Eosinophilic Esophagitis: Understanding & Managing the Condition (Recording)

This webinar was recorded on May 13^th 2025

Eosinophilic Esophagitis (EoE) is an increasingly recognized, immune-mediated condition that poses diagnostic and therapeutic challenges for clinicians. EoE affects about one in 2,000 people, according to the American College of Allergy, Asthma & Immunology (ACAAI). Join us as we delve into the latest advancements in understanding, diagnosing, and managing EoE.

Speaker:
Jay A Lieberman, MD

Born in Memphis, TN, Dr. Lieberman graduated from the University of Texas in Austin before returning home for medical school at the University of Tennessee Health Sciences Center. He completed his residency in internal medicine at Washington University in St Louis, Missouri, and then his fellowship in Allergy and Immunology at Mount Sinai Hospital in New York City. Upon completion of his fellowship, he returned home to work at the University of Tennessee, and LeBonheur Children’s Hospital.  He is the past Chair of the food allergy committee for the American College of Allergy, Asthma, and Immunology, and is the current co-chair of the Joint Task on Force Practice Parameters, an associate editor for Annals of Allergy, Asthma, and Immunology, and is a board member and current chair for the American Board of Allergy and Immunology. He lives in Memphis with his wife and 2 daughters.

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.

Sponsored by the American College of Allergy, Asthma and Immunology

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.

Ruthie Marker: All participants will remain on mute during today’s webinar. You can find all of our recorded webinars at allergy asthma network.org, scroll to the bottom of that page to access this reported — recorded webinar and any upcoming events. The ribbon are will — webinar will run for one hour and we will address questions at the end. However, you’re welcome to submit those at any time using the Q&A box located at the bottom of your screen. I team member will be actively monitoring the chat and if you have any questions or need assistance, you may do so at that time. We strive to answers many questions as possible before completing today’s session. This webinar is sponsored in partnership with the American College of allergy, asthma, and immunology. We offer CME’s for physicians and attendance credits for all others. You can create a free account and obtain attendance credits through that member portal for these webinars. All attendees will receive a certificate of attendance, no other continuing education is provided. A few days after the webinar, you will receive an email on supplement education and a link to download the certificate of attendance. We will also be adding the link for the certificate of attendance in the chat so keep an eye out for that. With that, we will go ahead and get started with today’s presentation. The title of our webinar today is Eosinophilic Esophagitis: Understanding & Managing the Condition. Eosinophilic esophagitis is increasingly recognized, according to the American College of allergy asthma immunology, it affects about one in 2000 people. Let’s go ahead and get ready for a great presentation as we delve into the latest advancement and understanding diagnostic and managing it. Dr. Jay Lieberman was born in Memphis, Tennessee and Raj waited from the University of Texas in Austin before returning home for medical school at the University of Texas health science Center. He completed his residency in internal medicine and Washington University in St. Louis, Missouri, followed by a fellowship in allergy and immunology at Mount Sinai Hospital in New York City. Upon completion of his fellowship, he returned home to work at the University of Texas and a children’s hospital. He’s the pastor of the food allergy committee 2011 college of asthma immunology and is a current cochair of the joint task force on practice parameters. Also he is an editor for the allergy and immunology and support member and current chair of the American Board of allergy and immunology. He lives with his wife and two daughters. Thank you again for being here today, Dr. Lieberman. I will turn it over to you.

Dr. Lieberman: Thank you very much, a very kind introduction. I want to thank both allergy and asthma network as well as the American color G — College of asthma and immunology for inviting me to go over the topic today of Eosinophilic esophagitis. I want to make this is clinically relevant as possible so we’re not going to dig too much into any kind of science, I will keep this as clinically relevant, we see highlighted for allergist, but also it’s relevant if there are any nurses involved our patients are parents of patients with EOE, hopefully it will be really good, practical take-home points from this talk. These are my disclosures, actually none of these are relevant for today’s talk and shouldn’t be any conflict of what we are going to go over today. The only conflict I will go over is where you pointed out, I’m cochair of what is called the joint task force of practice parameters, which we come up with topics such as EOE and a lot of the guideline recommendations are present today will be from our joint task force practice parameter, so maybe some conflicts of interest in that as we put it together, but that’s not a funding position in any way. Over the next about 40 minutes I’m going to go over these objectives and then we will have 10 or 15 minutes for questions at the end. So we will go over food allergy testing and dietary management as well as diagnosis of EOE , compare treatment approaches for EOE and develop a patient centered approach to treatment, nice what you notice in the guidelines as we go through them. In order to frame our discussion, a majority of what I’m going to bring to you today will come from one of two main resources, especially in the treatment section, I’m going to show you comparisons of these two resources.

The first resource is the joint task force practice parameters. This was a combined guideline that was the allergy society, the joint task force is a combined project between the American College of allergy asthma and immunology as well as the American Academy of allergy asthma and immunology. We came up with together guidelines for allergy and immunology topics such as EoE. But in these parameter,, the task force teamed up with the American gastrointestinal Association, the AGA, to combine the joint G.I. and allergy guideline and that’s what I’m going to present now. That is you will see was published in 2020. With the rapidity of medical knowledge and research nowadays, and some ways the 2020 parameter is almost not out of date but has some things that needed updating. And so we will use that resource and a more updated one and kind of compare the guideline using the American College of gastroenterology, the ACG guideline, which just came out this year. We will show the differences in treatment recommendations between these two documents I’m a between these guideline documents and kind of show where they are mostly similar, they are a little bit different, and talk about why. One quick slide, Ruthie kind of went over the prevalence in the introduction and I will not go too much into this. I always find it hard to kinda figure out the numbers, especially when they talk about the number of cases per year or something like that. All I know is when I started on the faculty about 14 years ago, we started a joint gastroenterology and allergy clinic through the eject — pediatric hospital and we started it once a week, seeing patients with EoE, and that quickly ballooned, — sorry, once a month, and now we are doing it essentially once a week because the need and demand became so much that we couldn’t just do it once a month. Now we are filling that clinic once a week. I was just telling Ruthie before this morning I had my clinic with gastroenterology and myself seeing the patients together, and really used a lot of what I’m going to talk about today. So let’s start out with the diagnosis of EoE. In the past, you may or may not have — the diagnosis of EoE required symptoms of esophageal dysfunction, and we will talk about what the symptoms might be, in addition to an endoscopy with biopsy, seeing at least 15 eos.

The current criteria or very similar but as you may be aware, major things happen in the diagnosis in the past seven years, eliminating the idea that you have to be PPI responsive, that you have to have a trial of a proton pump inhibitor before you diagnose a patient. So in the past you would get a biopsy, before you would get — before you could call it EoE they had at least four of eight weeks of proton pump inhibitor and then get another biopsy to show that the inflammation was still there. Newer kind of thought in diagnosis is we no longer require PPI treatment for we call someone having EoE. So patient gets a biopsy, greater than 15 Eosinophiles, you can essentially say they have EoE at this point. It gets a little bit confusing because for example gastroesophageal reflux disease can be the cause of that inflammation. So when you biopsy, when they are not on the PPI and you show — then you put them on an acid blocker and then it goes away, was that reflux or was that EoE? We will talk a little bit about how to differentiate that or why it may not matter in the section for PPI. Just realize most consensus criteria today does not require a trial of PPI, and you don’t have to give them a call of EoE but you can use that PPI is a treatment, and we will talk about that. So what are the symptoms I may present with? In the pediatric rural, typically that’s going to differ than the adolescent or the adult world. In pediatrics, we see kids in a very young presenting it’s going to be something like food refusal or failure to progress to solids. Once a get a little older, it’s kind of nonspecific symptoms, abdominal pain, nausea, vomiting, and regurgitation is what we often see. As they get older, to adolescent or adult age, it’s more going to be trouble swallowing, food not going down, or impaction where the food is stuck and often times I will end up in the emergency department needing the bolus to be retrieved her purse or something else. We looked at patients a few years ago and we show that with the pediatric and adolescent center, so we don’t have adults in this cohort, but are most common present in — presenting symptom of find a patient came to the doctor was abdominal pain followed by vomiting. Dysphasia we saw in her adolescent cohort but it was a little smaller than the total cohort and other things such as failure to thrive or they got up biopsy for something else, they got the rest of the diagnosis. I realize this would change if you had a cohort of adults where dysphasia would be more common but if you are taking care of kids, you really have to have it on your radar that if you have somebody with just abdominal pain, vomiting, especially in the setting of an atopic kid that it needs to at least be on the radar. The other thing you need to have on your radar is what they call the impact symptoms.

They use this acronym to assess the symptoms but essentially they’re all saying the same thing, meaning patients may not tell you they’re having the symptoms, and you may have modified their lifestyle so they’re not having the symptoms anymore because they stop doing the things that bother them. So when we are talking to patients, we will often say, are there any foods you avoid? We don’t just mean are you allergic to foods, maybe the patient stopped eating steak because the state cap getting lodged or it wouldn’t go down. So they may not tell you that, you have to actually asked them the questions. Is this the last person at the table for meals because they are eating so slow? Is this a person who has her drink a glass of liquid or water every time they take a bite of something that is a hard texture to get it to go down? Do they cut that steak or chicken breast into tiny pieces so that it doesn’t bother them when they swallow? These symptoms don’t mean everyone who is a slow eater has EoE by any means, but it’s definitely something you need to think about if you are a provider and you’re asking them these questions and trying to get, how much does this problem really bothered the patient? They may not say it bothers him because they’ve altered their lifestyle, but we don’t want them to have to do that, so we want to tease those symptoms out to know if we can improve on it. Endoscopy is still required for diagnosis. You have to have endoscopy with biopsies. You may start seeing this called EREFS which stands for the finding on endoscopy edema — this is from that guideline where they are showing examples of all of these findings. Edema is not so easy to visualize on these pictures, they say loss of vascularity or they can’t see the vascularity very well. The other ones are easier to see. Linear for Rose the kind of train track lines going longitudinally down the esophagus which are pretty obvious in that top middle picture, probably the best example of them. You can see really well on the top right, they are all over there, calmly thought to be candida, oftentimes they will think it looks like candida esophagitis. Then the rings on the bottom left, concentric rings going down. Once again, none of these are path on mnemonic, meaning if you find them it doesn’t mean the patient has EoE but they are most characteristic and in our patient population, the linear furloughs are the most common thing we see.

The U.S. course just a way to object if I am put a number to these findings so that you can see objectively if they change over time, with treatment you go from a higher to lower, suggesting that whatever you’re doing is helping. Just so you know these findings and you are well aware, you can see the scoring for each rings can be scored 1-3, and the higher the number, the more severe the disease. So you will kind of know what that means. The other way to follow this in time or to diagnose it would be use one of these newer diagnostic of Galilee’s. No one that I know is using these for initial diagnosis, probably not the best use, but we’re starting to see these more and more to follow disease without having to undergo a full endoscopy with biopsy. If you treat these patients or if you are a patient yourself, you know how annoying it is for the risk and the cost of going through biopsies every time you need to know if the therapy is working, and so novel, less invasive procedures are being developed. The one that is probably furthest along at least that I’ve seen is the esophageal string test, it has this little grade capsule and a little metal ball inside of it. You have the patient swallow it and there’s a string attached to it and then you take the string to the outside of the mouth and you let it sit there for one hour and then you drink a little water to get it down. Once you have it in their, for one hour you essentially just pull it out. It’s interesting, the metal ball probably stay in there and will get degraded and stay in their and they say not to get an MRI within 24-48 hours after it if the metal ball is still in there. But after you pull it out, you send it off to a special lab and then they will give you a readout essentially of Eosinophilia. It isn’t able to be sick tell you much else, so the way if you’re going to use this would be to follow a course in time when you’ve got a patient probably pretty stable overall, if you’re changing it a lot it’s definitely not useful — useful for the initial diagnosis. These side sponge is encased in this degradable capsule and you swallow it in the capsule will dissolve and then the spines will be pulled out, similar to the string test. I just haven’t seen it as much clinically as far along as the string test is.

There’s a nice review of the string test and how to implement it in your clinic, if you are a physician and wanted to do this, in that reference down there at the bottom. What we do it our center is the trans nasal endoscopy, and you will see more and more centers using this. This is a less invasive endoscopy in which the benefits are that the patient doesn’t have to undergo general anesthesia in order to do a trans nasal endoscopy. For example allergy clinics will use a scope to visualize nasal passages looking for things like nasal polyps and they can pass that a little further into the area of the voicebox, what you are seeing in picture B there. What the trans nasal endoscopy does is as has a little longer scope and he goes all the way down into the esophagus where you can visualize the esophagus and then take biopsies. The beauty is the patient never has to be asleep for this. So in the picture on the right, you’re seeing the gastroenterologist who works in our pediatric EoE clinic, what you can see is a patient there who is wide-awake, doesn’t have to be under general anesthesia. A pediatric patient, you can do this trans nasal and Skippy and get biopsies and save them the general anesthesia. It’s also obviously a lot quicker and can be done in a clinical setting. So just so you are aware, these are procedures that are less invasive or noninvasive, hopefully as a way to follow these patients in time and subject them to less general anesthesia. One final diagnostic thing is the I -SEE scoring severity system. It is a free app that you can download if you are a clinician and essentially just open up the app and tell the patient’s age and ask you a series of questions about their most recent endoscopy, what it looked like, maybe how bad was the histology, how many Eosinophiles there were, how often is the patient having symptoms, is it daily, weekly, monthly? It goes through a few questions like that and at the end it gives you a severity score, mild to moderate. This theoretically has an advantage if you want to use it, one is it tries to objectify the symptoms and the severity across centers, so that would be if the center or clinic is using the same thing and we all say they were 15 and now they are a six so it is better. The other way to do it is theoretically can follow a patient over time with it, so you put a baseline in their, like a 16, you give them treatment and get another endoscopy and next time you see them is down to a five, it just gives you some objective marker that perhaps the overall disease is better. So you can think of it somewhat like what we do and asthma, like ACT and a CQ score, the way to follow it somewhat objectively beyond just asking the patient questions. So a nice little thing if you want to use this in clinic is there, it’s free and easy to use. So that was the updates in the diagnosis, and I will — and we will get into the meat of it which is update in treatments and kind of where we are with that.

Here are the major changes over the past five years or so that are different than what I was doing when I started. Number one is I talked about it’s no longer required to put the patient on a PPI to either prove they have EoE, which we used to have to do, or b, as a first treatment. It’s an appropriate treatment but it no longer has to be the first thing you reach for if it doesn’t make sense for that patient. The next thing is shared decision-making. In the past, the algorithm was, OK, you have eosinophiles, you’re not responsive, I’m either going to give you diet or swallow topical steroids and that’s the only place we could have shared decision-making. Now you have shared decision-making from the onset of this PPI makes sense, the swallowing topical steroids make sense, does the diet or biologic makes sense? What makes sense for the patient and family beyond just here is the algorithm. Next thing, food allergy testing is not really helpful and not entirely recommended anymore. We will go over those recommendations. Next, dietary therapy, lots of data has shown that to tailor dietary therapies much better for the patient, lastly, obviously we have FDA approved therapies which we did not have at the time of the J TF practice parameters that we put out in 2020. We now have two that are approved, and we will go over those. So let’s start with the proton pump inhibitors. For each of these, what you will see is the guideline that put out the recommendations in 2000 and then the ACG which was just published in 2025. We will see how they are similar and different. For PPIs, what you will see is the AGA documents, we suggest using proton pump in addition over no treatment. We noted very low quality of evidence, giving it a condition recommendation. The ACG is similar, we suggest PPIs as a treatment for EoE and once again a conditional recommendation. What this conditional recommendation means, not everyone would maybe want this and it’s a great place to use shared decision-making, because we have other therapies, it’s not such a strong recommendation , like everyone should use this. That’s not what we are saying. So if were using PPIs, here’s the notes on what we can expect and how to use it. The high dose, what it looks like children is to mg per day and that could be twice daily dosing. Typically you max it out at 40 a day, there are some that go to 40 twice a day. Adults would be 20 milligrams twice a day or 40 millirems daily. There are some centers that we use 40 milligrams twice a day. So this is a little higher typically then what you would put a child or adult on right away for some reflux disease. You want to use it higher, most places will still recommend a good 6-8 weeks of therapy before you decide what the treatment response is. Getting back to why we no longer require PPI as a requirement for a diagnosis is there are no good predictive factors for who responds to PPI. So you would think if reflux is the cause of eosinophil you and you put them on a high dose of PPI and the eosinophil he a goes away, that’s why you would say, that rules it out and you need to rule it out before diagnosing with EoE. What is spent worrying it is it doesn’t really predict response. If you have an abnormal pH study, you’re not more likely necessarily to respond with PPI with your eosinophilia, nothing predicts if the patient will respond to PPI. Typically it’s between 30% and 60% and that’s between adult and pediatric patients in it similar whether you have done a pH monitoring study or not. If there’s no predicting factors and you have reflux you’re more likely to respond and you no longer require, if you say it’s appropriate for any patient who has esophageal eosinophilia.

We definitely don’t have any data on what is the real adverse effect of PPIs when used for patients with EoE because the idea is if you are an otherwise healthy person, and I put you on 20 years of a PPI, that’s going to look very different if you have PPI income and nation with a lot of other issues such as if you were in ICU or had kidney disease or something like that. In younger patients especially, I tell the parents I personally am not worried, but we don’t really have great data on otherwise healthy patients and putting them on a PPI for 10 or 20 years. But I don’t want to downplay their concerns with that respect , so if that is a concern, that’s where we use the shared decision-making on where — whether we use it or not. Swallow topical steroids have the strongest amount of evidence in agreement with both societies. Both recommend topical Lugo court accords, the strong recognition comes from well-designed trials and response rate above PPIs. Most response rate in the studies is about 60-80%. The most commonly studied swallow topical steroids, there are studies with others, as you’re well aware it’s in the form of a liquid that we normally would use in asthmatics. You put it in a nebulizer and have the patient inhale in for asthma, but obviously in this regard we’re having them swallow it for EoE. So we take 1-2 milligrams a day for children or2-4 milligrams a day for adults. We mix it with something to make it that, have them swallow it, and no food or drink for 30 minutes. The initial studies, obviously used Splenda, five packets of Splenda for one bio, making it into a slurry, but studies show you can really use anything. One of my patients exit with applesauce and had a very good response. There’s also putting, thickener, whatever.

Using the asthma inhaler, we use the same asthma inhaler, have the patience puppet into their mouth and swallow, tilted up to the roof of the mouth come puff it, you might see little smoke come out the side, that is normal. Do it again, no food or drink for 30 minutes. Those things anywhere from 44 microgram canister to twice a day swallowed, all the web to some studies using 24 puffs twice a day although that’s probably a little excessive. Most people use either the 44 or 22 puffs swallowed twice a day depending on the age or severity of the disease. There’s no one FDA approved formulation of a swallow topical steroid, it’s a two milligrams dose in a single dose pack that’s already viscous so the patient doesn’t have to mix it up with anything. It’s much easier. I will have to say the recommended dosage at two Ms. — at two doses — there’s no reason to think it is not clinically efficacious for longer-term use but the FDA said it’s for 12 weeks. So it’s great to have it FDA approved swallow topical steroid for EoE because we didn’t have one for years. How about dietary therapy? Dietary therapy, what you see here is the quality of evidence is low. Our documents against using a food elimination diet because that had the best data at the time. Both have low quality of evidence with a conditional recommendation. Because the ACG came out later, you will notice that it says providers may consider starting with the less restrictive Imperial elimination as the initial diet therapy choice, the other document said six. We have new data to show that you can just remove one food and almost issue similar or better responses in some cases. This is just one study that was recently published in the United States in which they randomize pediatric or adolescent patients with complete dairy emanation art dairy plus egg plus soy, follow them for three months and then look at biopsies scores and symptom scores. What you can see on this is the four food is in the light blue and the one food is in purple or lavender. On the left is symptom report breaking down parent versus child. The parent was a little bit better to remove more foods, but patients who had achieved less than 15 eos was absolutely no different. You look at the proximal and distal Eosinophilic counts and they were different, although the milk elimination was slightly better, not significant — not statistically significant, and the psychosocial changes, what you can see is the parent report maybe a little better with the four food but the actual patient that did like it was better but not statistically significant. In our clinic come based on this data and some others that it come out over the past five years, we essentially kind of leave it up to the patient and the family to say if you want to do a diet, could you do dairy and other foods, do you just want to do dairy? We do recommend dairy, though, because there is not as good data to just remove something like egg or wheat. So if you’re doing just one, use dairy. Once I start saying this is actually what you going to have to avoid, you like that mac & cheese, that pizza? You can put cheese on your burger anymore. Butter may not be the best way to do it, when you start going through all these, it hits a little bit harder. But it’s having that discussion essay what might work for you and your family and if this is something you want to do rather than use a medicine, let’s try at.

A couple of other things, most data would suggest that milk is the most likely trigger, like we talked about, and most studies egg and meat are probably two and three as a next most common triggers for EoE. When I started, there were a lot of people on elemental diets, meaning they swallowed a formula that was allergen free and it for almost every patient. I find the quality of life for these patients is just a lot worse. We typically don’t do that anymore, is still an appropriate therapy for a more severe patient that wanted to do it, but we try to take all of life into more count when advising that and we have — if we can have good success with less foods, let’s do it. Lastly, what we always tell her patients is, symptoms should not be used to say which food causes EoE. For example, you could have lactose intolerance every time you hit — eat dairy, but that doesn’t mean it’s your trigger for EoE because there are other things that come because symptoms when you eat. For a piece of steak that gets stuck, it may just be the texture of it. So you can’t use the food the patient or parent thinks is bothering them as the cause for EoE. How about testing for the diet? Back in 2020, it suggested using an allergy based elimination diet over no treatment, but the ACG took the opposite stance and said we do not suggest currently available allergy testing to direct food lamination diets. Once again, using the same very low quality of evidence. If you read our document, it does say in there, due to the potential limited accuracy currently available allergy based testing for the identification of specific food triggers, patients may prefer alternative medical or dietary therapies to an exclusively testing based elimination diet. So we were kind of saying, you don’t have to do this, and even more and more each year were finding less and less allergist doing testing. Anyone who gets referred to my clinic, I don’t do any form of allergy testing to direct a diet. The one time I will do testing is to say if you remove a food, especially if you’re younger and you have a positive skin test, is there concern that fight take it out for two years for EoE and try to add it back in we will see more symptoms consistent with an immediate food allergy like hives, swelling, or trouble breathing. In that case ABL would need testing to know if I take it out, should I be concerned putting it back in. But I don’t use any kind of testing to say this came up positive, you are eating a lot of peanut butter so you should take that out. I kind of stopped doing that in my own practice. The last therapeutic option we will go over for a few minutes is the Biologics. As you are likely aware, we now have one approved biologic within FDA indication for the treatment of EoE. Because it came out before the approval of that in our document, we said in patients with EoE that AGA recommends — as therapy for EoE in the context of clinical trial. We said use that only in a clinical trial because it wasn’t approved yet and we didn’t have enough data. We said that is a knowledge gap. Since he got approved so the ACG document is able to incorporate that, suggesting its use in individuals 12 or older who are not to PPI with a moderate quality of evidence, and gave it a conditional recommendation and suggested to use of age 1-11 who are nonresponsive to PPI. That’s based on the trials that patients had to have had a trial of PPI.

So we don’t have a huge number patients who got diagnosed right away — there’s a reason it couldn’t work but you notice the wording is because that’s how the trials were run. Message ATF and the AGA sought approval, we had a meeting and decided not to change the entire guideline at that time just for one approval of medication. With the American College of allergy and asthma immunology did and said was created yardstick, essentially authors on the guideline to give expert opinion on how to use it, this is published in 2023 so it’s a little more updated than the gout — then the guideline. You can see the expert opinion how to incorporate it such as when would you biopsy afterwards, but it also says he would be a good candidate. I like the ACG guideline that says you had to be PPI nonresponsive, it gives scenarios where it might be first-line. A patient gets diagnosed with EoE and for exam sent — for example they have — maybe makes a lot more sense to put that patient on Du pilumab and it could be cost-effective because one of the cost-effective — one of the downsides is the cost. The other thing about the yardstick here is if a patient has a strong preference to avoid diet or swallow topical steroids or PPI, there’s no theoretical reason Mike could be used first. So the yardstick if you little more leeway as a provider and prescriber to say maybe this is a good patient to use it on as first-line. This is the package insert for dosing, right now it’s approved down to one year of age for EoE. If they are 15-30 kilos, it’s 200 milligrams every other week, 30 having 40 kilograms is 300 milligrams every other week. Which is nice in a pediatric population. If they are 40 kilos or more is 300 milligrams every week. That is a slightly different dosing than allergies and asthma or atopic dermatitis. So just to finish up here, one thing to make sure you understand patients and families understand once you put them on therapy is that EoE is a chronic disease. None of these treatments are a cure. This quote is straight from the ACG guideline saying we advise providers to counsel patients have because it is a chronic disease, EoE disease activity almost universally recurs when treatment is stopped. I’ve had one or two patients who stopped taking their medicines, followed up a few years later and biopsies were normal. That is not the norm, it’s almost unheard of. So I always tell patients and families, as far as we know, this will be chronic and for your lifetime. Just because you started treatment doesn’t mean you have to do the treatment for a lifetime, we can change up the treatments, but were going into this thinking that whatever we do is going to be for a lifetime. Now if you find a food that causes it and you remove the food and that stops it, that is fine as well. Ideally medication should be weaned to the lowest effective dose. This is more specific for the PPI and swallow topical steroids.

What we will do in our clinic is let’s say they are on controlled , two puffs twice today, we will weaned it to 110 like we would do for asthma, follow them and that may not need a biopsy, and eventually weaned them to 44 twice a day. So is based on symptoms as well as biopsy. Clinical monitoring, optionally monitoring symptoms to incorporate the I-SEE app to follow them over time, we don’t use 15 as like whether or not we are successful. If you have a patient that goes from 80 eos and they are down to 20 and they have no symptoms, we discuss with them that is not perfect or completely normal, it may over time lead to some scarring, but if you are doing well, we can monitor you. We don’t have to reach the magic number of less than 15 before we say it is a treatment success, but we do want to see some improvement in eosinophil count. For going — for going to 80 and the patient feels better, we have a discussion with him and say I know you feel better but there’s still a lot of inflammation and the downside is , it could lead to scarring down the road and you will more likely have symptoms down the road. We would recommend treating that inflammation even though you feel better, and we have that discussion with the patient. So following treatment response is not just symptoms, it is symptoms and histology and then having shared decision-making with the family. I will close by showing the ACG guideline highlights. This is a free PDF that you can click on or follow that link or just Google it. When he shows is most of what I talked about in one little PDF that you can look at or put in your clinic. He gives you the recommended dosing, gives you the dosing and the PPIs and talks about the diet, it talks about everything we’ve talked about here. So nice little one-liner I like from that ACG guideline that you can go back to just for a quick refresher. In summary, I like this, the 1-2-3. One, it’s a chronic, relapsing condition. Management requires a multifaceted approach with treatment options. That’s taken family into account when deciding, and that’s number three, using shared decision-making to find the optimal treatment. With that I will stop right there at a quarter till and open it up to questions.

Ruthie: We have some questions, thank you for that presentation. I really like, and my background is as a respiratory therapist, in addition to my education role, but we talked a lot about shared decision-making with our asthma coaching participants, but also we talk about your feeling good, you are on a steroid, don’t stop, continue. So when you mentioned that clinical monitoring, just continue that even if you are seeing some improvement. I personally love that it all aligns because were saying the same message to our patients and asthma coaching participants, so thank you for that. I will start with our first question, it says what has been your joint clinical experience with patients who are identified on the spectrum and have components of food texture, color aversion, refusal or a tendency toward speeding, vomiting, or rumination?

Dr. Lieberman: That’s a great question. I was laughing because we have a current allergy fellow who does our EoE clinics, and they are convinced that EoE is not a real disease. So many patients have something like this that you’re talking about perhaps something else, we do have a ton of patients who may be on the spectrum or have speech therapy or issues with texture aversion and everything. It is really, really hard. Unfortunately we don’t have a speech therapist in our clinic. We used to have a nutritionist, which was nice. They don’t come anymore. We we referred them to speech therapy to work through it and we will message back and forth with the speech therapist, saying these foods are OK to try and these are not. What we try to do best from our standpoint is treat the disease part of it as best we can. What I mean by that is, if there’s inflammation there, how do I know that’s not causing their food aversion? That is what is hard. If I can clear their inflammation, until the speech therapist that I don’t think the EoE is any longer playing any role in their texture issues and the rest of that is up to the speech therapist. If they have active inflammation and how do you know the swallowing isn’t bothering them too? So I do everything to clear the histology and then work with the texture and aversion issues, but it’s very hard. It’s a great question.

Ruthie: We have a couple of questions that I will try to combine the best I can. Related to allergies, how do you coordinate care with patients that have multiple allergic comorbidities, and there are a couple people asking about asthma and how pollen and mold allergies exacerbate EoE.

Dr. Lieberman: It’s a good question. I am a board-certified allergist and I run the clinic of the board-certified gastroenterologist. We make a treatment plan together. If the patient has atopic dermatitis, allergic, I manage that during our patient visit along with CEO we. The gastroenterologist manages that at the same time because a lot of these play a role in that patient. So if they have constipation, it’s probably calling abdominal pain. If they — it’s making it confusing as to what the symptoms are. So it is important to treat those comorbidities by an allergist and a gastroenterologist. If you’re lucky to do it at the same time, and as far as the rolling EoE, there are lots of reports that there’s probably some role being played there. Some of that is based on seasonality of diagnosis. There’s a few studies which looked at a few patients and they got their EL we under control. They scoped them throughout the year and they did show an increase during pollen season, that was only a very few occasions. So we think that maybe it’s getting to the food pipe in addition to the nose and airways can exacerbate or cause eosinophilia. For example, I don’t ever put a patient on EoE on allergy shots because I think it’s going to help their EoE, but if it does help their rhinitis, maybe you get some benefit to the EoE, but it’s definitely an not the main cause and it’s not something I would target beyond just saying target the comorbidity and it will help with the disease.

Ruthie: There’s kind of like a follow-up question to that as well regarding testing for environmental such as pollen, mold in animals and it would typically show on that biopsy.

Dr. Lieberman: Not on the biopsy, once again, as best we know for the majority of patients, but managing the comorbidity. In our clinic, if the patient also has symptoms of rhinitis or asthma for example, most of those patients are going to get allergy tested, even if that wasn’t there primary complaint. I’m going to taste you and look to see how allergic you are, treat those allergies but not necessarily things like the DOE itself.

Ruthie: Shifting to pediatrics, are there any red flags for EoE that a pediatrician or allergist should be aware of?

Dr. Lieberman: The younger kids failure to thrive, they will get referred to G.I. anyway and usually it’s bad enough in scope. I don’t have any red flags, the worst possible outcome in EoE for most patients is the acute food impact, they won’t show in the sense of they can breathe, although they feel like they are choking, and it’s very, very uncomfortable and they will end up in the emergency room. But there is nothing to predict that, unfortunately. There is no red flag in that sense. But symptoms of food getting hung up is something that, you need to be evaluated because that steak is always getting hung up and you are having trouble swallowing it. Unfortunately there is no red flag

Ruthie: Our last question, what are your thoughts on esophageal dilation for both pediatrics and adults.

Dr. Lieberman: It’s funny, if he asked new diagnosis EoE patients is anyone else in the family have this, no. Does anyone have trouble swallowing and it feels like you’re getting your pipes stretched? They are like, yeah, that patient has EoE. The dilations make people feel better but they don’t treat the underlying disease. If that is what a patient chooses to do, that’s how they can treat it. We tell families, some of our patients get dilated and we say there, you don’t want this happening again but we would recommend treating them for the inflammation. It’s kind of a Band-Aid, is not treat — not treating the underlying cause.

Ruthie:  Thank you. Thank you so much, Dr. Lieberman, it’s been a great presentation and for answering so many of our questions. For all those in attendance, we will be mailing you in a few days with a link to this recording. An evaluation also supplemental resources. We are thrilled to share that we have two upcoming webinars. The next one on June 4 at 4:00 p.m. eastern time, we invite you to join us for our virtual conference series, is going to be session six, a closer look at food allergies in the black community. We have a monitor and patient advocate who will share her lived experiences, she talks about her journey and triggers as we present that an different skin tones. Then on June 12 at four puppy Mason, join us for the Vance webinar. Our title is anaphylaxis. And current guidelines, emerging therapies to improving patient outcomes, which offers practical insights on the acute treatment and prevention of anaphylaxis and the involvement in the treatment landscape. Thank you from all of us at the allergy and asthma network where we strive daily to be your trusted resources for people with allergy, asthma and related conditions. Thanks again, Dr. Lieberman. Have a good afternoon, everyone.