This webinar was recorded on Wednesday, June 22, 2022

There are a lot of advances in the medical care of atopic dermatitis.  Dr. Luz Fonacier will share the latest information and discuss atopic dermatitis in skin of color.


  • Dr. Luz Fonacier


 CME and CNE are available for this webinar (CNE available for a reasonable cost)

Transcript: This transcript is automatically generated. While this transcript is believed to be accurate, errors sometimes occur. It remains your responsibility to evaluate the accuracy and completeness of the information in this transcript. This transcript is not intended to substitute for professional medical advice.


Welcome to today’s webinar on new treatments in atopic dermatitis. This webinar series is sponsored by the American College of Allergy, Asthma and Immunology, and we work together to share the latest information and advances in allergy and asthma with you. This is Sally Schoessler, director of education for Allergy & Asthma Network. Today’s webinar helps our network live out our mission and the needless death and suffering. Due to asthma, allergies and related conditions through outreach, education, advocacy and research, we’re pleased to welcome today’s speaker, Doctor Luz Fonacier. Doctor Fonacier is a professor of medicine at NYU Long Island School of Medicine. She is at the head of Allergy and Training program director in Allergy and Immunology at NYU Winthrop Hospital.


You can move the slide forward one that will be great. She completed residencies in dermatology and internal medicine, a fellowship in allergy and immunology at New York Hospital, Cornell Medical Center and a fellowship in dermal immunology at the New York University Medical Center. Doctor Fantasizer is immediate past president of the American College of Allergy, Asthma and Immunology and past chair of the American Board of Allergy and Immunology.


She is the recipient of the 2020 Edward Jay O’Connell Lectureship 2014 are trust quad AI Lectureship 2012 of the colleges, John P McGovern, Lectureship in 2010 college Gene a Chapman, Memorial Lectureship and the 2009 ACAI Women in Allergy award and the 1998 Presidential Award of Asian Pacific Association of Allergy and Clinical Immunology. She served as president of the Long Out Long Island Allergy society, Doctor Fonacier’s numerous publications and textbooks and journals.


Because of her training in dermatology, allergy and immunology. Her special interests are the dermatological manifestations of allergic diseases. Thank you for being with us today, Doctor Fonacier, and for sharing your insight into this important topic of atopic dermatitis. Thank you. Today will discuss the emerging challenges in the diagnosis and treatment of atopic dermatitis. Sally has introduced me and I thank her for this lovely introduction. These are my disclosures. The research grants were paid to NYU, Long Island and I am Advisory Board in our Regeneron at Italy and Pfizer.


There are many treatments for atopic dermatitis that have recently been approved and professionals need to be familiar with the many treatment options. At the conclusion of this activity, participants should be able to demonstrate the ability to discuss underlying pathophysiology of atopic dermatitis and targets of treatment. Discuss the use of assessment tools for identifying patients with moderate to severe atopic dermatitis and discuss current and new treatments for moderate to severe atopic dermatitis. Let’s look at the challenges. So challenge one. The first is the diagnosis and comorbidities. The morphology of atopic dermatitis is not static. They can manifest as erythema, vesiculation, exudation, crusting, scaling, and back to erythema during the course of this atopic dermatitis.


There are however features that define atopic dermatitis. It is essential that the skin is sporadic, has to be itchy. There has to be an eczema, either acute, subacute or chronic. There are age specific patterns, for example in infants and children there is more involvement of the face, neck and extensor areas and in any age group the current or previous flexural lesion sparing the groin and axilla is typical. History is chronic. For relapsing there are also important criteria that support the diagnosis that is the early onset of the dermatitis and the sort of API, their personal and or family history.


An elevated total or specific IgE or seborrhea and dryness of the skin. And finally, some nonspecific associated findings such as keratosis pilaris, Prurigo Nodularis and Enthesis. Challenge number two, how do you identify the triggers of atopic dermatitis? Do tests for secondary bacterial infections with disease exacerbations, food allergies for patients less than five with refractory atopic dermatitis despite optimal treatment and or clinical history of allergic reaction to certain foods? Contact dermatitis for refractory atopic dermatitis despite optimal treatments, especially if involving the phase and or defeat.


Do not test for food allergies on a routine basis. Go by the history. Serum IgE batch testing, skin biopsy and or genetic testing should be done if necessary to rule out other differential diagnosis. Both allergic contact dermatitis and atopic dermatitis present as eczematous lesions making differentiation making differentiating the two very difficult. Biopsy for both will be spongiosis and can be indistinguishable. Let’s consider allergic contact dermatitis in the differential diagnosis of atopic dermatitis and as a coexisting condition.


It was previously thought that atopic dermatitis patients had less. Allergic contact dermatitis, but recent data from the US and Europe have it as common or more common, depending on the studies. The most common contact allergens in atopic patients include metals, topical antibiotics, fragrance, formaldehyde and other preservatives, lanolin, sesquiterpene, lactone mix, composite, and rubber mix. Consider contact dermatitis in atopic dermatitis. Patients who have dermatitis that worsens, changes its distribution, fails to improve or immediately rebound. Also consider those with atypical distribution or pattern such as the head predominance under foot, eyelid predominance, lips, eyelids or perioral predominance.


Think of contact dermatitis in therapy, resistant hand dermatitis or hand eczema, adult or adolescent onset atopic dermatitis without childhood eczema, and severe or widespread dermatitis before initiating immunosuppressant treatment. One challenge in treatment is that the medication that the patient is using is actually making him worse. Overall, between 2 to 5 % of all dermatitis patients have topical corticosteroid allergy. 85 % of these patients have multiple topical corticosteroid allergies. Suspect topical corticosteroid allergy not only to the active molecule but also to the vehicle and preservatives in the product in all patients who don’t respond to topical critics steroids.


Those who get worse with topical corticosteroids and those who improve initially and then flare in this population, public corticosteroid allergy is seen in 19 to 22 % of adults and 25 % of these children. Corticosteroids can be grouped based on their potency and allergenicity. Potency and side effects are related to the saturation of the glucocorticoid receptors in different cell types and are classified from class one, which are the Super potent topical corticosteroids for Class 7 which is a low potency. Allergenicity is based on 2 immune recognition sites. In red are steroids that service markers within the cross reacting groups.


If there is a reaction to more than one screening agent, it is reasonable to use a Class 3 steroid, which is the lowest prevalence of reactivity. A more comprehensive list of corticosteroids and cross reactivities can be seen in the most recent. And also subscription and the article on contact allergens for the allergies. Challenge three, determine the severity of atopic dermatitis. Different components should be considered. One is a body surface area at least more than 10 % to be considered moderate to severe. Areas involved, such as those highly visible as the face or those that are highly functional, such as the leg, genital spasms and souls. The severity of the lesions, which includes excoriation like unification and even secondary infections.


And of course, the quality of life providers, sleep quality, emotional and mental health disturbance, and interference with daily activity. There are eight topic dermatitis disease severity tools used in research trials, but it’s not practical in clinical practice. Until recently, the Investigator Global Assessment, or IGA, has not been validated. For a busy practice, it is probably the easiest to use and includes the physician assessment. However, it does not measure the extent of lesions and the patients reported symptoms or quality of life. So in our practice we would do the validated IGA, the body surface area and the PARIDO score to capture all three.


This is the validated IGA. There are five possible scores, clear, almost clear, mild, moderate and severe. The morphological descriptions are also better defined, and you can use this tool every time the patient comes in for an office visit. For body surface area, we use the rules of nine. As you can see, it’s a little different in children. They have a bigger surface area in the head and a smaller surface area on both legs. But it is useful to know that the patient’s hand is about 1 % of the patient’s total body surface. The quality of life in atopic dermatitis is predominantly measured by each, and sleep.


So in a scale of 1 to 10 asked the patient then is the worst imaginable age 8 weeks you up from sleep and six distracts you from activities which are you during the previous 24 hours. For every patient visit, we document IGA, body surface area and provider score. Challenge for is the clinical features in darker skin types. Erythema may be difficult to see. There’s hyperpigmentation, follicular accentuation, and a grayish white skin discoloration or ashy skin. There’s a higher rate of lesions in the trunk observed in African American patients, and assessing the body surface area becomes challenging.


Let me discuss this individually and show you some examples. This is an example comparing the white and the dark skin on the left is severe erythema. But in the darker skin, it’s more violaceous and may be missed. In fact, scoring systems that rely on erythema underestimate the severity of atopic dermatitis in darker skin. Some studies have shown that after adjusting for erythema scores, black children have six times greater risk of severe AD than their white counterparts.


Ad in darker skin types may present as grayish white skin discoloration, or what you would see here as the ashy skin. Hyperpigmentation may present differently as well. It’s hardly perceptible in the white skin, looking almost like freckles, but definitely a cosmetic issue in the black skin. Follicular accentuation is prominent in brown and black skin. And for prurigo nodularis is common. There is prurigo nodularis and lichenification, as you can see in this baby. There’s also a higher rate of lesions in the trial observed in African American patients.


As I said, this would be a challenge in assessing the body surface area. Adverse effects from topical corticosteroids are directly related to their potency and duration of use. Local reactions such as tree and atrophy of the skin, telangiectasia, perioral dermatitis, rosacea and allergic contact dermatitis should be monitored at every visit. Systemic adverse effects are more rare and more important in small children and infants. However, telangiectasia street A and atrophy may be difficult to monitor index skin.


It’s also important to address patient fears of steroid side effects to improve adherence. It’s not just the skin color. That affects the care of black compared to Caucasian or white patients in the United States, black children have a higher prevalence of AD, increased persistence of childhood AHD, more severe AD, and more sleep impairment. The Black and Hispanic with 80, compared to Caucasian children, have a lower household income as more likely to be uninsured or underinsured and report insufficient time during patient physician encounters. Black children and adults with AD are less likely to have an ambulatory visit for AD and or more likely to have an emergency room or urgent care visit or even be hospitalized for atopic dermatitis.


The interplay of the epidermis and the immune system in patients with atopic dermatitis demonstrates targets for new therapy. Badger defects promote the ingress of epicutaneous antigens that interface with epidermal Langerhans cells and dermal dendritic cells, leading to immune activation, particularly of the PH two and the PH twenty two signaling pathways. Crt H2A chemoattractant receptor homologous molecule expressed on TH lymphocytes, a prostaglandin D2 receptor on a variety of inflammatory cells promotes TH2  migration into the skin. Phase2 cytokines which are IL 4, IL three thirteen and i five lead to IgE Class switching in those peripheral using ethos and mast cells and increase PDE 4.


The increase PDE four also increases TH2 cytokine expression. The H2 cells produce IL 33 which induces epidermal hyperplasia and is prominent in patients with chronic disease TH2 and TH22 impairment, which is thought to increase the risk of infection. Barrier impairment also increases the risk of infection. Staph aureus is increased and bacterial diversity is decreased with flares. The TH2 cytokine IL31is upregulated and associated with causing H, but not much of the inflammation. So what challenges finding treatment? Since September of 2021  four new treatments for atopic dermatitis have been approved. Where will each drug fit in the treatment algorithm and what is our patient’s access to care? Let’s start with topical treatments for mild to moderate atopic dermatitis.


Corticosteroids are still the first line, but can cause side effects such as skin atrophy and thinning. Also, there is no consensus regarding optimal dosing or frequency. Calcineurin inhibitors which is the Protopic and Pimecroliumus are non steroidal anti-inflammatory and are especially useful in areas prone to atrophy. Your eyelid, very oral, genital, axillary and inguinal areas. There under inflammatory potencies about 1 % tacrolimus equivalent to about the intermediate strength corticosteroids. Both are more potent than 1 % to micrologus. PDE-4 inhibitors such as your crisaborole is another non steroidal topical medication that inhibits the cyclic amp levels. PDE-4 directly regulates peritus, the reduction of continuous neuron in dorsal root ganglion neuron activity.


The drug has a favorable safety profile. Our newest drug approved for moderate to severe atopic dermatitis is the topical JAK Inhibitor ruxolitinib. These drugs block intracellular signaling pathways on which many pro-inflammatory cytokines elicit their pathophysiologic functions. So ruxolitinib is for mild to moderate atopic dermatitis not adequately controlled with topical prescription therapies or when those therapies are not advisable for non immunocompromised patients 12 years of age or older. It is a topical, short-term and non continuous chronic treatment. It’s applied twice a day to affected areas. Up to 20 % of body surface area comes as a 60 gram tube and limits used to more than 60 grams a week.


The package insert and limitation of use says using combination with biologics, other JAK inhibitors or potent immunosuppressants such as azathioprine o r cyclosporine is not recommended. It has a bllack box warning, including serious infections, mortality, malignancy, major adverse cardiovascular events, thrombosis, which are observed in the systemic use of the drug. So which patients need to be stepped up to systemic therapies and how do we define failure of topical therapy? Unfortunately, there’s no standard definition. The expert panel proposed inadequate clinical improvement.


The lack of stable long-term control or flares continue. The quality of life is also important. For example, facial eczema is associated with worse quality of life as compared with examinations, dermatitis and the rest of the body. Sleep quality, emotional and mental health disturbances, and disease interference with daily activities of living and work are important quality of life issues that need to be addressed. Finally, unacceptable adverse events leading to treatment discontinuation. There’s also no generalizable time specified for treatment failure, but rich research protocols have suggested at least 28 days or the maximum duration. Recommended for example 14 days for a super potent topical corticosteroid. When we differentiate biologic agents and small molecules, our focus of systemic therapies today.


Biologic agents, by definition, are produced from living organisms. They’re larger in size, typically administered parenterally, that’s IV or sub Q, and can interfere with pathologic pathways such as soluble receptors, antibodies against hypocrites themselves, or as antibodies against cytokine receptors. Small molecules, on the other hand, are compounds manufactured through chemical synthesis, are smaller in size and can be given orally. So 90 % of global drugs are small molecules and that inhibitors are classified as such.


Our first therapeutic targets are approved biologics. Today we will discuss drugs that target different sites in the pathogenesis of atopic dermatitis, dial 4 receptor alpha, anti IL13, anti IL31 and your JAK inhibitors. Let’s look at the role of IL4 and IL13. In atopic dermatitis there is increased signaling of IL 4 and 13. This amplified signaling of the Type 2 cytokines and chemokines increases the recruitment of inflammatory cells, increases sensitivity to allergens and inappropriate IgE Class switching.


This then results in a weakened epidermal barrier function, decrease antimicrobial peptides, decrease keratinocyte differentiation, and decrease epidermal lipids. Let’s discuss two approved biologics. Dupliumab is an anti IL 4 receptor alpha approved for moderate to severe atopic dermatitis, not responsive to topical therapy. It has recently been approved for six months and above for atopic dermatitis. Tralokinumab is an anti IL 13 also approved for the treatment of moderate to severe atopic dermatitis in adult patients 18 years of age and over whose license is not adequately controlled with topical prescription therapies or when those therapies are not advisable. The dosing of tralokinumab is 600 milligrams subq an initial dose, followed by 300 milligrams every two weeks.


The difference between Dupilumab and Tralokinumab is that a step down option for every four weeks is given for patients below 100 kilograms who are clear or almost clear after 16 weeks. Another difference is that tralokinumab comes in 150 milligram syringe, therefore the maintenance dose is 2 shots. Every time. At least in fact, events include higher rates of nasopharyngitis against placebo in both. Conjunctivitis is seen in both. But more frequent would try looking them up. Done placebo but also same in both dupilumab and tralokinumab. Yes in the eosinophilia is also seen involved. Now let’s review the mechanism of peritus. In atopic dermatitis. There are histamine dependent and histamine independent signaling pathways that mediate right as antipyretic drugs are target to block each periodic pathway.


Targets include IL 4, IL 13, and IL 31 and they elicit their function through the JAK stat signaling. Il 31 is believed to be critical in the development of HT in atopic dermatitis and there are clinical trials ongoing for this. The FDA has approved 2 JAK inhibitors in January of 2020. Abrocitinib which is a JAK1 and upadacitinib.


Also a JAK1 is awaiting FDA review is baricitinib which is a JAK 1 and JAK2. There are different JAK pairings in different cytokines and this influences their function and possible side effects. The therapeutic profile of individual JAK inhibitors depend on multiple factors, including the relative potency towards different tracks and the selectivity. Note that no Jack inhibitor is specific for only one JAK  isoform. Abrocitinib and upadacitinib are approved for moderate to severe atopic dermatitis. By definition, it means that there’s more than 10 % body surface area affected, an easy score of over and equal to 12A score out of over equal to 25 and an IGA score of or equal to three.


Most frequent adverse events are headache, nasopharyngitis and nausea. All drugs include black box warning for serious infections, mortality, malignancy, major adverse cardiac events, thrombosis, drug interaction in the CP, CYP four fifty. Thus there is blood monitoring for TB, hepatitis, CBC, CMP and pregnancy. It’s also suggested that immunizations are completed before starting Jacks, and there’s no live vaccine to be administered while on the JAK. Both can have an up titration of the dose.


Before this, new biologics and small molecules, the only approved systemic treatment for atopic dermatitis are corticosteroids in UV therapy. As we know, patients with moderate to severe atopic dermatitis are treated off label with immunosuppressants. You can see on this slide the more commonly used systemic therapies for moderate to severe atopic dermatitis all carry significant side effects and need regular monitoring. Let’s look at this. Four new therapies for atopic dermatitis. Two biologics which are injectable and two small molecules both JAK1. Dupilumab has the youngest indication of actually six months of age and older. These biologics can both cause conjunctivitis, the tralokinumab and dupilumab.


JAKs are based in include an antiplatelet therapy of more than 81 milligram of aspirin during the first three months of treatment is discouraged. The biologics do not require lab monitoring, while the oral JAKs need your baseline blood test monitoring, drug interaction, and recommendations for immunizations. The American College of Allergy, Asthma and Immunology published a yardstick providing guidance on step up therapy from mild to moderate to severe atopic dermatitis. Initial treatment includes basic management, recommendation for skin care, antiseptic treatment and avoidance of triggers. If the patient is symptomatic, despite appropriate use of low to medium topic, medium potency topical corticosteroids, PCI or crisaborole, and adherence, the therapy regimen stepping up from mild to moderate atopic dermatitis is indicated and this includes consideration for referral to a specialist and allergist or a dermatologist. Dupilumab,  Phototherapy and possible systemic immunosuppressants will then be considered since this publication, which is currently being updated for new therapies, have been approved by the FDA. Where do we think these medications will fit in? Our yardstick? Well, this is my guess. My guess is ruxolitinib will be after topical therapies fail since that is in their package insert.


Tralokinumab  would be for 18 and above and likely at the same level as dupilumab for this age group. If you are looking at the age group of six months and above, then it’s only dupilumab that has been approved. Systemic immunosuppressive therapies such as cyclosporine was our next line before our abrocitinib and upadacitinib were approved. These two JAK inhibitors will probably be before systemic immunosuppressive therapies. So that would be before cyclosporine since it is approved for the indication of atopic dermatitis and cyclosporin is not approved for atopic dermatitis in the United States.


Challenge SIX is probably the hardest to provide our patients and that is supportive care. Emotional factors, increase peritus, and scratching stress induced immune activation in atopic dermatitis. Atopic respond to stress, frustration, embarrassment with increased providers and scratching may be associated with secondary gain or just become a habit and behavioral modification and distraction of therapy may be helpful in these patients. Challenge 7, prevention. Can we prevent atopic dermatitis? Then we discuss a few studies and guidelines on emollient therapy from birth, maternal avoidance, neonatal avoidance, breastfeeding and how do we stop the atopic March? As we know, there are some vast majority of patients with moderate to severe atopic dermatitis also associated with asthma, allergic rhinitis, allergic conjunctivitis, and other allergies including food allergy and EOE. This is an interesting and randomized controlled trial in the United States and UK of 124 neonates high risk for atopic dermatitis. Either they have a family history of atopic dermatitis in first degree relatives. Or history of atopic disease. Full body emulsion therapy at least once a day, starting at three weeks of age. A protective effect was found on the cumulative incidence of atopic dermatitis, relative risk reduction of 50 % and no emollient related adverse events and no difference in adverse events between groups were noted.


The conclusion of this study is that emollient therapy from birth. Represents a feasible, safe and effective approach for AD prevention. Emollient therapy from birth could be simple and is a very low cost intervention that could reduce the global burden of allergic disease. The American Academy of Pediatrics has replaced the 2000 policy statements on the effects of early nutritional intervention on the development of atopic dermatitis. There is no major role for maternal dietary restriction during pregnancy or lactation.


Breastfeeding for at least four months prevents or delays atopic dermatitis, comic allergy, and wheezing in early childhood. There is modest evidence that the onset of atopic dermatitis and atopic disease in infants at high risk of atopic. And not exclusively breastfed for four to six months may be delayed or prevented by the use of hydrolyzed formulas. There is little evidence that delaying introduction of complementary food spy and four to six months actually prevents atopic disease. In fact, there is no evidence that early introduction of complementary foods may help prevent food allergies. Our biggest challenge yet? These emerging new therapies have the potential to revolutionize atopic dermatitis care, but as we move towards precision medicine, we need to consider the role of age, race, concomitant activation of other immune pathways, the FILAGGRIN mutation or other barrier components, environmental factors and the microbiome.


The extent of their effect on patient care will depend on their affordability and accessibility, patients from a broad range of socioeconomic groups and with different insurance status. The college has several tools including physician and patient education, practice management and prior authorization toolkits, which can help you navigate in the complex world beyond patient care. In addition, the college has an interactive atopic dermatitis E yardstick that is very educational and the link is here in this slide. Thank you very much for attending this webinar. Well, thank you so much Doctor Fonacier for so many great points. I really appreciate all you bringing all of your expertise to the table today and we do have several questions for you today.


Our first one is why are live vaccines not appropriate during therapy with a JAK inhibitor? The JAK inhibitors are immunosuppressants, so because they’re immunosuppressants, no live vaccine should be given in any immunosuppressant therapy. Ok, thank you. If people are concerned that they may have atopic dermatitis, would you suggest they see an allergist or a dermatologist? I think there’s a role for both. The advantage of seeing analogies is trigger factors, skin. Can be investigated. We can give a good history on environmental factors that can worsen the atopic dermatitis as well. We also have access to skin testing and blood testing to determine if there are any figures like dust mite or foods that are based on the history of patient, but both.


Dermatologists and allergies have access to these different medications that we have discussed today. Ok. Thank you. And our next question is Grover’s disease and atopic dermatitis and is there treatment? Grovers disease is not a topic dermatitis, but yes, there are some treatments for Grover’s disease. This is a disease that the dermatologist will probably be treating. Ok, thank you. Our next question comes from Tracy. Is there any data showing a diverse efficacy for JAK inhibitors in different races? Very interesting question because we are looking at that.


We know that the diagnosis is that. atopic dermatitis. If you remove the erythema is under diagnosed, the severity of atopic dermatitis is under diagnosed. What we don’t know is if these different medications including your biologics, your dupilumab trailer, Chenab or your other two jacks have more efficacy in different races at this point in time. But we are looking at that. There’s just not enough African Americans. Enrolled in the studies to make that determination. All right. The next question is when asked when does aspirin need to be avoided with which biologic or small molecule inhibitor? Yes, so I brought that up in one of the slides there.


Abra sitting there actually has that in their package insert that anything above 81 milligrams of aspirin should be avoided. In the first three months of treatment of upadacitinib we did not see it in the upadacitinib package insert. The question though is both of them are Jack inhibitors. And most likely functioning the same way. Why they’re different results in these two different JAK inhibitors that were studied will need to be determined at a future date.


Ok. Thank you very much. Our next question is what emollients do you recommend patients use? So I am a contact dermatitis person, so I always say the fragrance free emollients and the I like Vaseline, I like the survey, I like the vanicream and vanadium products as well. The important thing is how you tell them to apply their moisturizers. Moisturizers are best applied on wet skin, so when the baby or the atopic dermatitis patient after their shower, they’re still wet, just a very light drip dry.


And applying the moisturizers on wet skin is actually going to supply the moisture and trap the moisture in this very dry in. Thank you so much. We have a question from a patient who’s asking is atopic dermatitis contagious? Definitely not. So there is sometimes confusion on the broad range of eczema, is actually if you think about eczema is the skin condition where on biopsy there is what we call spongiosis, there are different diseases under eczema, atopic dermatitis is the most common and in delay in most patients will consider eczema as atopic dermatitis.


However, contact dermatitis is an eczema. Psoriasis is an eczema. So atopic dermatitis is not contagious. What the problem is that the patient may have colonization with stap areus, but these patients are prone to this staph aureus because of the condition of their skin. They actually are more prone to get the stuff Oreos than transmitting these to other people. Thank you. Actually that leads into our next question is what is the difference between atopic dermatitis and psoriasis? Totally different diseases. Atopic dermatitis, as I said, you have this essential requirements for atopic dermatitis. Usually there is a genetic factor underlying it. The skin is dry, it’s chronic, it’s it comes, it’s very poetic and you have the exam at this lesion.


In psoriasis you have an over, you have an increase in over of the skin scale. So,you, what you have here are you scaly white lesions on certain areas that are predisposed to psoriasis at your elbows, your scalp, or your knees. The treatments differ for both diseases. Thank you so much. Our next question is, does atopic dermatitis usually occur on the scalp first in children in infants? There is such a thing as cradle cap and., in some literature they will say that cradle cap could be a manifestation of atopic dermatitis, but there are children who will have greater cut because of seborrheic dermatitis, because of the seborrhea in the scalp, and not necessarily go on into atopic dermatitis.


But yes, it can be one of the manifestations. But the more common area in infants and children is actually the face. You’ll see them with red red. Mixed with the eczematous lesions in the face. Thank you so much. So someone is asking when the skin itches, scratching it is temporarily satisfying, but that leads to more itching. How do we stop that? Yes, that is the very true observation. And in fact with this itching scratching cycle, we thought initially way back then that this is the reason why atopic dermatitis just propagates in itself.


How to stop that is a problem, but the most important thing is to try to stop the itching. We know that antihistamines don’t work for the itching many patients do get. Benadryl just to make them sleepy at night so that they won’t scratch. But otherwise the most important thing is to treat the atopic dermatitis, so topical corticosteroids will decrease that itch. And the other topical medications such as tacrolimus, pimecrolimus, these are the ones that we need to apply on the skin and dry skin is also an itchy skin, so making sure that we have moisturizers, liberal moisturization. Is very important in controlling the edge in atopic dermatitis.


Thank you for that one. Our next question is, do you find wet wrap therapy very efficacious with treatment in young children? Way back before we have anything approved for infants. And we know that we have now one biologic approved for six months, and above that was the only treatment that we had for the very young children with atopic dermatitis. And we know that when these children are admitted in the hospital, and wet wraps are done. And by the way, let me explain what wet wrap is first as you soak the baby until they’re.


Skin is well moisturized. You get one, then you apply liberal moisturizer. Sometimes you can apply a very low dose topical corticosteroids in the area for one or two days. Then you get a first pair of onesies. You soak that onesie, you ring it and lukewarm water and put it on the baby, and then get a second pair of onesies a little bigger than the first one and put it.


Put the dry one over and the baby will sleep on that is the classical wet wrap. It’s very tedious. As I said, it’s very hard for infants to stay on it, but. As long as you can get it four to six hours into the baby, it does work. It hydrates the skin and we know that it does improve the skin. Thing is we cannot sustain it. It’s very hard to go more than four or five days with a wet wrap.


So we use it as an emergency tool when we have to acutely treat a severe atopic dermatitis patient. But beyond that, I think we have to think of some other ways of controlling. Atopic dermatitis based on their pathophysiology and that’s what we have are still the first line, our topical corticosteroids, but we have three other first line topical medications available now and then we have our biologics injectable and our oral jackets.


Thank you, that was a great explanation of that. Our next question says my baby has atopic dermatitis. Will they ever grow out of it? Most atopic dermatitis do get better as they get older. The problem is if you can find triggers then it’s best to eliminate triggers. So there is such a thing I was talking about that’s what we would call atopic march. Atopic March is the children initially have atopic dermatitis. As they get older, their atopic dermatitis improves and then they start to develop the asthma and then they develop the allergic rhinitis.


This is the atopic March where most people would actually what they call outgrow the atopic dermatitis, but developed the other atopic diseases. Unfortunately, there is. There are other populations for example, but over 12 percent, 12 to 20 %, it depends on the literature that you’re looking at also have what we call adult onset atopic dermatitis. In other words, it’s very mild when they were young and then it just got worse. There are also the very severe atopic dermatitis patients where they don’t really outgrow their atopic dermatitis and they just it’s just there and it flares. It improves and it flares again. So yes, there is atopic march where the baby may outgrow it, but then watch out for those who do not outgrow it and those who have adult onset as well.


Is there ever a break where a child will have it when they’re young, have it go away and then come back as an adult? Yes, there are some, I mean remember the break means that you might be doing something to prevent exacerbation. You are moisturizing. So we know that the atopic dermatitis waxes and wanes if you have exacerbations and remissions. So you can have a prolonged remission if you’re doing the right things, but you can exacerbate at some point. Especially when you get concomitant contact dermatitis. As they’re getting older, they become. Allergic to fragrances and now they’re starting to apply moisturizers and creams and ointments on their skin and even using a lot of personal products that may have fragrances or preservatives, for example, and they get sensitized.


And for these people, then you have a double whammy, you have both atopic dermatitis and allergic contact dermatitis causing an exacerbation or worsening of the skin. Thank you. Our next question comes from Mary Jane. She says what about using cold wrap therapy, does it work? I’m not sure what you mean by cold wrap therapy as against one wrap therapy. I don’t know about temperature. What we do with drug therapies is we recommend lukewarm water because that’s more comfortable. Remember, especially in children, they’re going to sleep on that.


And it’s not that it’s not the temperature that’s affecting the wrap therapy, it’s actually the moisture. It’s actually the liquid, the water that you’re putting and the moisturizer that you’re putting on the skin as well. Thank you so much. So someone’s asking. So what I’m hearing is that atopic dermatitis is best controlled by good skin care. Yes, it is. Let me put it this way. Skin care is always, always going to be a part of atopic dermatitis treatment.


Whether you’re on biologics or jacks or whatever medications you’re on, you still need to do skin care. You’ll prevent infections. You will moisturize the skin. But in many patients, those who go beyond the mild atopic dermatitis spectrum, those who are moderate or severe, do skin care alone with moisturizers, for example, will not be sufficient. And therefore in these patients you may need intermittent use of topical steroids or intermittent views of the micrologus or tacrolimus and if. That becomes a persistent use. Or that’s not enough. Then you move on to other treatments, including biologics and small molecules. Well, thank you so much. That’s the end of our questions for today.


Doctor Fonacier, thank you so much for joining us. You are so patient answering questions and yet we really appreciated the great responses. And I’d also like to add, I’d also like to thank our listeners for being with us today. So at this time, please download the certificate of attendance from your control panel. If you haven’t had a chance to do it, if you have any difficulties, please email us using the link in your emails. Please join us for our next advances in allergy and asthma webinar.


As we discuss the phenotypes of COPD, we’ll look at the latest information and gather insight into this health issue with Doctor Vick Tejwani. This webinar will be on July 26th at 4PM Eastern Time. You can register for this webinar on our website at Scroll to the bottom of our home page to webinars. You can also view our recorded webinars on this page. Of our website.


Visit our website for quality guidelines based resources on allergy and asthma. Also access important medical information on allergies and asthma from our partners, the American College of Allergy, Asthma and Immunology at Thank you again for joining us today. This is Sally Schoessler for the staff at Allergy & Asthma Network. Please stay online for two to three minutes to complete the evaluation survey. Thank you for exploring the latest treatments in atopic dermatitis today and we look forward to having you join us next time on advances in allergy and asthma.

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