped a lot of my patients because they couldn't come to the office. We had restrictions on how many people you could let in. We had patients who didn't want to come in even if they could. And home phototherapy certainly helped many of them continue in their treatment. Do I think in office phototherapy is better? Well, it depends on the, and it depends on your treatment outcome. But yes, home phototherapy has been something very helpful, and it continues to be an important part of my therapeutic armamentarium.

Can AMZEEQ be combined with benzoyl peroxide?

You. So with the advance, with topical minocycline being available, and there's a 4% foam that's available once a day for the treatment of acne. There's a 1.5% topical minocycline foam approved for the treatment of papilla plush lesions of rosacea. But we're typically going to get into a situation where we want to use topical minocycline 4% foam in a patient with acne, where we also want to use benzo peroxide. We have to recognize that benzel peroxide is an oxidizing agent and it can actually break down or degrade certain other agents that we use for acne. We've known about that for years with tretinoin. So we separate benzoyl peroxide from most of the formulations of tretinoin. With topical minocycline foam, benzoyl peroxide degrades the topical minocycline foam, so we expect it to be less active or inactive, and it also is going to create a discoloration. So it is recommended, and actually, it's in the labeling that you separate by at least 8 hours application of benzo peroxide from when they apply a topical cycling foam.

How long should you hold dupilumab prior to live vaccine injection?

So first let's talk about some of the common live vaccines that may come up during our discussion, and they include yellow fever vaccine, sastavax, measle, mumps, rubella and rotavirus vaccines, intranasal influenza vaccine and BCg vaccine. So the current recommendation is to hold dupilumab injection for twelve weeks, give the live vaccine, and then wait another four weeks before you give the dupilumab injection. And now, this particular practice is not really based on a lot of data because we don't have a lot of data in this area right now, but it's a recommendation that's based on maximizing safety and also not interfere with our body's response to mount the antibody response as a result of receiving the live vaccination. Now let me also talk a little bit about non live vaccines and its use with dupilumab here when we're talking about our Covid vaccines, for example, the mrna vaccine, there is really no consideration with regards to when you give the mrna vaccine versus the dupilumab injection. So typically really have people schedule their mrna vaccine appointment first, and then they should be able to continue the dupilumab injection as recommended on the original dose. This goes the same for the adenovirus vector Covid vaccines as well, as long as they have that first, have them schedule the earliest vaccine appointment that's possible for the adenovirus vaccine, and then they can continue their dupilumab injection at the regularly scheduled interval.

Do you ever use triple therapy cream for Post-Inflammatory Hyperpigmentation?

You. I do get asked a lot. Do I ever use triple combination therapy for PIH? And the answer is I do. However, it's not something that I use for every patient with post inflammatory hyperpigmentation. You have to be careful because remember, if it's pih from acne, you don't want to just put spots everywhere and then get a halo effect from the hydroquinone. You want to be able to use something that's more uniform on the space. So retin, azalic acid, chemical peels, antioxidants, really like those for ph and yes, hydroquinone based triple combination for the stubborn areas. But I don't use it exclusively all the time as much as I do in melasma, for example. And.

Can you address potential long term side effects from finasteride after discontinuation?

You. Mostly, we've seen that long term finasteride after discontinuation does not have any long term side effects. The main ones that we get asked about or that have been reported in some recent studies are potential sexual side effects in men. But from what we've seen, the risk of this is incredibly, incredibly low, less than 1% in some studies, 0.1% percent. I do talk people through it, particularly men, but women as well as one of the risks, and that there are some studies that, as I mentioned, show long term issues. But I feel comfortable prescribing finasteride in both men and women and through the process.

How do you manage patients on biologics when they undergo orthopedic surgery? Do we need to hold the biologic?

So orthopedic surgeries are typically considered low risk surgeries and low risk surgery. Definition is where procedures where the GI, the respiratory, or the geotracks are not entered during surgery and for those the National Psoriasis foundation recommending not holding biologic during the surgery. So continue the biologic regimen as usual through these low risk surgeries. Now, if you do have a patient who is undergoing high risk surgery and that is defined as if the respiratory GI tract, or GU tract is penetrated during the procedures, then the recommendation there currently is stop the biologic for about five half lives prior to the surgery and then resume the biologic one to two weeks after the surgery. If there is no infection and.

Do you see WINLEVI replacing ACZONE?

You. We now have available a topical androgen receptor inhibitor, which is topical cliscodorone. It's FDA approved as a 1% cream applied twice a day in patients with acne that are at least twelve years of age. This is the first time we actually have an FDA approved androgen receptor inhibitor. It's available topically. So the data showed that it can be used in males and females with oral spironalactone, which is an androgen inhibitor that we use off label. It's utilized only in females, but it's important to recognize that topical closcodarone was studied in males and females and can be safely used in both. It's a unique mechanism of action. So a lot of people ask, is this going to replace topical dapsone or topical benzero peroxide or retinoids? It doesn't technically replace anything because it's working on a different pathophysiological pathway. So there's no immediate replacement of any other agent, whether it be topical or oral antibiotic for that matter, it doesn't replace any other therapies. It targets a specific pathophysiology, which is inhibition of androgen activity.

Are you excited about delgocitinib?

I am very excited about delgocinib. Delgocitinib is a panjack inhibitor. It inhibits throughout the jack family. And it's actually being studied for chronic hand eczema, which is, I think, why I'm so excited about it, because it's a topical. It's a panjack, and it's being studied for hand eczema, which is a really vexing chronic disease, too, which we have no cure. We don't have a great fix for that. So it certainly is an unmet need, and I'm excited about it.

Can you comment on hot topic of J Lo and her olive oil and non use of BOTOX?

Here's what I will say. Look, ideally, people have integrity and don't misrepresent what types of things you're doing for the face. I would argue that just because JLO is not or anybody else is not necessarily doing Botox doesn't mean there aren't a lot of other things they might actually be doing. So there are ultrasonic wave tightening and all sorts of stuff, chemical peels and serums that you can use to help keep your skin flawless. Also, hey, some people just have good genes, but given that she now actually has her own brand of skincare, I would say she probably is definitely doing more than olive oil, even if she isn't, in fact, using.

How do you transition a psoriasis patient from methotrexate to a biologic? Can you use them concurrently?

You. In most of my patients, if I had to transition from a patient from methotrexate to a biologic medication, I first would not do anything to the methotrexate dose and I would continue the methotrexate while the biologic is getting started. And then I wait until the patient is clear or almost clear or really significantly better year, at which point I then would discontinue the methotrexate altogether. Methotrexate is a medication that can be discontinued without tapering. So I tend to do that at that point because I wanted to see how the patient will do on monotherapy of biologic and then if the patient later on start to have return of disease on this monotherapy of biologic, then I would add a little bit of methotrexate back until the lowest methotrexate dose that's needed to maintain patient clear or almost clear. In this case, I shall say the reason in the beginning why I would continue methotrexate and biologics in combination together until the patient is a lot better. The reason for that is typically if you are adding a biologic to methotrexate in the first place, probably because the patient is not under very good control and some of our biologics may need also some lead time for their full efficacy to kick in. So that combination of methotrexate and a biologic together in the beginning of that transition just really helps the patient to be under good control.

Is vitamin supplementation important in treating vitiligo? Are there supplements that you recommend for your vitiligo patients?

Vitamin supplementation in combination with jack inhibitors and tcis. All those questions are critical and important in vitiligo. The short answer is I do use vitamin supplementation for my patients with Vitiligo. I do make sure they've had their vitamin D checked, they're getting their thyroid and iron checked with their pcp supplement as needed for those based on lab work. But I also recommend alpha lipoic acid with vitamin C and vitamin D, typically in a 100 to 150 milligram dosing for the combined capsule. And I recommend polypodium leukotomas twice a day for my patients, which helps to increase their body's own uv protective factor. All.

Are there any differences in the side effect profiles between ABSORICA LD and traditional isotretinoin?

You. So with the advent of isotretinoin formulations that are presolubilized in the lipid matrix, so you don't need a fatty meal like you do with branded generics or accutane, which was the original brand, which is now available from a company. Those original agents, the branded generics like amnestine, Clarivis, xenotane, myoricin and Accutane. To get optimal absorption, you need to give a high fat meal, and they were studied with 50 grams of fat, which would be needed with each dose. With the presolubilized formulations Absorica and Absorica LD. Absorica LD is micronized. It's absorbed even better. Even with water, you don't need a fatty meal. We have to recognize that that correlates with a lower risk of relapse because they get greater systemic exposure. But the side effect profiles are the same. The formulations like Absorica and absoric LD do not have any additional safety signals as compared to any oral isotretinoin. So the monitoring and the side effect profiles are the same.

Any tips on how to reduce the risk of ring warts?

You. The main tip that I use is I use an autoscope connector that goes on the end. I use that, and I actually use the cryo tank. I spray that through there to get it right on the size of the wart. I use different, I have about three different sizes of those in my practice. And so I actually use that and put it on the wart to keep the actual whole, the temperature and the coldness really focused that you don't have this situation which causes a lot of ringwarts where you have a lot of cold density in the center, but externally not as much. And then also, I do a ton of education. Another way that I see that there are a lot of ring warts are that if people don't understand that if there is a blister there, they actually should pop it and unroof it. So I make sure for work care that the instructions are very clear.

Should we consider the JAK inhibitors more broadly immunosuppressive than the biologics?

You. A lot of clinicians have questions about how immunosuppressive are Janus kinase inhibitors compared to some of the biologic agents that we use, whether it be dupiliumab or il 13 inhibitors that are coming along for atopic dermatitis or some of the injectable biologics that we have for psoriasis. You really have to look at the specific Janus kinase inhibitor and look at what Janus kinases are being inhibited, realizing that even if they're selective, there may be some spillover into other Janus kinase enzymes being inhibited. And then you have to look at what's downstream from that Janus kinase stat signaling, what the end effect is, because there are many different cytokines and mediators that interact with different Janus kinase inhibitors, and they have different implications in terms of what they signal downstream. So, for example, if you're inhibiting Janus kinase one, you're going to have a modulatory effect on interleukin four, interleukin 13, interleukin two, interleukin 615 22, 31, interferons, some of the interferons and TSLP, thymic stromal lymphopoietin. So you have a broad inhibition or modulation of the effects of those different cytokines. So in general, yes, Janus kinase inhibitors are more modulating of the immune system than targeted antibodies that affect specific, but you still have to look at each individual case.

Do patients need to be maintained on PRP therapy? If so, how often?

You. I recommend a series of three treatments, separated out every four to six weeks, and then I have them do one touch up treatment yearly after your last treatment. So you would come in a year after your series for that one touch up.

Do you support dupilumab for all of the AD spectrum conditions if moderate-to-severe and failing?

Yes, I think this is a great question, and one of the nice things about our diagnosis and our diagnostic criteria that are often used for atopic dermatitis by George Reich and John Hannifin. These are wonderful criteria because they really only ask three things. It has to be itchy, it has to be chronic or relapsing, and it has to be basically in the pattern and distribution of one of the known forms of eczema. So that gives us a really big way to think about this, and it gives us a lot of leeway. So I would argue that, definitionally, the spectrum of ad really is all part of AD. It's not necessarily just the perfect, I guess, the erythematus, scaly patches in the elbow creases. Right. Just those anacubidal or papatel faucet. That is not just Ad, it's much bigger than that. But I will freely admit that the spectrum can be bigger than some people are comfortable with, because. Do you include pragonodularis? Most people don't. They think prigonodularis is a separate condition, but of course it can have prigonodules in ad context. I have many patients like that, but some clinicians I've met, even really seasoned ones, say, no, it's the same thing. It's all part of the same. It's ad fascinating. Other ones that can be a little bit different, I think dyshydratic eczema, quite different. Sometimes just localized to the hands, little blisters. Is that part of the spectrum? I think, largely speaking, yes. But again, I can also see why splitters might say we should separate that out. And even things like separate dermatitis are sometimes included under the general subheading of eczema. But we really think of that as quite different. That being said, of the things that really fit into the spectrum and subderm would not fit into my concept of the ad spectrum. I find that dupliumab has worked great for all of these diseases. It's a little bit funny, it's bittersweet, because in the very beginning, I think a number of us were excited about using it as a tool to help figure out which ones are different. Maybe we'd say, well, what if certain subtypes respond beautifully and others don't respond at all? Then we'd say, wow, they're not mediated by Il four and Il 13. They're really different. The latin term for this is diagnosis ex uventibus. You can make a diagnosis by what's helping. So if the dupliumab helped, then we know. Well, it turns out it does really well across the whole spectrum. So I guess they're all pretty related. And now we have it FDA approved for paragonodularis as well. And even other things coming down the line, there's discussion about bullis, penfagoid and even things like chronic ridicaria, so these may be more connected than we understand.

How do you have your patients take oral tranexamic acid? Is there any benefit to splitting the 650 mg tablet?

You tranxemic acid orally. We've talked about in length in many of my talks. It's in the US, available as a 650 milligram dose, and I usually have patients split it bid 325 in the morning or 325 at night. I like to split the dosing. I feel that that can be more compliant. And also I can monitor for those early side effects of headache, nausea and vomiting early on. Based on the dose and the frequency. Some people say you don't really have to split it, but that's what I do. And if you look at the asian studies, the doses were divided by D in most of the large papers, particularly from the Singapore group that published in the Blue journal.

What is your favorite biologic in geriatric patients?

You I will say that all of our biologics can work very well in our geriatric patients. If I were to consider all of them and pick some of my favorites among our really great options I would say it will probably be the IL 23 class of medications for a number of reasons. Number one that they have fewer injection frequency. Number two, for example when we are looking at medications such as chodrachizumab for example, I could potentially take advantage of the Medicare part be part of my patient's insurance plan who are solely covered by Medicare. In addition to that, when we think about eustachinumab in our elderly patients, we just have a lot of good long term safety data with eustachinumab and also it's a medication that has really good I would say coverage as well when we are thinking about our elderly population who typically have Medicare and a supplemental insurance. So I will say that our IL 23 class of medications are one of my favorites when it comes to caring for for our geriatric patients with psoriasis and.

What are your thoughts and dosage of finasteride for androgenetic alopecia in post-menopausal women?

You. Finasteride for treatment of androgenic alopecia is one of my favorite tools. I tend to use it for postmenopausal women in a 2.5 milligram dosage, and sometimes I go up to a five milligram dosage depending on tolerance and any potential side effects. I think it is likely an underused tool, but it's definitely something I have in my armor. Material. When people, when we work them up for other forms of hair loss and we really see that it's mostly androgenic, I feel comfortable using it and usually start at that 2.5 milligram dosage.

How do I transition from cyclosporine to dupilumab for patients with atopic dermatitis?

You when a patient is on cyclosporin and then he or she then gets approved for dupilumab. Typically I would add dupilumab while the patient is still on the current dose of cyclosporin. I would wait until the patient is a lot better clear or almost clear or pretty much very mild disease on both a combination of dupilumab as well as cyclosporin. Once they are clear or almost clear or really extremely mild, then I would taper off cyclosporin from bid dosing to QD dosing for about two weeks and if they're still doing well and then go from QD dosing to QOD dosing for another two weeks. And hopefully by then you can then after that have patient come off of cyclosporin completely while they're being managed on dupilumab.

How do you get oral JAKs covered by insurance for alopecia areata?

How do I get jack inhibitors covered by insurance? Boy, if I had an answer to that question or had a way to fix that, I think I'd get all the referrals from around the country. I don't have a great answer. Most of the time I get these for patients who are willing to pay cash. I have been able to get oral tofacitinib as compassionate use for some of my patients. Remember, it is approved for rheumatoid arthritis. So if you do have a patient who has uncommon at RA and vitiligo for example, which isn't uncommon, talk and coordinate with your rheumatologist buddy. See if you can get it covered through the RA indication because it is on label for that. Also, the topicals fairly inexpensive depending on which compounding pharmacy you use. So that's something to keep in mind.

Can dupilumab cause cutaneous T-cell lymphoma (CTCL)?

There have been some recent publications, some of them in the Journal of the American Academy of Dermatology regarding utilizing depiliumab in patients that you're treating them for atopic dermatitis, but it turns out that they actually have cutaneous T cell lymphoma. Right. And so the question is, did they have cutaneous T cell lymphoma from the start, and the clinician just thought it was atopic dermatitis? Did the atopic dermatitis emerge into becoming cutaneous T cell lymphoma, and did dupliumab have any role in that particular situation occurring? To answer the last part of the question, that's a very difficult thing to determine because you're finding out somewhat after the fact that the patient had cutaneous T cell lymphoma. And they may have had that from the start, because we know, especially with patients, adult patients, that have a diagnosis of atopic dermatitis. And I would suggest looking carefully at how you're making that diagnosis, especially with adult onset, because that's a relatively uncommon condition. Think about the possibility of cutaneous t cell lymphoma, and you may want to get a biopsy if there's any question about the diagnosis. I had a patient recently where that happened, where I'm convinced that they didn't have atopic dermatitis before, because I went back and drilled down on the history, and the diagnosis of atopic dermatitis really wasn't that strong. They didn't get better. I biopsied them, and they had atypical lymphocytic proliferation. They didn't have called a cutaneous T cell lymphoma, though that may emerge. We treated them as parasiriasis with phototherapy, and they're doing very well. So you have to really make sure you feel comfortable, especially in adults, with the diagnosis of atopic dermatitis. And if there's any question, you can do a biopsy and try to differentiate.

What is your favorite biologic in those with treated latent TB?

You. I work in an area where many of my patients have latent TB or have had treated latent TB. And for these patients with a moderate to severe plaque psoriasis, my go to biologic, if I can get them access to it, is either an IL 17 or IL 23 inhibitor. The reason for that is that the risk of reactivation is very low of their tb with IL 17 or IL 23 inhibitors. So if I can for those patients, I don't prefer to use TNF inhibitors in them. Rather I would probably pick an IL 17 or IL 23 inhibitors for these patients.

Which cosmeceuticals do you recommend for lightening?

You for lightning. Mostly I recommend things that have athalaic acid and vitamin C. If someone's not on a prescription retinol, I also like to have them use some type of retinol or vitamin A product. Those are my main go to for lightning brown spots and keeping the skin nice and light with eclo.

Why does clascoterone work for acne and not minoxidil since they are both anti-androgens?

You. I've got a question here about classicodarone, which is a new topical medication that's coming out that's actually been approved for acne and has completed trials for use in male pattern hair loss. And the question is, why does minoxidil not work for acne and closcorone does? And the question was around those medications, both being antiandrogens. Well, the first issue is that minoxidil is not an antiandrogen. Minoxidil is actually in its own class. It's nothing to do with hormones. It just happens to prolong the antigen phase. We think that it has to do with potassium, inhibition of receptors in the follicle. And so there's no antiandrogen effect from minoxidil. So it's a totally different class from classcodorone. So it would not make sense for minoxidil to work in its current form. It is typically a little bit of an irritant to the skin, so we don't typically have patients apply it to their face or if they do very sparingly to eyebrows in patients with alopecia of the eyebrows, potentially a few times a week. So we wouldn't want to try to think about using minoxidil for acne because that would not be a good use of that medication.

How would you address live vaccines in pediatric patients on Ixekizumab?

When we think about our pediatric patients that you want to put on ixicizumab, for example, and the issue of live vaccinations, it's important to know that the key live vaccine that we're really thinking about is the MMR vaccine or the measles mumps rubella vaccine. And in these children, it's also good to know that typically the children get two doses of the MMR vaccine, the first one typically at twelve to 15 months of age, and the second one typically between four to six years of age. And I shall also say that eustachinumab is also approved for children six years and older. And etannercept is the one that is approved for children four years and older for moderate to severe plaque psoriasis. So for the second dose, children can receive the second dose earlier as long as it's at least 28 days after the first dose, according to the CDC recommendations. So with that being said, there's very little data currently in this topic, and we definitely need more research here. But if you have a child who haven't had MMR vaccine, I would probably just have that child get their second dose of MMR vaccine prior to starting the biologic. And let's say you have already started the biologic, and then you realize, oh, they haven't gotten their second dose of MMR vaccine. Then here, the recommendation by some experts is to really hold the biologic for two to three half lives, give the live vaccine, and then wait another two to four weeks. Depends on the viremia level of the live vaccine. So, for example, let's say you start ixychizumab already on the child, and then you realize the child hasn't gotten their second dose of the MMR vaccine and that they need to get that. In this case, I would then hold the ixicizumab injection for 30 days. So that's about two half lifetimes because ixicizumab's half lifetime is about 13 days. So you would hold IXI for 30 days and then give the MMR vaccine, and then you wait another 30 days. In this case, the reason for that waiting period is because the viremia level for some of the mumps component can last up to four weeks. So you wait four weeks after the child receives the MMR vaccine before you resume the next shot of execution. Map for the child and.

Do you need to monitor any laboratory testing with topical JAK inhibitors?

You. A common question we receive is, do you need to monitor any laboratory testing with topical Janus Kinase inhibitors? We certainly know that there are recommendations to date, and we'll see what happens as these drugs get approved for dermatologic conditions given orally, we know there's laboratory monitoring and involved. However, the data we have, and I've been involved with some of these studies with topical application of the Janus kinase inhibitors do not appear to elicit any of the systemic safety signals that we see with systemic administration. So in my mind, I don't believe you need to do laboratory testing. Some clinicians may want to do it because these agents are new, and as they get approved, we'll see what the FDA puts in the labeling, but we certainly don't see the systemic reactions with topical application that have been associated with these agents given orally. Depending on what Janus Kinase inhibitor you're giving.

Is there any evidence for the use of oral or systemic glutathione?

So glutathione skin pigmentation? Is there any evidence the answer is intravenous and oral? Glutathione has never been studied in randomized, double blinded, placebo controlled trials for lightning the skin. It has been thought to be an antioxidant due to its effect on pheo and umelanin low oral bioavailability, which is why in some countries, even parts of the US, you can get it. Iv in my opinion, we should not be advocating for this until we have better studies and better safety outcomes.

How frequently do you recommend bathing children with atopic dermatitis?

You? Well, you know, that's going to differ depending on how severe the skin disease is. But generally speaking, you can bathe them up to once daily, and especially if they're pretty dirty people, if they play sports or run around a lot or get in the dirt up to once daily. Certainly, you don't have to do once daily. Every other day is reasonable. The key is, though, using moisturizing cleansers and applying moisturizers after the bath or shower, those are really the key. So if you're going to do the bath, there must be moisturizing cleansers and moisturizing creams applied afterwards to all areas of the body, especially those that are affected. So that's the key. It's not so much how few or how many baths the kids get. It's really more about what you're doing after the bath or shower.

How do you discuss PRP for hair loss with your patients?

PRP or plateletrich plasma has been a mainstay of treatment for androgenetic alopecia and even telogen effluvium in my practice for about six to seven years. One of the objections that patients have to using this treatment is the expense associated due to the fact that it is a chronic treatment. I simply explain to patients that treating hair loss with PRP is no different than any other lifestyle modification, no different than a nutritional or dietary change or going to the gym. When you go to the gym, everything looks the way it should. You stop going, you get back to your baseline. So if your patient has a success with PRP initially, they do need to continue with those treatments. My treatment algorithm is to do once monthly injections for three months, take a three month pause, and then reassess the patient. If the patient is happy and it's a success. We continue with yearly injections twice a year, up to four times a year in some patients. Now, every now and again somebody will need a booster if they have a new medication or telogen effluvium that's coming through and that's also okay. But the chronicity of the treatment is very important to explain from the get go. So your patients understand that this treatment is for them for as long as they care about their hair loss.

What level of impact is teledermatology having on dermatology and will it persist?

You. I would say telermatology is an amazing tool if used in the right way. I have lectured and like to use it as a triage tool to really be able to tell patients, hey, you need to come in immediately or be seen later. I think we will see it used more just because people have perhaps moved out of some larger cities and want to still maintain that relationship with their dermatologists, or are going to be doing more remote work and don't want to have to leave their home and come to a practice. I would say long term, the challenges are that there are certain things you can't assess as well by a tele dermatology. So my opinion is really that it's a great tool if used in the right way, and I think we'll continue to see it, likely not as much as we saw it during the height of the pandemic, but we will continue to see it in some form.

Can hypochlorous acid products be useful for staphylococcus aureus decolonization and can they be sprayed on the scalp?

The simple answer is yes. There's multiple studies that show that hypochlorous acid, and there's a number of products on the market, OTC products such as lasersin, that could go through the office. There's a levicin that can be also prescribed. But the data shows very clearly that they have a very high degree of eradication of staph aureus and really multiple different bacteria, not just staph strep and others. And yes, it's very nice on the scalp. I can tell you the other thing that works very nice for are conditions such as polyculitis and even acne. And acne. You can use this as a wipe down because it does is really destroys c. Acnes, number one. And number two, it's anti inflammatory. So those aspects go together. I tend to use product epicin for that because it's a higher concentration of hypochlorous acid.

Do you prescribe oral JAK inhibitors for your pediatric patients with vitiligo or alopecia areata?

You. So the answer to that is that I have not yet prescribed oral jack inhibitors for any of my pediatric vitiligo patients. I have prescribed it for my adult vitiligo patients. And in those situations, I've used oral tofastidinib, and I do prescribe oral jack inhibitors for my alopecia. Pediatric patients who are over 16. I haven't gone less than 16 yet. And again, I use the tofacidinib and it's five milligrams twice daily. I do have several patients who are in open label studies taking oral jacks, and unfortunately, none of those are pediatric trials, so I can't comment on that. But certainly in my pediatric patients, again 16 and over, we've had good success using the oral tofacidinib in many of those patients, and they tolerate it quite well.

What are the advantages of the Sensus device over older radiation therapy devices?

So I have to disclose, I am a consultant for census healthcare. I have helped develop some of the not only technologies, but of this I'm also president of the American Continuous Oncology Society. There are a couple of new, not just census, there's one or other especially new computer controlled radiation therapy devices. And superficial radiation therapy has dramatic benefits over a lot of other radiation therapy aspects, such as electron beam, because there's actually higher curates and lower side effects for non melanoma skin cancer. The tremendous advantage of the census device is that it's computer controlled. It really is much more accurate at dialing in exactly what you want to do. There are a great amount of different options you have from 50 to 100 kb, so you can look at different depths of tumor. You have the ability to have very large areas for keloid. We've published extensively on this for in Q wide recurrence following excisions. So there's a great degree of flexibility with that device you never had before. And as I said, you have the computer controlled aspect as well to be able to give you really good calculations from that perspective as well.

How do you decide whether to use a JAK first line vs monoclonal antibody?

You both classes of medications, be it jack inhibitor or monoclonal antibodies or biologics, really will play a big role in our management of patients with moderate to severe atopic dermatitis. This is not a quick question to answer, because the different jack inhibitors or the different biologics that are emerging for atopic dermatitis all have different efficacy profiles, different safety profile, and different dosing profiles. So the decision on which one to use for our individual patient really needs to be customized or individualized based on the patient's disease severity, their experience with past therapies, and possibly their comorbidities as well. So the key, when we look at these different data that's coming out is really also looking at the subpopulations that are responsive to the different therapies. So, let me give you a few examples. For example, for those who have done really well on dupilumab, there would be really no reason to switch, in my opinion, if they haven't responded optimally, then we want to look at the head to head trial data that they may have with another agent, and also the switch data that there may be available of looking at dupilumab failures and how they would do, let's say, on another il 13 inhibitor or on a jack inhibitor. Some jack inhibitors have shown really robust efficacy, and this is very promising in terms of the use of jack inhibitors for long term control of atopic dermatitis. However, they will likely need to be monitored in terms of laboratory monitoring at some frequency. And so when we think about that, in addition to using jacks as a long term control therapy for atopic dermatitis, I think they can also be very helpful in terms of controlling flares, in that some jacks have a really fast onset of action, and they can be used more on and off because they're small molecules. So we don't really have to worry about things like antidrug antibodies. So they can be used like how we currently use cyclosporin, but with a greater safety profile. So I can see scenarios where jack inhibitors can be used, for example, in combination with biologics with regards to controlling flares that may happen when a patient is not well controlled on the biologic. And then finally, the clinical data for the emerging IL 13 inhibitors show that they have good safety data and will likely remain really an excellent choice for long term control for AD patients. And then, very importantly, patient preference need to take their preference into account whether they would prefer an oral medication or injectable medication. And that will be another key factor in terms of ultimately deciding what may be a good therapeutic option for them.

What are the recommendations on how to monitor patients on oral JAK inhibitors?

You. A very common question is what are the recommendations on how to monitor patients that are on oral Janus kinase inhibitors, specifically with laboratory testing? I want to refer you to an article by Nash in the Annals of Rheumatic Diseases in 2020. And you can go to PubMed, it's open access and you can actually print the article. And there are recommendations from clinicians that utilize a lot of Janus kinase inhibitors because these agents, although they're not yet approved in the United States for dermatologic disorders, there are many of them that are used for other conditions in other specialties, like in rheumatology, for example. So patient selection is important. So in the history we want to get the vaccination status of the patients, if they have any history of severe infections or malignancies, if they have any history of thromboembolic disease. And then as far as pretreatment screening, we look at obviously getting the history and physical exam, as I mentioned, but looking at complete blood cell counts, liver function tests, hepatitis B and hepatitis C testing, TB screening and HIV testing in patients at high risk. Those are important as far as baseline evaluation because, remember, these agents, depending on what Janus kinases they're inhibiting, can impact on a variety of different organ systems in terms of potential adverse events, even though they may be uncommon in many cases. Then as far as follow up monitoring, complete blood cell counts and liver function tests at month one and three, and then periodically there after around every three months, lipid levels at about three months and maybe periodically thereafter. And don't forget, skin examination, annual skin exams and skin cancer detection are recommended. So this article really gives you a good framework until we get further direction as we see approvals and recommendations in package inserts and from further information from studies.

How often do you recommend shampooing with seborrheic dermatitis?

You answer to that is going to be different depending on the hair type and how you wear your hair. So for african american patients who have sebric dermatitis, especially women, generally, they're not going to wash their hair any more than once weekly, and probably they're going to be, on an average, about every two weeks. So when you have separate dermatitis, I recommend once weekly because I think that if you can keep your scalp cleansed and minimize the oils that build up and also use a good antidandruff shampoo to the scalp once a week, that helps to take down the itching and the build up of the scaling, et cetera. So once weekly would be my recommendation at the very least for women of color, for those who can wash their hair every day, and if they don't wash their hair, they get the greasies, you can certainly wash your hair every day. Generally, I recommend that you use anti dandruff shampoos, especially prescription ones, only about three times a week, two to three times a week. So I wouldn't keep using those. They're very harsh on the hair shaft. So I do recommend putting the shampoo on the scalp and using your nice moisturizing shampoo on the hair. So it really does depend on hair type and what your hair style is going to be. But I think that you want to make sure that it makes sense for the patient, because if you tell someone who's an african american woman who wears her hair in a relaxed style to wash her hair every day, she won't follow any of your recommendations. So you really have to know what the hair care practices are before you give that information.

Do IL-17 inhibitors work more quickly than IL-23 inhibitors and what does that mean for my patients?

You. So to really answer the question of does one drug work better or more quickly than another? You really need a head to head study. And fortunately, we have that in a couple of cases. So we have Exora R, which was a study, a head to head study of ixicizumab, the IL 17 inhibitor, versus gaselkumab, the IL 23 inhibitor. What that study found was, looking at the first twelve weeks, that there was a faster response to ixicizumab versus biselcum. However, looking at 24 weeks and using Pazi 100, so complete clearance of the skin, there really was not a difference. Both drugs performed equally at 24 weeks, although the Pazi 100 response at twelve weeks was a little bit higher for ixicizumab than with gaselchumab. There's another study called emerge. This was secukinumab versus risenkizumab, a head to head study. And that study really found a similar speed of onset, or PasI 100 response rate at week twelve. This study went out for 52 weeks and actually showed that risen kizumab had a higher Pasi 100 response rate at week 52 than did psychicinumab. So about two thirds of patients on risen kizumab, we had a Pasi 100 versus 40% treated with psychicinimab. What does that mean for our patients? I think it depends. Does your patient, are they looking for their response in two weeks or four weeks? In that case, you might want to consider, for example, executionab, or are they looking at what's their long term durability? Um, so I think it depends. I think most patients are really looking for a treatment for the long haul, but there are going to be some who really want that quick response, and that might be a situation in which an IL 17 could be preferable for that patient.

How do you compound your topical JAK inhibitors like tofacitinib or ruxolitinib?

You. I often get asked about the compounded jack inhibitor topical creams like the 2% topacitinib and 1.5% ruxolitinib cream. How do I compound them? What kind of base do I put them in? The answer is talk to your compounding pharmacy about the best vehicle that has the least amount of preservatives. I typically like to recommend using pf base or preservative free base. Most compounding pharmacies can actually do that for you. It really also depends on the cosmetic elegance you're trying to achieve, but preservative free base in my hands has worked quite well all.

How would you compare and contrast the utility of the information from 31-GEP vs. SLNB?

You. So both GEP and sentinel node biopsy are attempting to answer the same question. Is or will this melanoma metastasize distantly? One does it genetically, one does it by actually looking for tumor in the lymph nodes. So the differences that we see are that if we look at sensitivity or how likely if a metastasis is present, is it that the test picks it up? It turns out that GEP is more sensitive. So there are going to be more melanomas called high risk by GEP than by sentinel node biopsy. Probably a couple of reasons. One is that not all, most but not all melanomas do metastasize through the lymphatics. So if you have a melanoma that never goes through, the lymphatics, metastasizes heterogeneously. You may pick that up with GEP, but not by sentinel node biopsy. Now, the flip side of this is that there are going to be cases where a melanoma may have a genetic signal suggesting metastasis, but it doesn't go on to metastasize. Maybe it's treated, maybe it's excised. Maybe the test is over calling it so you'll have more false positives with GEP than you do with sentinel node biopsy.

How far laterally will you inject the frontalis?

You. It really has to do with the patient and what their needs are. Generally, if you draw a line up in the lateral aspect of the little upward bulge of the lateral eyebrow and go up, that's probably a good place. You don't want to be too medial because then you can have the quote Bach look, and being too lateral may drop the lateral brow. So as a general rule of thought, I think if you're looking at this general normal curve of the eyebrow and go straight up from there, generally you want to go up at least 2 cm from there to inject the frontalis.

Is hair recoverable in pattern hair loss?

You as long as you still have fine or intermediate hairs present, you can oftentimes use medications or other modalities to prolong the antigen time of those hairs. So to understand that, you have to kind of understand what's happening in pattern hair loss. In pattern hair loss, the antigen phase is shortening, so the hair stays on the head less time. So instead of staying on the head five years, it might stay on the head six months or a year or however long it is. But it's shortened and it doesn't have time enough to thicken, increase in diameter and provide density. So if you can use a medication such as oral or topical minoxidil that prolongs antigen and the hair stays on the head longer, it gets larger in diameter and it starts to contribute to density. So in that case, we're not really reversing hair loss such that we're bringing hairs back that weren't there. We're just sort of pushing the hair growth in the opposite direction. Instead of getting smaller, it's getting larger, and therefore your density looks better and the hair looks fuller. So if you're lucky enough to respond to one of the topical, oral, or Prp type injections, then yes, that's going to happen and you're going to have what looks like a reversed hair loss process, but it's really just prolonging of antigen.

What is the data on PLA positivity for dysplastic nevi?

You. We did a study in which we looked at dysplastic Nevi with severe atypia or severely dysplastic nevi, and we looked to see if they expressed link and or prime, and also if they carried turp promoter mutations. It turns out that 61% of the severely dysplastic Nevi did express link and or name. Now, interestingly, only 4% of these had a turt promoter mutation, and that is, by contrast, melanomas. About 70% of those had a turt promoter mutation. So what that tells us is that severely dysplastic nevi have some of the early features of melanoma, particularly link and or prem positivity. However, they're very unlikely to have a turt promoter mutation. So if I have a nevis that has all of these features and is read as a severely dysplastic nevis, I will personally go back and re excise that to make sure that it's completely out.

Are stronger retinoids more effective for Post-Inflammatory Hyperpigmentation compared to weaker retinoids?

You retinoids in PIH is a story than a plot that continues to thicken. In my opinion. There have been some studies that have shown, for example, that tazaratine point one cream was more effective than adaptane .3 gel in treating PIH. So the question is, are all retinoids created equal for post inflammatory hyperpigmentation? And in my opinion they're not. And I think you have to use the strongest retinoid vehicle you can with minimizing irritation because you don't want to get a retinoid dermatitis, especially in a skin of color patient, and then subsequently get PIH from the retinoid dermatitis. So make sure you're selecting based on vehicle and skin type and having that discussion with your patient.

Can you comment on the impact of biologics on COVID vaccine efficacy?

You. So one of the big questions that has arisen among our patients treated with biologics is what do we tell them about getting vaccinated? So, one, we certainly are telling patients, if you're on a biologic, you should certainly be vaccinated against Covid. We have had some recent studies that have given us some information about how those patients respond. And so I think that one of the most interesting studies looked at the response to the Pfizer mrna vaccine, and they found that patients on tnf inhibitors, IL 17 and IL 23 inhibitors, compared to healthy controls, really had very similar antibody titers to the vaccine and neutralizing antibody activity. They also looked at patients with methotrexate. Their antibody levels and neutralizing activity were slightly lower, but still were adequate. Now, the other thing that this study looked at was they looked at t cell responses, and interestingly, they found that t cell responses across all those therapies, biologic methotrexate really were comparable to those in healthy controls. So I think it really does suggest that patients on biologics for psoriasis will mount a good vaccine response. They should be encouraged to get vaccinated. I will say that other studies that have looked at other biologics that we use in dermatology, specifically b cell depleting therapies like rituximab, that is a drug that really does impair vaccine responses. So patients who have had rituxim map, particularly those who've had it within the past six months, are unlikely to mount a good vaccine response. They should be counseled to use good social distancing and precautions, and it probably makes sense to monitor titers in those patients.

Can you make a comment on rate of blindness in fat injections?

The rate of blindness from fillers per se, fat as well as ha, et cetera, is very low, but it has gone up over the years. And the key issue is not necessarily the type of filler that you're using, it's where you're injecting. So there are certainly risk areas. The globe, bella, is one of the highest. Lower forehead and nose are probably the key areas that you have to be extremely careful or avoid for blindness because you have the chance, obviously, of the retinal artery being embolized. Now, there is a data that fat is, ah, highest up on the list in a sense, but that has to do with where some of the studies are published, where they're using fat more ha, certainly can cause blindness as well. There are many reported cases of this. So it's really about being careful in terms of where you are injecting, no matter what you're using. From that perspective.

Do you compound any currently available JAK inhibitors into creams for topical use by your patients?

You? I do. I recommend typically topical topacidinib, which we have mixed up in a 2% topical ointment, and we use it for our alopecia patients. I haven't found it to be greatly successful on the scalp, but in my patients with eyebrow involvement, we sometimes do find that it can be very helpful. I've had a few patients who've used it for vitiligo, and again, it's usually the topical topacidinib. I have compounded ruxolidinib as well, but that's a little less commonly used and a little bit more expensive, in my experience. So I've used topacidinib, the topical topacidinib, and that's worked out pretty well for patients. There are some people who feel that the mixture where I've been compounding it is a little tingly when they put it on, but it kind of goes away very quickly, so people tolerate it quite well.

Can you explain how the new 31 GEP reporting has changed and what it means?

You if you order 31 GEP decision DX testing, it used to be that you would get a report that said a lesion was class one or class two, or it may have read class one a, class one b, class two a, class two b, and going from lowest to highest risk. And that gave you information about the patient's likelihood of having a distant metastasis. But it was really grouped into these four buckets. Reports now actually have a little more granular detail, specifically that you will get a GEP score that is continuous, and you will get a. I think what's really helpful is a percentage likelihood that that patient is going to have a positive sentinel lymph node biopsy. So that's taking into account out their GEP profile and factors like their age, the thickness of their melanoma, ulceration status and things like that. So a little more detail in the newer reports.

Are there any concerns with the use of IL-23 or IL-17 inhibitors in patients with a history of cutaneous squamous cell carcinoma (cSCC)?

You. Based on the currently available data looking at skin cancer and IL 17 and IL 23 inhibitors, there is no safety concerns or substantial safety concerns when it comes to using IL 17 or IL 23 inhibitors in patients with a history of cutaneous squamous cell carcinoma, and even if that particular history can be quite recent. That being said, it is very important that we see our patients who have psoriasis on these biologic agents in person at least once a year to make sure that we do a full skin check. Oftentimes, for my patients who are well controlled, I see them actually twice a year, and I do a full skin check at every one of those visits. But I will say at least once a year. Full body skin check is very important to screen for skin cancer in these patients and.

Gwyneth Paltrow is promoting Xeomin as a 'natural' Botox. In my 13 years, we mostly use Xeomin for people that are resistant to Botox or Dysport. Thoughts?

So, number one, all type a toxins, every single one of them, work. It's exactly the same. And the reason that xiaomin is different is that it doesn't have in its native state, the complexing proteins that either Botox or dysport or jubo has. And those are obviously the approved toxins. However, it's been shown very clearly that you get disassociation of those proteins, literally in the syringe, if not immediately after it's injected. So those complex proteins don't seem to have a factor in this. From that perspective. The reason it's called natural, they're saying, is because it's the 150 kilovolt protein and not the complexing proteins. However, there is no evidence, or virtually no evidence that having those complexing proteins, number one, is increasing the immune resistance to toxin, either botox or dysport. And there's also no evidence that those people who are, quote, resistant, and I'll talk about that in a second, get better results from Xemin. It's all about the issue of molecular potency, and I've published on this. You can just look my name up. I published on Journal of Cosmetic Dermatology last year on this for the paper on the science of botulinum toxin, the postulate paper, so you can look that up. It's really about molecular potency. There are people who are genetically more resistant, and there probably is a mechanism where the receptor gets toned down as you inject more. It really does not seem to be an immune response for any of these toxins, per se.

What other topical medications with novel mechanisms of action are in the pipeline for atopic dermatitis?

So this is actually a really exciting time because we've got three different drugs that are really in the pipeline and getting close for atopic dermatitis that are pretty distinct. Right. So we've got ruxolitinib, which just hit the market. Topical jack inhibitor. Main benefit, incredibly fast and incredibly effective. Main down inside comes with some box warnings. They may or may not matter a whole lot. They may or may not be relevant. We're still going to have to deal with them with patients. Second drug to Pinoroff, which is an aerohydrocarbon receptor modulator. Great part about that drug is in the psoriasis world and maybe in the atopic dermatitis world, it looks like if a patient does have a really good response and get the clear or almost clear, they will have the potential for a long term remission, where they won't have to continue to use topical. Don't expect there to be any box warnings on it. And then the third drug that's in development, reflumalast, which is a topical PDE four inhibitor, several hundred times more potent than anything that's on the market right now. And this one probably is the best, what I would describe as a jack of all trades, meaning relatively fast, very good efficacy, no box warnings, very tolerable. Going to come in a foam form as well as a cream form. And I think that that's going to be very helpful for sebderm, psoriasis, and atopic dermatitis. So those are the three main different drugs that we have in development right now.

What are the advantages of JAK therapy vs. monoclonal antibody therapy for atopic dermatitis?

You. So as a provider, as we're thinking about Jack inhibition, whether topical or systemic, versus monoclonal antibodies blocking Il four, IL 13, IL 31, the big thing to think about is that the jack inhibitors are much broader spectrum. So the monoclonal antibodies are very specific and blocking one antibody that may signal through the Jack pathway. But the Jack pathway, if we block it, we're actually the equivalent of hitting the person with multiple monoclonal antibodies. And so broader spectrum of action, which means there can work in things that are th one, like psoriasis, things that are th two, like atopic dermatitis, and things that are just inflammatory, like allergic contact dermatitis. So very broad spectrum activity compared to monoclonal antibodies. That being the main benefit. The other benefit, probably a significantly faster onset of action compared to monoclonal antibodies.

Is there any data on contact dermatitis with use of topical JAK inhibitors for atopic dermatitis?

You. So no studies that I've seen out there looking at topical jack inhibitors for if they're triggering allergic contact dermatitis. I'm not aware of any reports of allergic contact dermatitis from ruxolitinib. However, there is propylene glycol in the vehicle. So if you have somebody who's propylene glycol allergic, it is certainly possible that they are going to have allergic contact dermatitis from the cream. More interesting question. Question for me is, is topical recolitinib going to work for allergic contact dermatitis? It's a really interesting question. I actually expect that it will work for allergic contact dermatitis. My experience is that monoclonal antibodies do not work for allergic contact dermatitis. But I am betting that jack inhibitors, both topical and systemic, will, because they are broader spectrum, just like I talked about a minute ago. Talk about their comparison to monoclonal antibodies.

Can pregnant patients use ruxolitinib cream?

So can pregnant patients use rex solidity cream? As far as I'm concerned, pregnant patients can't use anything. If a pregnant woman is in my office and says, I'm thirsty, can I have a glass of water? My answer is, you know what? You better check with your ob gyn before we get you that water. Right. I don't want pregnant women using anything. The more interesting question here is women of childbearing potential. So do if somebody is of childbearing potential. So a 30 year old woman, and we're giving them recollective cream. Do we need to tell them to avoid pregnancy? The best answer we have there, the limited data that's out there about tofacitinib and other systemic jacks in pregnancy is that there don't seem to be big issues with them. So with the very limited systemic absorption of topical recollective cream, I don't have any concern about woman of childbearing potential using it. But what I would tell them is the minute you find out you're pregnant, you should stop using it. So I would not use it in a pregnant woman, but in a woman who was of childbearing potential or trying to get pregnant, I would tell her, you're fine to keep using it until the minute you find out you're pregnant. Those stop.

How concerned are you about the risk of thrombosis mentioned in the boxed warning for ruxolitinib cream?

You. I am very minimally concerned about the risk of thrombosis associated with ruxolinidib cream. So we do know that there's some risk of thrombosis associated with oral jack inhibitors. We do know that a very small amount of topically applied ruxolinib, so about 6% will get absorbed systemically. So there is potential for systemic effects. But we also know that the side effects of the oral jack inhibitors seem to be very ghost related. And since we know that the systemic exposure to topical rexylin inhibits can be very low, I think that if there is any thrombosis risk associated with it, it is extremely, extremely minimal.

How concerned are you about the risk of infection mentioned in the boxed warning for ruxolitinib cream?

So I'm even less concerned about the risk for infection mentioned in the in the box warning that I am for the risk of thrombosis. So again, the risk of infection associated with systemic jacks very clearly and directly related to the dose. The higher the dose, the more risk of infection. This is even much clearer, especially with something like zoster than it is with thrombosis. Since we know about this really strong dose relationship, dose response relationship in terms of the immunosuppression, and we know that the systemic absorption is very low, I am essentially completely unconcerned about the risk of infection. The thrombosis. I could more imagine there being that's more of a black white like if you get over a certain level, maybe you're more susceptible, the thrombosis a little less clear, still very minimally concerned about that. But the risk of infection is essentially zero, not at all.

How concerned are you about the risk of death mentioned in the boxed warning for ruxolitinib cream?

You. So I am not at all concerned about the risk for death. This maybe goes back to the thrombosis question. I suppose if there's a minuscule chance that it increases your risk for thrombosis. Well, if you get thrombosis, turn into a PE. A heart attack, stroke, whatever. So I can't be like, this is impossible and it's ridiculous. But you know what? I've prescribed topical recolinitive to probably a dozen people since it came out a couple of weeks ago. And the way that I say this to them, look, it's going to come with these warnings that says it might cause blood clots, it might increase your risk for infections, it might even increase your risk for death. As long as you're not eating the cream, I don't think you need to worry about any of that. So I just want to warn you about that so that whenever you get it, you're not startled. Just don't eat the stuff. That's the way that I talk to patients about it. Do I think that there is the possibility that there's some minuscule risk? It's possible because there is systemic absorption. Again, if it's a risk, it is incredibly minimal. And you also do have to always take this in context of what are your other options? Your other options. So, topical steroids. We know topical steroids increase the risk of diabetes. They increase the risk of osteoporosis. We know there are lots of local effects or potential for HPA access suppression. So it's not like we're comparing ruxolitinib to nothing. If we compare it to high potency topical steroids, certainly even the risk of those kind of systemic side effects, I think is going to be, in my mind, is certainly lower. With ruxolitinib is what makes the most sense.

Does atopic dermatitis always start in childhood?

You. My experience is that the vast majority of adults with atopic dermatitis have adult onset atopic dermatitis. Now, I was trained in residency that atopic dermatitis always starts in childhood, is always flexural, and is always associated with strong personal history of atopy. None of those things are true. Whenever you look at the AAD census criteria, which I think are fantastic. It's itchy, it's chronic, it's spongiotic, it spares the groin and axilla if it has those four characteristics, and it's not allergic contact dermatitis, it's not scabies, it's not sebraic dermatitis, it's not psoriasis, it's not any of those other things that we can easily rule out. So really, it becomes that atopic dermatitis is your default diagnosis for everyone with spongiotic dermatitis, unless it involves a groin and axilla or you are certain that there's some other type of dermatitis. So, again, does it always start in childhood? No. And in fact, my experience is, in adults, the vast majority of people who meet the criteria had no history of childhood dermatitis at all. In a purely adult onset disease.

Does atopic dermatitis always involve the flexural areas?

You. So my experience is that atopular dermatitis in adults rarely involves the flexural areas. The vast majority of patients that I'm treating with monoclonal antibodies, methotrexate, mycophenylate, cyclosporin, phototherapy, topical rexalinib, all of these things. It is very rare that, for me, any of these patients have flexural involvement. The vast majority, it's upper back, flanks, face, hands, thighs, backs of the thighs, fronts of the thighs, places like that. Adult onset atopic dermatitis. Incredibly different animal compared to the classic pediatric atopic dermatitis that we were taught about in residency. We just have had this wrong for years. Again, the vast majority of patients with adult atopic dermatitis this do not have flexual involvement.

Do people with atopic dermatitis always have atopic co-morbidities?

You? Absolutely not. It turns out, while there is a powerful and important connection between atopic dermatitis and other atopic comorbidities, for example, food allergy, asthma, allergic rhinitis, allergic conjunctivitis, all of these things are very common. And it turns out there is a common connection, especially that gets stronger as the disease severity gets higher. So more severe atopic dermatitis really does seem to be more likely to have allergic comorbidities. That being said, many patients have none. And I have a fairly sizable group of patients with even severe ad that really do not have asthma, hay fever, allergies of any sort. And in fact, even when you do serology, they don't even have elevated ige. So some people have actually talked about calling this a different disease altogether that maybe we would call atopic dermatitis if they have atopic comorbidities in this one atopiform dermatitis that's in the literature. Other people call it intrinsic versus extrinsic eczema. And the answer is we just don't really know why and what some of the other key ideas here, fundamentally from a pathophysiologic standpoint, are. But absolutely, it is true that we have patients with some or a lot and other patients with none, and.

Is there any basis to the concern about delayed nodules with the Voluma group of products?

Every single filler, hyaluronic acid filler has different manufacturing attributes. And some of the manufacturing attributes of the voluma group have been published and have been shown to perhaps cause more of a reaction. It's not clear whether that's an immune reaction, whether it sets up a little bit of an increased ability to have an indolent infection, a biome infection, but there is definitely published data now. It's still limited, meaning you don't see this very often. And it's very clear that if you use small aliquats of any filler, and that includes voluma, you will dramatically decrease the risk of any delayed nodules for these products.

Can you discuss your thoughts on the NEJM article on melanoma overdiagnosis and how GEP may fit into this?

So highlights of this New England journal article were that we are potentially experiencing an overdiagnosis epidemic within melanoma. And so overdiagnosis was kind of defined several ways. One, was we biopsy too many things, particularly too many benign lesions. Two, we are more likely, when is biopsied, if it has some histologic atypia, to actually call it melanoma, whereas in the past, a similar lesion maybe would have just been called an atypical nevis. Three, we are more likely to have these more, what would be called indolent melanoma. So, lesions that are melanoma, they're treated as melanoma, but they didn't have the same potential for metastasis as what we would maybe have thought of as melanoma, for example, 50 years ago. So how can GEP help with this? I think what GEP can do is provide objective data. So, one, in terms of what we biopsy, we're not just saying this mole has a little bit of an irregular border. We're saying we can actually measure some degree of genetic atypia. Two, in terms of, do we call an equivocal lesion linoma or benign? Again, you can use some genetic information, not just the histologic features. And then three, one of the really, the bad outcomes of over diagnosis is over treatment. So by getting genetic information on a lesion's behavior, then we have the potential to actually de intensify treatment for some patients.

How do you manage the diarrhea associated with apremilast?

You. So, diarrhea occurs in about 16% to 18% of the patients on a premolast, and it's about three times greater the rates than that seen in the placebo group. Typically, when diarrhea were to occur, it usually occurs during the first two weeks of therapy. And the duration of the diarrhea is usually about two weeks. In most cases, diarrhea can be managed while on premalast and is not a reason for discontinuing the medication. And some of you may wonder, gosh, what is the mechanism of this premolast related diarrhea? It's a type of secretary diarrhea and it's thought to be really a class wide effect for RPDE four inhibitors. And the proposed mechanism is that premilas can increase, as we know, the intracellular cyclic amp level as a result of that, that can lead to extra activation of the chloride channels in the crypts of the small intestine. So what happens is that there will be an excess secretion of these chloride ions which lead to this secretary diarrhea. And it can take the large bowel, really a couple of weeks to really adapt and adjust. Now, how do we manage this? Typically with over the counter therapies include things like pepto bismol or fiber supplements. Those are typically sufficient for most patients. Sometimes you may need to resort to some prescription medications. Oftentimes the oral prescription agent crofellamer can be very helpful in terms of reducing the secretary diarrhea. One can also use lamodal as another option for our patients. So again, the premalass associated diarrhea can occur in about 16% to 18% of patients. Typically mild can be managed without discontinuing a premalis. Through these methods and.

How are noncompete agreements handled in dermatology practices?

It's really a legal state to state issue. And what's interesting is that the Biden administration just put out an executive order essentially looking to limit non compete agreements because they feel it's anti competitive. Most states, the way it's looked at is it's got to be reasonable, meaning you can't say you can't practice dermatology, you can't practice forever. You can't practice normally. It's somewhere around 5 miles, because if the practices patients are not yours, but the practices, they don't want you opening up across the street and saying, hey, patients come to me. What generally happens is it's about 5 miles is considered reasonable all in most states. And there is normally now also a monetary aspect that goes along with it. In other words, you can do non compete and go 5 miles. Or if you break that, there is a specific set monetary aspect as well that you have to pay back the practice.

What are the age indications for upcoming JAKs?

You. If we take oral jack inhibitors, the age indication will be, so far, 18 years of age older, because that's what we are doing the clinical studies for. However, as we know, roxalutinib topical jack inhibitor has been approved for twelve and above.

Is there an ideal time to apply emollients?

You because of the trans epidermal water loss when you take a bath. Actually, the water is going to evaporate very, very fast in the atopic dermatitis skin. So what would be nice is to apply the emollient or the moisturizer right after a bath. And we usually tell patients, don't use a towel. Air dry yourself. And while your skin is wet, apply the moisturizer so it keeps that moisture within the skin.

Can you explain the different types of moisturizers for atopic dermatitis?

You. The moisturizers are very complicated, even though we think it's a very simple issue. But there are two major types. We have occlusive moisturizers, just like vaseline, that occludes the skin. But if you occlude the dry skin, what good is it going to do? Absolutely nothing. Then we have humectants. Humectants, they actually attract humidity and water from the deeper layer of the skin as well as from the atmosphere. So then the humectants bring humidity and water to the skin. However, because of trans epidermal water loss and impaired epidermal barrier, especially in atopic dermatitis patients, the water is going to come as fast as it's going to live as fast as it comes, and it will evaporate. So we do need occlusive moisturizers. So the combination of those two is the ideal moisturizer.

Can you prescribe dupilumab to patients with a history of malignancy?

You? Well, that's a great question. When we do any clinical study, we exclude all the patients with a history of malignancy. But when people come through the door into my clinic, I cannot say, okay, you had skin cancer or you had breast cancer. I'm not going to be able to treat you. Right. So what I usually do is I call the oncologist and we make a coordinated effort. What we can or we cannot use in those patients.

Which areas of the body can you and can’t you apply ruxolitinib cream to?

You. So unlike the topical steroids, we don't have a concern when it comes to the location or the body area where we can use rock scream. We can use it on the face, we can use it on the intertrignous areas. When we did the study, because of the skin texture on the palms and soles, the skin is very thick. We did not use it on the palms and soles. But other than that, everywhere else was used. And there is no issue using rock scream anywhere else on the body. It's not like the steroids. I'd like to mention that.

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

When starting a patient on an oral beta blocker for rosacea, how do you counsel them about side effects?

What are high risk features of cSCC?

What is the best sunscreen to prevent skin cancer?

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

How was the 40-GEP test developed?

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What are the advocacy priorities of the AAD?

How are PBMs and Health insurance companies related to one another?

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What is Budget neutrality, and how does it affect our reimbursement?

How do I get involved with the AAD?

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

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