This webinar was recorded on June 12, 2024

People with atopic dermatitis have higher rates of allergic diseases than the general population. About 50% of children with atopic dermatitis develop asthma, 33% develop food allergies and children with atopic dermatitis are at a higher risk of developing allergic rhinitis. This is often referred to as the atopic march or allergic march. In this webinar, you’ll learn about this complex relationship.


  • Luz S. Fonacier, MD
    NYU Grossman Long Island School of Medicine

Luz Fonacier, MD is Professor of Medicine at NYU Long Island School of Medicine. She is the Head of Allergy and Training Program Director in Allergy and Immunology in NYU Winthrop Hospital.

Dr. Fonacier is the past president of the American College of Allergy, Asthma and Immunology (ACAAI) and the past chair of the American Board of Allergy and Immunology. Dr. Fonacier has numerous publications in textbooks and journals. Because of her training in dermatology, allergy and immunology, her special interest is the dermatologic manifestations of allergic diseases.

This Advances webinar is in partnership with the American College of Allergy, Asthma & Immunology. ACAAI offers CMEs for physicians for this webinar. If you are a member of ACAAI, you can obtain CME through the member portal for Advances webinars.

All attendees will be offered a certificate of attendance. No other continuing education credit is provided.

CME is available through ACAAI for this webinar.

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Transcript: 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.

Catherine Blackwell: Hello. We’re just waiting a minute or two for everyone to join and while we’re waiting, if you could put where you’re dialing in from so, I can see who’s here, that would be great. OK. We’re going to go ahead and get started. Hello, everyone, and thank you so much for joining us today. My name is Catherine Blackwell and I’m the Chief Health Equity Officer for the Allergy & Asthma Network. Welcome to this afternoon’s webinar. We are really in for a great treat today with Dr. Luz Fonacier as today’s presenter.

We have a few housekeeping items first. All participants will be on mute for the webinar. We will record today’s webinar and post it on our website within a few days and you can find all of our recorded webinars on our website at Allergy & Asthma Scroll down to find the recorded webinars and any upcoming webinars. in webinar is going to be an hour long and that it includes time for questions. We will take these questions at the end of the webinar but you can put your questions in the Q&A at any time and that qxa box is right at the bottom of your screen. So, we’ll have someone monitoring the chat if you have questions or need help. We’re going to get to as many questions as we can before we conclude today’s webinar. This webinar is in partnership with the American College of Asthma and Immunology. It offers credits in end answer for all others. You can obtain C.M.E.’s or attendance credits. All other attendees will be offered a certificate of attendance. No other continuing education credit is provided. Now, a few days after the webinar you’ll receive an email with supplemental information and a link to download the certificate of attendance. We’ll also try to add the link to the certificate in the chat so let’s get started.

Today’s topic is “The Complex Relationship Between Atopic Dermatitis and Allergies.” People living with atopic dermatitis have higher rates of allergies than the general population. today you’re going to learn how to identify and treat food allergies, environmental will, contact allergies and treatments associated allergies in patients living with atopic dermatitis of the it is my great pleasure to introduce our speaker, Dr. Fonacier is a Professor of Medicine at NYU Long Island School of Medicine. She is the Head of Allergy and Training Program Director in Allergy and Immunology in NYU Winthrop Hospital.

Dr. Fonacier is the past president of the American College of Allergy, Asthma and Immunology (ACAAI) and the past chair of the American Board of Allergy and Immunology. Dr. Fonacier has numerous publications in textbooks and journals. Because of her training in dermatology, allergy and immunology, her special interest is the dermatologic manifestations of allergic diseases. Thank you for being here today, Dr. Fonacier. I’ll turn it over to you.

Dr. Fonacier: Thank you very much, Catherine and I thank the Allergy & Asthma Network for giving me this opportunity to talk about a topic nearby and dear to my heart and that’s the complex relationship between dermatitis and allergies. This is the Allergy and Asthma Network mission and as Catherine said, I’m professor of medicine NYU Long Island School of Medicine. These are my disclosures and related objectives. which is describe the related allergic conditions that may impact people living with atopic dermatitis. We want to talk about the different times of allergens.

What is atopy? It’s a genetic tendency to produce Ige ab to common proteins and we call these allergens. These include atopic dermatitis, rhinitis, asthma and food allergies. People with atopic dermatitis have a higher percentage of dermatitis. The converse is true as well. Patients with allergic diseases have a higher rated of atopic dermatitis. Teens with asthma have a higher rate of AD than those without asthma. And 10% to 20% of patients with AD have food-induced urticaria compared with 1% to 3% of the general population. The more severe atopic dermatitis is associated with high hen’s egg, cow’s milk, and/or peanut-specific Ige. Patients with AD and concomitant hen’s egg, peanut or dust mite allergy are more likely to develop atopic dermatitis at higher than 5 years of age.

Food allergies are more common in less than two years of age and asthma and rhinitis are more common in more than 4 years of age. And there are multiple factor that combine to contribute to atopic dermatitis. The genetics, we talked about. There were mutations in the genes. Environment, there are allergens that are present and the immune system. There is an activation of other cell types and there’s the microbiome or microbacteria.

Triggers are important to be evaluated. Allergic triggers include food, aeroallergens and contact allergens and that can be irritant or allergic determine tights. You can have back tear infections, eczema. fungal infections. There are other factors, including irritants, temperature, sweat, and stress.

So, atopic dermatitis is a skin barrier defect and this leads to sensitization and questions moms always ask is can your child’s eczema cause food allergy or can eczema trigger a food allergy? Not all those with sensitization, however, will manifest as allergic. So, you look at children with atopic dermatitis, they also have Ige antibiotics but no signs of allergy when they eat the particular food. This is sensitization with tolerance. They sensitize to whatever they’ve been sensitized to. Such as coming up with hives and anaphylaxis but occurs consistently with every exposure to that particular food. In such cases, referral to an allergy expert can do food tests if necessary.

First, let us do no harm. Take an example of a child with eczema eating a food without problems. Blood test was taken and we see elevated food-specific IgE. That child is sensitized, has the IgE but toll rates the food. However, what is the harm we can do?

You have the same child with eczema eating food with no problem. We find out that they have elevated specific IgE to certain foods and then we tell them to avoid that particular food. This gives rise to sensitization plus increased allergy. So, we recommend avoid testing with food panels. You have to be targeted. There is no index reaction to a particular food and no serum IgE test have a high negative protective but a low positive protective value. With over 90% if it’s negative, there will be no reaction but if it’s positive you only have about a 50/50. The size of the test confers the likelihood of the allergy being present, not the severity of the reaction.

There is prevention of food allergy by early peanut introduction. You have high risk infant, those that have severe eczema or egg allergy, consider introducing peanut at 4 to 6 months after tolerating other solid foods. If is peanut-specific IgE and/or skin test sell slated consider a formal oral challenge by allergist. Infants with mild to moderate eczema, you can introduce peanut around 6 months of able and infants without eczema or food allergy, introduce your peanut-containing foods freely as you would with your other solid foods.

The American Academy and American College joint tests have recently published their most recent guidelines at the end of 2023. They talked about elimination diet with or without skin testing in atopic dermatitis so the recommendation is in patients with atopic dermatitis, the panel suggests against the use of elimination diet. Because you have to consider infants are very hard to do elimination diets. One, there’s the risk factor of developing an IgE-related allergy and of course you also have the risk of malnutrition. the effects of early nutritional intervention in development of atopic dermatitis. The American Academy of Pediatrics has replaced the 2000 policy. They say now, there’s no major role for maternal dietary restrictions from pregnancy or lactation, breast feeding for at least 4 months prevents or delays atopic dermatitis, allergy and wheezing in early childhood and there’s modest evidence that the onset of atopic disease in infants at high risk of atopy may be delayed or prevented by the use of hydrolyzed formula. There is little evidence that delaying introduction of complementary foods beyond 4 or 6 months private atopic dermatitis.

That’s food and now let’s talk about environmental airborne allergies. Again, you have allergens, pathogens, irritants and toxins that can more easily go through the skin and cause allergic sensitization. There are indoor and outside air pollute ants. The indoor ones include combustion and particulate matters. The sources of these are rare. You can find them in tobacco smoke but in furniture, air conditioners, stoves, wall paint and even in the human body itself. Eczema has been associated significantly with certain pollutants including benzene, particulate matter 10, nitrogen compounds and carbon monoxide.

There is less data on the role of environmental allergies than in the food allergies. There are reported allergens such as dust mite, which is more common in atopic dermatitis. cat, and grass pollen. There is a Malassezia which is both an IgE and t-cell related response. It’s found in several areas. This is an organism that can worsen atopic dermatitis. It has been found in patients with refractory head and neck atopic dermatitis and they may respond to anti-fungal theory pi.

What about allergy shots or allergy immunotherapy? This is what the joint task force recommended. In moderate to severe atopic dermatitis, refractory, intolerant or unable to use mid-potency topical treatment, they suggest adding allergen immunotherapy to standard therapy. They’re likely more responsive to immunotherapy. The recommendation in mild atopic dermatitis is against adding allergy immunotherapy to the standard topical therapy.

Moving on now, to contact allergens. we discuss food, airborne environmental and now we’ll discuss contact allergens. again, same problem. Epidermal barrier defect permits easier entry for allergens. That will lead to antigen presentation and sensitization for prolonged and frequent periods of exposure to potential allergens, confer greater sensitization risks. A 2009 study showed that Dutch children with AD had significantly higher rates of sensitization to lanolin and fragrances. The review found that patients who patch tested with lanolin were more like low to have problems. Lanolin is found in many of the topical treatments for AD.

Risk of allergic contact dermatitis in atopic dermatitis. Dysfunctional skin barrier allows for increased penetration of chemicals. It may increase susceptibility to AD through some form of immune signaling. So, there is an increase in exposure and chronic use of emollient in chronic atopic therapy. A lot of patients come in and say we only use natural products. Note that all natural is not hypoallergenic. A survey of the so called hyper allergenic cosmetic products show that they often contain fragrances and preservatives and common natural products are lanolin. the products we’re using to treat them, we are actually causing contact allergens.

Allergic contact dermatitis may actually complicate the course of your contact dermatitis so who should you suspect? When their dermatitis starts to worsen, when they start to change the solution, when they fail to improve with your treatment, when they improve and then immediately rebound or when they have atypical distribution or pattern. Eyelid predominance, hand and feet, lip. Those who have persistent hand eczema adult onset or adolescent onset and they don’t give you a history of childhood eczema and those with widespread or severe dermatitis before initiating your systemic suppressants. Specific contact already generals are treatment associated.

So, as I said, emollient are very common: preservatives like benzoates, emulsifiers. You can see lanolin, propylene. You can see these in the ingredients. topical antibiotics. surfactants. and compsitae are all very common in your cosmetics as well. Preservatives are common. They prevent rancidity and fungal overgrowth and extend the shelf life of products and these are the most common found in preparations that are being used for atopic dermatitis. I just want to give you a few of these products.

Methylisothiazolinone because there is what we call an epidemic of this. The positive active rate is 13.8%. only second to nickel, a very common contact allergen. You’ll find it in personal care products, household and industrial products, in paint. There’s a very high clinical relevance and you can find it either as mci/mi. in the product label. known as a trade name of Kathon CG. You can find it in paint. This is a case that was brought up in 2014 of a mother who breaks out in a rash every time she goes into a lounge that was painted in a certain paint and you can see that the concentration of the preservatives is very high in paints. Different types of the paint and this is something that could be airborne. Something you will need to consider if your patient is getting worse in certain environments because of contact dermatitis.

Fragrance is the most common cause of allergic contact dermatitis in cosmetics.

Frequent in personal care products, household products, and medicine occasions. Leave on fragrances and watch off product, detergents or soaps or shampoos are less likely but they can still cause fragrance allergy. With a product that is scent-free already or you cannot smell anything, it doesn’t mean there are not fragrances. Sometimes they put in fragrances to mask a chemical smell.

Cocoamidopropyl betaine is the most common allergen in shampoos and if you look at the shampoos here, you’ll see it as the more common use of these products from shampoos. There are very few shampoos that will not have these surfactants and they do cause contact dermatitis, mostly in face, neck but is can also affect your eyelids, scalp and hands. You see that in baby products.

So, treatment associated already generals. We talked about lanolin. antibiotics. Topic corticosteroids is the first line of treatment for atopic dermatitis and the risk factors are severe disease and others. Neomycin is the contact allergen of 2010. The top 15 most common allergen in North America? Why so high? Because it is found in over the counter products either alone or with polymyxin and bacitracin. Both bacitracin and neomycin cause sensitization. Those at risk are those with patients with a lot of antibiotic in the skin. The committee on Infectious Disease no longer considers contact hypersensitive to neomycin as a contraindication to vaccines containing neomycin. There’s too small an amount in vaccinations and you can go ahead and vaccinate the patients. We talked about steroids. This is a patient that I had that had a facial dermatitis and eye patch and this led to the product that she’s using so you can see here the positive patch that she was allergic to her product.

So overall about .2% to 5% of all dermatitis patients have topical corticosteroid allergies. Those who get worse, condition improves and then players, if you take this population and test with them for this, close to 19% to 22% of the adults and 25% of children, you will actually pick up allergy to their product. We have steroid classification either based on potency with the very potency you use in very thick skin and then your lower potency which you will tend to prescribe for the face but if your patient is allergic to hydrocortisone acitate, you would have to avoid all of these in this group and if you have a patient allergic to have to avoid it as well. If a patient you suspect to have allergy, put them on Group C, which is the least prevalent allergy until I’m able to patch test then and see when they’re allergic too and then I can open up more of the other products to them but it’s a good process to just switch them over to group c until you can determine what group they’re actually reacting to.

We talked about the lanolin and it’s very common in personal care products but this is more common in lip products so if you have lip sticks, children with atopic dermatitis will react more to lanolin and these are tests with lanolin alcohol and patch tests. There is a lanolin paradox where the sensitivity is low in normal skin, moderate in atopic skin and high in stasis eczema and ulcers.

Microbiome. You’ll have atopic dermatitis flares associated with this because it was produce exotoxins and stimulate the immune response system. They worsen TV bacterial lipases. Bleach bath thought to de degrees AD severity by reducing s Aurerus.

There is also a reduction in microbial diversity is a focus for potential therapeutics. So, there is therapy of potential bacteria. A fecal transplant and we know the higher, the less likely they will develop allergies.

New studies are showing that topical organisms or bleach baths may be beneficial for atopic dermatitis. We’re waiting for products that would do this. So, what about use of topical antimicrobials? The recommendation is in uncontrolled atopic dermatitis and no serious bacterial skin infection, that is there’s no weeping, no crusting, no pustules, there’s no sign of infection, they suggest against adding topical antimicrobial as a standard of care. Bleach baths, they suggest that in addition to topical therapy. You can consider diluted bleach baths if they fit into the patient’s routine. This is an important shared decision making in the patients with in mild atopic dermatitis. The joint task force actually suggests adding diluted bleach baths to topical therapy.

It’s time to summarize the testing recommendations from the integrated guidelines to identify triggers. What do you want to test for? Food allergies in patients if they have a history of an immediate type food allergy that occurs consistently with every exposure to the particular food and with refractory atopic dermatitis despite optimal treatment. For concomitant environmental aeroallergies, especially these with other atopic diseases, consider testing for environmental allergies and contact dermatitis despite optimal treatment, especially if you have involvement of the face, hands or feet. Do not test for food allergies on a routine basis. Best targeted food will, that has a history of an IgE reaction and consistently have an exacerbation of atopic dermatitis if they eat this particular food.

So, principles of therapy, after avoiding the irritants and specific allergens, general supportive therapy includes skin hydration, emollient, baths, wet wraps. Get the disease under control — use of anti-inflammatory medications, strength based on the disease severity. The stronger steroids only for shorter bursts and systemic treatment if needed. Keeping it under control — steroid sparring agents, immunomodulators such as emollient creams and proactive treatment.

Basic skin care, bathing should be fine. Soak for 10 to 20 minutes. You may or may not use oatmeal. That’s not a must. Quickly clean with a mild soap or cleanser but pat dry and immediately apply your emollient or topical medication. Improve skin barrier functions, reduce susceptibility to irritants and its strengthen the skin. So, this application of emollient is extremely important after you hydrate. So, soak and seal, hydrate and then seal with your emollient. The emollient layer actually reduces your water loss, improve your barrier and decreases drying and itching. They can be oil based and they are effective for restoring skin barriers. You have creams and locates but these are more water based and less effective than ointment so between the three, ointments are probably the most potent and then you have creams and lotions that are water or alcohol based. Use them regularly once or twice a day and use the preventative strategy even if the skin is clear. Use at least 30 grams per day or one kg per month. Using the soak and seal method.

There’s an interesting randomized controlled trial in the U.S. and UK of 124 neonates with a high risk of atopic dermatitis. This is very young. Starting at 3 weeks of age, they have full body emollient therapy, at least once a day. A protective effect was found in accumulative incidence of atopic dermatitis and reduced the risk by 50% of atopic dermatitis developing within three months. Their conclusion was emollient use from birth represents a feasible, safe, and effective approach for AD prevention. Emollient therapy from birth could be a simple and low cost intervention that could reducing the burden of those.

What are your topical treatment choices for mild to moderate disease? Corticosteroids is your first line of treatment. You have your calcineurin inhibitors. You can use it especially from areas of atrophy like eyelids, perioral, genital, axilla and inguinal areas. Up your PDE4 inhibitors and then recently in a couple of years, you have the JAK inhibitor, which blocks the intracycle already signaling of many pathophysiologic functions.

So, when you fail topical therapy, you move on to systemic therapies and how do you define treatment failure? There’s no standardized treatment but a panel prosed this — if you have an adequate clinical improvement, if you’ve flares, in other words, you improve but it’s not stable. You have no long-term control. You have no relief from itching, pain, not sleeping or poor quality of life or unacceptable adverse events leading to stopping of treatment. And the next step would be your systemic treatments and what are available. We have dupilumab and tralokinumab, which are both biologics. We see the recommendations here. The joint task force recommends having the dupilumab over the standard therapy. The same recommendation in patients 12 years and older for the tralokinumab. As a next step for patients who have failed topical therapy. What about systemic co corticosteroids as a systemic therapy? Their recommendation is against using systemic steroids, why? Because of a transient benefit with little or no improvement in the quality of life or itch or sleep disturbance. As soon as you stop your steroids, you are back to your atopic dermatitis flares. Of course, it has a lot of adverse events and there is existing overuse of oral or other systemic court co-steroids. It may also have a recommendation against their use even for flare management. Again, because it becomes very chronic and you keep on using it and now it’s not only during a flare but you use it three, four, a five, times a year and you do get your side effect even from intermittent use.

So, let’s summarize the street strategy for atopic dermatitis. For mild to moderate, hydration emollient, decrease the itching. Then a step-up therapy would be moderate to severe atopic dermatitis. You can use your atopic corticosteroids. We move on to biologics if you fail this. If you go on into severe then you can consider biologics, minor immunosuppressants if you fail that. There is such a thing as proactive treatment where this was as needed as against routine use where patients who are under control and may use two or three times a week topical inhibitor or topical steroid on areas that tend to flare. They recommended the use of proactive therapy to areas that frequently flare with a mid-potency, topical steroids. This is a strong recommendation because we know that atopic dermatitis will flare, and reactive treatments don’t give you good control. This is the reason for doing a proactive treatment. Prevent the exacerbation. Patient education and other resources are available in both the allergy in the American College of Allergy, Asthma and Immunology and the Allergy & Asthma Network. Please make use of this for yourself and your patients and that’s it. I think we can open it up to questions.

Catherine Blackwell: Thank you. Dr. Fonacier, that was a lot of information. Very informative. I learned a few things myself so thank you. So, we have a couple of questions in the Q&A and I’ll read the first one to you. If the IgE is positive for a food allergy, what is the likelihood that there will be an aggravating factor for atopic dermatitis?

Dr. Fonacier: If the IgE, if it’s very elevated in someone who has clinical symptoms then you just have a marker. It’s just a marker that you have an atopy there. However, a specific IgE to a food may be elevated and yet the patient is tolerant to it. Meaning they don’t have symptoms and yet you would have an elevated IgE and that is why the joint task force is very against doing panels. In other words, you’re testing for 20 foods, example, and the patient doesn’t report any reaction to it. Then you might pick up a patient with an elevated IgE that is actually tolerant to it. But the problem goes beyond that. The problem is then you discontinue the food. You make them avoid the food. Not only could they be prone to nutritional problems but then they can get sensitized. They’ve tolerated it in the past, developed a tolerance and then you took it out and now you’ve actually developed a sensitization and an allergy component.

Catherine: Thank you. We have another question and it’s three questions in one. Does the rise of Malassezia. If so, why and does a topical anti-fungal do that?

Dr. Fonacier: When I brought Malassezia up, it’s not because of treatment. It’s found mostly in the face. And patients have been found with IgE or allergy anti-to it and treatment of it led to the improvement of the atopic dermatitis so that is did not worsen the condition. The other question was, why does it increase? It does not.

Catherine: And then the third part was can they use any antifungal topical to decrease that?

Dr. Fonacier: Yes, some of the studies showed oral but you can use antifungal and topical to treat it, yes.

Catherine: The next question — there’s been shown to have a link between eczema and oral hygiene, if you will and then the question is should they look for certainly certain dental products? Because you had mentioned some certain product use. Is there any kind of special toothpaste or oral products you would recommend?

Dr. Fonacier: You’re bringing up contact allergens here and dental products, in contact with face and mouth. The most common allergens are cinnamons. If you look at the ingredients of dental products, these are the more common ingredients found in there and in general patients who are atopic and may develop contact dermatitis, you might want to give them products that don’t have fragrances. Again, it’s not scent-free. It’s got to be fragrance-free. Very hard to find, especially in toothpaste and mouthwash and then with lip products, you have the problem of lanolin, which is very commonly put in lip products.  Vaseline may be the best thing. Aquaphor has lanolin. So plain Vaseline is probably the best thing to give for lip products.

Catherine: Another question — how effective is Aquaphor in the treatment of atopic dermatitis long-term?

Dr. Fonacier: Again, the problem with Aquaphor is that it has lanolin. If you just go with Vaseline, it’s probably cleaner and the properties is the same. In my practice it is interchangeable. I actually use more of Vaseline but the important part is the soak-and seal part. I seal with Vaseline. You soak them for 10 minutes. They’re still wet. Just drip dry. Apply your Vaseline and I do in at night. During the day it’s very hard to convince teenagers to use Vaseline because they’re shiny and oily so I would adjust. Again, shared decision making. If they’re not going to use it what’s the points of my giving it to them so during the day I would have a cream, hypoallergic creams, and then at night I go with Vaseline.

Catherine: OK. one other question here is, what is the best treatment or symptom treatment of atopic dermatitis on the eyelids?

Dr. Fonacier: Yeah, if this is a new onset or predominantly — eyelid, please consider contact dermatitis on top of atopic dermatitis. This is very common. Eyelid is a very thin skin so if it’s very severe, I will put them on a 1% hydrocortisone and always say no more than three days. After that I will switch them over. But you can use on the eyelid things that will not thin the skin and you can switch. During a bad exacerbation, corticosteroids three days and then switch back.

Catherine: Let me see if there’s any more here.

Dr. Fonacier: I think there was a question about proactive treatment. Proactive treatment has been shown effective for topical corticosteroids and topical inhibitor. So, what was the study? The study was once you have your eczema under control, two days a week and the study was weekends. So, you have a holiday of medications from Monday through Friday. On Saturday and Sunday you apply your others. Let’s say you have more of the eczema on the areas so you would apply your pimecrolimus or your low-dose hydrocortisone on these areas on Saturday and Sunday to prevent exacerbation. In atopic dermatitis there are areas that are almost always prone to exacerbation.

Catherine: There were a couple who asked the same question. Is there a specific emollient that you specifically recommend. I think you had a list of them.

Dr. Fonacier: You just want something to seal. So, plain Vaseline is what I use and then you can use CeraVe. These products tend to eliminate the fragrances but the important thing is to give the patient something that they will use, especially the older children. If they are willing to apply — whatever they’re willing to apply, I would go for it.

Catherine: OK. I think we have time for one more. I just saw this one come in. Is there any role for withdrawal of a food and then reintroduction?

Dr. Fonacier: This is actually — if you’re talking about a sort of period of time, probably be but if you’re waiting long periods of time, you’re actually giving them time to sensitize. I kind of hesitated because this is what we do with challenges. Food testing was done and they come to us positive to peanuts. What do we do now? Now we try to prove or disprove the peanut allergy and we do the challenges. By then they probably would have avoided it. Depends on when we get them but they would have avoided it for a few months so we would have to challenge them because they could have been sensitized already during that time and our challenges are very controlled. We do it in the office. Small increase in doses of the food. If it’s a challenge usually we divide it anywhere from three to five doses of whatever the patients would have consumed in one sitting.

Catherine: There was a question on deodorants. What can I do to help my skin? Avoid the deodorant? And what about bleach baths?

Dr. Fonacier: You addressed three things. One is contact dermatitis. Deodorant is a very common cause of contact dermatitis and the fragrance is the most common part of it. Talking about bleach baths for skin. If you have severe atopic dermatitis that looks like it’s colonized and — obviously is a good topical treatment for atopic dermatitis.

Catherine: Let’s see if there are any other ones.

Dr. Fonacier: There was a question what do you recommend for antibiotic cream. The one that doesn’t cause a reaction is perazin ointment. If I think there is an infection but you don’t use it on normal looking skin. I’m talking 15, 20 years ago where one of the recommendations was to apply topical antibiotic on atopic skin, right? Thinking that it would take off the colonization, take out the staph but actually we don’t recommend that anymore. If there’s an infection and it’s localized then topical antibiotics and I use parazin. machine severe and I would use oral antibiotic.

Catherine: There was something about laundry detergent recommendations?

Dr. Fonacier: All is fragrance free but there are many other products. The American Dermatologic Society has a list. Let’s say from the laundry detergent it was fragrance and the surfactant they’re allergic too. It’s hard to say without doing a patch test but anyway, this database, after you put in what the patient is allergic to, will generate a list of safe products. This is then when you can recommend to the parents. The safe products do not have whenever they have tested to in the patch test.

Catherine: We are just about out of time. Thank you, Dr. Fonacier. It was an outstanding presenation. We have several webinars coming up in the next month.

Join us on June 26th for the next Unidos Hablemos virtual conference series presentation about food allergies and the Hispanic/Latino Culture. Then on July 16th, we’ll welcome Dr. Nancy Joseph to talk about health disparities in allergy, asthma and immunologic diseases. And on July 25th, Dr. Angela Hogan will discuss SMART therapy and other patient-centered approaches toward asthma management.

You’ll receive an email from Zoom in a few days with a link to the recording, an evaluation, and supplemental resources.

Thank you again from all of us at Allergy and Asthma Network.  Join us as we work every day to breathe better together.