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JAK Inhibitors

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Welcome to Dermbits! Watch short videos of KOLs answering your questions

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Dermbits

SCC June 2023

What is the best sunscreen to prevent skin cancer?

What are high risk features of cSCC?

Is SCC more deadly than melanoma?

How do I order the 40-GEP test?

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

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

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

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

How was the 40-GEP test developed?

How do GEP tests work?

Incyte AD May 2023

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

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

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

Does topical ruxolitinib work for pruritus or pruritic disorders?

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

Does tralokinumab have a higher rate of conjunctivitis versus dupilumab?

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

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

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

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

PrimusRX Psoriasis June 2023

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

How important are vehicles in topical Plaque Psoriasis therapy? 

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

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

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

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

How do you utilize product samples in plaque psoriasis? 

How do access, tolerability and efficacy improve compliance? 

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

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

BI Spevigo July 2023

What is Generalized Pustular Psoriasis (GPP)?

What is the clinical presentation of GPP?

What are some of the systemic associations of acute GPP?

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

Who is at risk for GPP?

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

What are some known triggers of GPP?

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

What is the pathophysiology of GPP?  

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

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

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

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

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

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

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

What are treatment options for GPP?

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

What is the safety profile for spesolimab?

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

Arcutis Zoryve July 2023

How quickly do patients experience clearance results with topical roflumilast?

How would you describe the overall tolerability of topical roflumilast? 

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

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

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

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

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

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

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

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

Castle SCC August 2023

What is the 40-GEP test?

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

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

Why do we need to better assess SCC prognosis?

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

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

How does the 40-GEP test work?

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

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

What SCCs are appropriate for the 40-GEP test?

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

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

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

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

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

Is the 40-GEP test covered by Medicare?

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

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

What are the traditional SCC prognostic paradigms?

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

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

What are the trends in US incidence of SCC?

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

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

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

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

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

Why doesn't SCC get the respect it should?

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

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

Lilly Olumiant AA August 2023

In what ways can alopecia areata affect quality of life?

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

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

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

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

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

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

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

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

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

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

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

How soon can patients start seeing results on baricitinib?

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

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

What is the mechanism of action of baricitinib?

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

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

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

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

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

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

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

What is the recommended dosing regimen for baricitinib? 

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

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

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

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

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

Incyte AD August 2023

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

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

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

Can ruxolitinib cream be used in combination with therapeutic biologics, other JAK inhibitors, or immunosuppressants?

<p>In the case of ruxolitinib cream, there are some dos and don'ts when you're thinking about the actual FDA approved prescribing information. So because ruxolitinib cream was studied as a monotherapy, you'll notice that there's an indication on the label that suggests that it's not for use in combination with therapeutic biologics, other JAk inhibitors or immunosuppressants. Now in the real world based on data that our group and others have published, it looks like people are sort of mixing and matching therapies in that regard. Remember not the way that the medication is approved per label, but in the real world it looks like there's going to be some patterns of people using it in combination with other therapies. Luckily, it looks like there's going to be some great studies going on where we can actually see and make sure if this is going to be efficacious and safe for individuals.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya addresses the question of whether ruxolitinib cream can be used in combination with therapeutic biologics, other JAK inhibitors, or immunosuppressants. According to the FDA approved prescribing information, ruxolitinib cream was studied and approved as a monotherapy. Therefore, the label indicates that it should not be used in combination with therapeutic biologics, other JAK inhibitors, or immunosuppressants.&nbsp;</p><p>However, despite this indication on the label, real-world data from various sources, including Dr. Chovatiya's group, suggest that some individuals are combining ruxolitinib cream with other therapies successfully. This practice deviates from the approved label usage. Nevertheless, ongoing studies are being conducted to evaluate the efficacy and safety of using ruxolitinib cream in combination with other therapies. These studies aim to provide valuable insights into the potential benefits and risks of such combinations, ensuring informed and evidence-based treatment decisions for patients.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Ruxolitinib cream was studied and approved as a monotherapy.&nbsp;</li><li>The FDA-approved prescribing information for ruxolitinib cream indicates that it should not be used in combination with therapeutic biologics, other JAK inhibitors, or immunosuppressants.&nbsp;</li><li>Despite the label indication, real-world data shows that some people are combining ruxolitinib cream with other therapies successfully, deviating from the approved usage.&nbsp;</li><li>There are ongoing studies to determine the efficacy and safety of using ruxolitinib cream in combination with other therapies. These studies aim to provide more insights into the potential benefits and risks for individuals who use the cream in combination with other treatments.</li></ul>

What limitations of other atopic dermatitis therapies does ruxolitinib cream address?

<p>We've had topical therapies for a long time when it comes to atopic dermatitis, but we've always had some gaps in our care. One big one has been the fact that generally, all of our topicals are pretty broadly acting. So in the case of topical corticosteroids, really, a blunt instrument, and one which has oftentimes has a lot of side effects associated with it. Thinking about thinning of the skin, pigmentary issues, loss of subcutaneous fat, and even potential systemic absorption of steroids as well. In the case of topical calcineurin inhibitors, modest potency and also sometimes adverse events related to actual use themselves in terms of stinging and burning, along with the box warning that at least suggests the potential risk of lymphomas that hasn't been borne out in the long run. For that reason alone, there's been just general desire for a topical therapy that's going to be safe, that's going to be effective, and something that comes in a non-steroid package. And in the case of ruxolitinib cream, it kind of checks all those boxes that you're looking for, potency that rivals some of the stronger topical corticosteroids, and a very nice steroid sparing effect as well, with safety that seems to be borne out both in terms of actual clinical trial data and the real world data as well.</p>

<h6>Summary&nbsp;</h6><p>Dr. Raj Chovatiya discusses the limitations of other atopic dermatitis therapies and how ruxolitinib cream addresses these issues. Historically, topical therapies for atopic dermatitis have had some shortcomings. Topical corticosteroids, while effective, are considered a "blunt instrument" and may lead to various side effects, such as thinning of the skin, pigmentary issues, loss of subcutaneous fat, and potential systemic absorption of steroids.&nbsp;</p><p>On the other hand, topical calcineurin inhibitors have modest potency and may cause adverse events like stinging and burning. There has also been concern about a potential risk of lymphomas, although this has not been supported in the long term.&nbsp;</p><p>Therefore, there has been a need for a topical therapy that is safe, effective, and non-steroidal. Ruxolitinib cream appears to meet these requirements. It offers potency comparable to some of the stronger topical corticosteroids, and it has a favorable steroid-sparing effect. Furthermore, both clinical trial data and real-world evidence suggest that ruxolitinib cream is a safe option for managing atopic dermatitis. This addresses the limitations of previous therapies and provides a promising treatment alternative for those with the condition.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Ruxolitinib cream addresses limitations of other atopic dermatitis therapies.&nbsp;</li><li>Traditional topical therapies for atopic dermatitis have some gaps in their care and there is a general desire for a topical therapy that is safe, effective, and non-steroid-based.&nbsp;</li><li>Topical corticosteroids are broadly acting but often associated with side effects like thinning of the skin, pigmentary issues, loss of subcutaneous fat, and potential systemic absorption of steroids.&nbsp;</li><li>Topical calcineurin inhibitors have modest potency and can cause adverse events such as stinging and burning.&nbsp;</li><li>Ruxolitinib cream offers potency comparable to strong topical corticosteroids and a steroid-sparing effect.&nbsp;</li><li>Ruxolitinib cream's safety has been supported by both clinical trial data and real-world data.  </li></ul>

How quickly can patients expect to start feeling itch reduction with ruxolitinib cream?

<p>One of the more impressive features of ruxolitinib cream, both in terms of actual studies and the real world, has really been how fast its resolution occurs. So I remember some of the first times that I used the therapy, I had patients respond, “This stuff works extremely fast,” and what's ended up happening is a lot of the analysis from the phase two trial programs has really matched what's been seen on the real world. So you can actually see that typically within minutes to hours you're actually going to be significant changes in the actual itch scores for patients in the way these studies were designed. I will say in my clinical experience, this is kind of what I've actually seen in my patients as well.</p>

<h6>Summary&nbsp;</h6><p>According to Dr. Raj Chovatiya, ruxolitinib cream has shown impressive itch reduction results both in clinical studies and real-world applications. Patients using the cream can expect to experience significant itch relief within minutes to hours after application. Dr. Chovatiya's clinical experience aligns with the findings from phase two trial programs, where patients reported fast and noticeable improvements in their itch scores shortly after using the cream.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Ruxolitinib cream provides rapid itch reduction.&nbsp;</li><li>Both real-world experiences and clinical studies have demonstrated the fast resolution of itch with ruxolitinib cream.&nbsp;</li><li>The cream has been praised for its quick and effective action in reducing itch, as acknowledged by patients and healthcare professionals alike.  </li></ul>

Ruxolitinib cream is indicated for short-term use; when should patients discontinue use?

<p>With any therapy, there's going to be people that respond and potentially people that don't respond as well. So a question that oftentimes comes up is how long should I be using ruxolitinib cream in somebody that's a good candidate? Should I stop? Should I keep going? What should I do? Well, there is some really helpful guidance that's baked right into the actual prescribing information that suggests that this is something you're going to use twice daily for eight weeks and assess. If you're having actual improvement, right, you're gonna keep using it. If you're not really seeing what you want to at that point in time, really good point that you want to sort of reassess and figure out if this is the right treatment. This is kind of what's meant in terms of short term. If you read along the actual indication statement, it then talks about sort of a non-continuous chronic use. This is exactly how the trial program was designed to take a look at people who sort of used it on a need to use basis in the long run and this is oftentimes the discussion that we're going to be having with our patients in the real world.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya discusses the appropriate use and discontinuation of ruxolitinib cream, considering patients' responses to the therapy. According to the prescribing information, ruxolitinib cream is meant for short-term use. For patients who are good candidates for this treatment, the recommended usage is twice daily for eight weeks.&nbsp;</p><p>After the initial eight-week period, patients and healthcare providers should assess the response to the treatment. If significant improvement is observed, patients should continue using the cream. However, if the desired results are not achieved at that point, it is essential to reevaluate whether ruxolitinib cream is the right treatment option.&nbsp;</p><p>The indication statement for ruxolitinib cream also mentions "non-continuous chronic use." This refers to the trial program's design, where some patients used the cream on an as-needed basis in the long run. The decision to continue or discontinue the treatment should be based on the individual's response and the discussion between the patient and their healthcare provider in real-world scenarios.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>The duration of use depends on the patient's response to the treatment.&nbsp;</li><li>The prescribing information recommends using it twice daily for eight weeks and assessing the results.&nbsp;</li><li>If there is improvement, patients should continue using it.&nbsp;</li><li>If there isn't significant improvement after the initial eight weeks, it's essential to reassess whether this treatment is right for the patient.&nbsp;</li><li>The indication statement also mentions the possibility of non-continuous chronic use, as seen in the trial program design.</li><li>&nbsp;In the real world, healthcare professionals will have discussions with their patients about using the cream on an as-needed basis in the long run.</li></ul>

What is the recommended dosing regimen for ruxolitinib cream?

<p>Ruxolotonib cream is recommended for use twice daily to all the areas of active atopic dermatitis from head to toe. In the trial programs, people had involvement of all sorts of areas. The head and neck a common one where we're really limited by what we can actually use, almost 40% of people there. So really it's something you can use safely across the skin surface area twice daily. And no more than about one 60 gram tube per week.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya explains the recommended dosing regimen for ruxolitinib cream. The cream should be used twice daily and applied to all areas of active atopic dermatitis from head to toe. In clinical trial programs, it has been found effective for various areas of the body, including the head and neck, where traditional treatments might be limited. The cream can be safely used across the skin surface area twice daily, and it is advised not to exceed the usage of one 60-gram tube per week.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Recommended dosing regimen for ruxolitinib cream: Twice daily application&nbsp;</li><li>Application area: Apply to all areas of active atopic dermatitis from head to toe&nbsp;</li><li>Common involvement areas in trial programs: Head and neck (limited to approximately 40% of people) • Maximum weekly usage: Not to exceed more than one 60-gram tube per week</li></ul>

What is the maximum dosage per week recommended for ruxolitinib cream?

<p>Depending on how much body surface area and the severity of someone's atopic dermatitis, there's probably going to be differences in use for any individual. Now, in general, based on the way that the prescribing information is written, you're going to be thinking about twice daily use and up to one 60-gram tube per week. So in the course of four weeks, or about a month, no more than four 60-gram tubes. Now, this may not actually be the amount you end up using just based on how much someone’s body surface area is. For instance, if somebody has less than 10% BSA, you may find that one tube can actually last in quite a while compared to somebody who's hanging out in that 10 to 20% range.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya explains the recommended maximum dosage per week for ruxolitinib cream, considering individual variations in atopic dermatitis severity and body surface area. Generally, the prescribing information suggests twice daily use of the cream, not exceeding one 60-gram tube per week. So, over the course of four weeks (approximately a month), the maximum usage should not exceed four 60-gram tubes. However, the actual amount used may differ based on the individual's body surface area. For example, if someone has less than 10% body surface area affected by atopic dermatitis, one tube might last a long time, while someone with a body surface area in the 10 to 20% range may use the cream more frequently. It's essential for patients to follow their doctor's specific instructions and not exceed the recommended dosage.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Maximum dosage per week recommended for ruxolitinib cream depends on body surface area and the severity of atopic dermatitis.&nbsp;</li><li>Individual usage may vary based on the person's body surface area.&nbsp;</li><li>If someone has less than 10% body surface area (BSA), one tube may last longer compared to someone with 10 to 20% BSA.&nbsp;</li><li>The prescribing information suggests twice daily use and up to one 60-gram tube per week.&nbsp;</li><li>Over the course of four weeks, the maximum usage should not exceed four 60-gram tubes.</li></ul>

When should oral antibiotics be used in the treatment of atopic dermatitis?

<p>A common historical misconception is that oral antibiotics may actually be a helpful monotherapaputic option for patients with atopic dermatitis. Now there is a kernel of truth to this in that we know that infections both cutaneous and systemic can be important comorbidities in patients with atopic dermatitis. Where might an oral antibiotic be useful? Think about that patient, oftentimes quite severe, that has a lot of open areas that are oozing and weeping that have a lot of golden crusting, AKA impetiginization, bacterial colonies that are hanging out right over those open areas of atopic dermatitis. Beyond that, you're typically not going to be thinking about oral antibiotics as a long-term treatment strategy. Really, you should be thinking about more targeted treatment approaches that get at some of the immunopathogenic roots of atopic dermatitis.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya discusses the use of oral antibiotics in the treatment of atopic dermatitis. He points out that there is a historical misconception that oral antibiotics can be a helpful standalone treatment for atopic dermatitis. While infections, both on the skin and throughout the body, can be significant comorbidities in patients with atopic dermatitis, oral antibiotics should be considered in specific situations.&nbsp;</p><p>The appropriate scenario to use oral antibiotics is when dealing with a patient, usually with severe atopic dermatitis, who has a lot of open and oozing areas with golden crusting, also known as impetiginization. In such cases, bacterial colonies are present in those open areas, and oral antibiotics may be useful in managing the infection.&nbsp;</p><p>However, beyond this specific context, oral antibiotics should not be considered a long-term treatment strategy for atopic dermatitis. Instead, more targeted treatment approaches that address the immunopathogenic roots of atopic dermatitis should be considered for managing the condition.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Oral antibiotics are not a recommended monotherapy for atopic dermatitis.&nbsp;</li><li>Oral antibiotics can be useful in cases where the patient has severe atopic dermatitis with oozing, weeping, and golden crusting (impetiginization) in open areas, but not as a long-term treatment strategy for atopic dermatitis.&nbsp;</li><li>Instead, targeted treatment approaches should be considered to address the underlying immunopathogenic factors of atopic dermatitis.</li></ul>

What do you recommend for patients with atopic dermatitis who require long-term treatment?

<p>Atopic dermatitis is a chronic disease. I'll say that again, atopic dermatitis is a chronic disease. This mantra there is something, I repeat to my patients who oftentimes, maybe are used to thinking about a quick fix for their problems. And really once you get that educational point across, you really unlock the possibilities that can be unearthed for long term treatment. So with atopic dermatitis, we have a few good options for long term treatment. Biologic therapies, of which we have a couple available to us, even oral JAK inhibitors of which have a couple available to us as well, phototherapy potentially, even old school oral immunosuppressants based on the patient type. These are all going to be part of my discussion of my patients, but primarily what I really want to do is frame the idea of it being a chronic disease. So at least my patients will understand that wee oftentimes have to go with chronic approaches that can provide control in the long run.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya discusses the long-term treatment options for patients with atopic dermatitis, emphasizing that atopic dermatitis is a chronic disease. He stresses the importance of understanding this fact, as many patients may be seeking quick fixes for their condition. Once patients comprehend the chronic nature of the disease, they can explore more effective long-term treatment options.&nbsp;</p><p>Dr. Chovatiya mentions several long-term treatment options available for atopic dermatitis. These include:</p><ol><li>Biologic therapies: These are advanced treatments that target specific molecules in the immune system to control inflammation and symptoms.&nbsp;</li><li>Oral JAK (Janus kinase) inhibitors: These are medications taken orally that also work to suppress the immune system and reduce inflammation.&nbsp;</li><li>Phototherapy: This treatment involves controlled exposure to ultraviolet light to improve symptoms.&nbsp;</li><li>Oral immunosuppressants: Old-school medications that can be considered based on the patient's type and condition.</li></ol><p>Dr. Chovatiya acknowledges that all of these options will be part of his discussion with patients. However, he primarily focuses on framing the idea of atopic dermatitis as a chronic disease. This understanding will help patients realize that long-term, chronic approaches are often necessary to achieve proper control over the condition.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Atopic dermatitis is a chronic disease that requires long-term treatment.&nbsp;</li><li>Biologic therapies are available as a long-term treatment option for atopic dermatitis.&nbsp;</li><li>Oral JAK inhibitors are also an option for long-term treatment of atopic dermatitis.&nbsp;</li><li>Phototherapy can be considered as a potential long-term treatment approach.&nbsp;</li><li>Old school oral immunosuppressants may be prescribed based on the patient's type and condition.&nbsp;</li><li>The focus should be on educating patients about the chronic nature of the disease.&nbsp;</li><li>Emphasizing the chronic aspect helps unlock possibilities for effective long-term treatments.&nbsp;</li><li>The goal is to provide long-term control of atopic dermatitis using chronic approaches.</li></ul>

When do you recommend the use of wet wrap therapy for patients with atopic dermatitis experiencing a flare?

<p>Wet wrap therapy is what I like to think of as an oldie but a goodie, something that we all learn about as residents and have in our armamentarium, but not something we're necessarily whipping out for every patient just because it can be kind of cumbersome, particularly at home. So I find wet wrap therapy being particularly effective if you're really in need fast control of highly acute, very severe atopic dermatitis, especially for somebody that may be a good candidate for a systemic therapy, but you just know that you're not gonna be able to get them on that therapy in time. So one way in which I use acute wet wrap therapy quite a bit is patients who end up being hospitalized for a day or two. A lot of people just don't have the actual wherewithal and ability to be able to do wet and dry and wraps and changes, it's a whole messy process, at home, so the hospital setting can be a place where you can ensure somebody is having appropriate wrap therapy to really cool down that atopic dermatitis flare and hopefully buy you some time to actually get that systemic therapy on board that you're looking for.</p>

<h6>Summary&nbsp;</h6><p>In the video, Dr. Raj Chovatiya discusses the use of wet wrap therapy for patients with atopic dermatitis experiencing a flare. He describes wet wrap therapy as an effective approach for achieving fast control of highly acute, severe atopic dermatitis. Wet wrap therapy involves wrapping the affected areas in wet bandages, which helps to cool down the skin and provide relief.&nbsp;</p><p>Dr. Chovatiya mentions that wet wrap therapy is particularly useful for patients who require urgent control of their atopic dermatitis but may not be able to start systemic therapy immediately. It can be used in cases where a patient is a good candidate for systemic therapy but cannot receive it promptly. For example, patients who end up being hospitalized for a day or two due to the severity of their condition can benefit from wet wrap therapy during their hospital stay.&nbsp;</p><p>While wet wrap therapy is an effective option, Dr. Chovatiya acknowledges that it can be cumbersome for patients to manage at home. Therefore, its use may be more practical and achievable in a hospital setting, where healthcare professionals can ensure appropriate application and changes of the wet wraps.&nbsp;</p><p>Overall, wet wrap therapy is considered a valuable approach for rapidly managing acute, severe atopic dermatitis, especially when systemic therapy may not be immediately accessible.&nbsp;</p><h6>Key Points&nbsp;</h6><ul><li>Wet wrap therapy is recommended for patients with atopic dermatitis experiencing a flare.&nbsp;</li><li>It is particularly effective when fast control of highly acute, very severe atopic dermatitis is needed.&nbsp;</li><li>Wet wrap therapy is not used for every patient because it can be cumbersome, especially at home.&nbsp;</li><li>It can be beneficial for patients who may be good candidates for systemic therapy but cannot start it immediately.  </li></ul>

How is cantharidin applied?

On what areas of the body can cantharidin be applied?

What is the mechanism of action for cantharidin?

Can you reuse the cantharidin applicator?

Why is denatonium benzoate included in the ingredient list for cantharidin?

What are some important instructions you should give to give patients being treated with cantharidin?

Why are patients with atopic dermatitis more at risk of contracting molluscum contagiosum?

What are some complications and long-term effects associated with molluscum contagiosum?

What are some of the biggest challenges in treating molluscum contagiosum?

What classification from the 40-GEP test would make you consider referral to a radiation oncologist and adjuvant radiation therapy?

Can the 40-GEP test be performed on superficial biopsies?

How long does it take for a report to be delivered for the 40-GEP test?

Do you consider imaging for patients with class 2a or 2b results on the 40-GEP test?

How do accuracy metrics of the 40-GEP test compare with those of the AJCC8 and BWH?

How does the 40-GEP test influence your decision to use radiologic imaging to check regional lymph nodes and distant organs for metastasis?

What clinicopathologic factors have significant prognostic value?

How do you undertake a multidisciplinary approach to SCC management?

What patient and disease characteristics do you consider when choosing a systemic therapy for patients with metastatic SCC?

How does the test inform the clinical management of patients with high-risk SCC?

Is there drug monitoring required for bimekizumab?

What is the dosing regimen for bimekizumab?

Which patients are eligible for treatment with cantharidin, and are there any notable exclusions?

What are some of the most common adverse reactions associated with cantharidin?

Does cantharidin provide any benefits over other treatments for molluscum contagiosum?