Chapters Transcript Understanding Eosinophilic Esophagitis: Tips for the Primary Care Provider Sandeep Kumar Tripathy, MD, PhD presents on eosinophilic esophagitis and explains the pathogenisis. And then while you do that, I will introduce you. So, our next speaker is Doctor Sandy Tripathy and Trip is it Tripathi Tripathi Tripathy? Um He earned his medical degree at the University of Chicago at Pritzker School of Medicine. He then did his residency in internal medicine and his fellowship in Gastroenterology at Barnes Jewish Hospital with Washington University School of Medicine where he is currently an associate professor with the Division of Gastroenterology. Doctor Drath sees patients at Barnes Jewish West County Hospital and the Center for Advanced Medicine in South County. So, thank you so much. I appreciate uh your time today. Excellent. Well, thanks for letting me participate. Like, like you mentioned, I'm a Luminal gastroenterologist here in our division of Gastroenterology at Wash U. And today I'm gonna be talking about eosinophilic esophagitis. All right, let me see if I can. All right. So, um my conflicts of interest, I do own stock in Boston Scientific, but there's no products that I'm gonna be talking about from this uh from that company I will discuss off label uses of PPIs and fluticasone and Budesonide for the treatment of EOE. The reason for that is just until recently, uh we now have two FDA approved treatments, but we've been using PPIs for some time and we'll discuss that in this session. So, objectives uh you may have are to define the Sinop esophagitis. Explain the pathogenesis of eoe uh recognize patients symptoms that would suggest referral for evaluation of eoe uh describe how eoe disease progression is followed and then list some treatment options for eosinophilic esophagitis. So I wanted to start off with a case. A 28 year old man presents to the clinic to establish care. Uh When you're going over the review of sym symptoms, he mentions that he's been having some difficulty swallowing. So he has a past medical history of childhood asthma at topic dermatitis and he said he's had issues with swallowing that's been going on for 10 years, but feels that things have gotten worse in the past year. When you further ask questions about his dysphagia, he mentions that foods like breads or bagels and rice cause problems. He says he's always needed to drink a lot of water with meals. And he also states that he's almost always the last person in the group to finish because he has to chew his food carefully. It just takes him a long time to eat. So, a little background on eoe or eosinophilic esophagitis. It's a chronic disease. It's a th two cellular mediated disease and it's a clinical pathologic disease. So you need to have symptoms of dysphagia and then on pathology, you see an eosinophil predominant inflammation in the epithelia. So there's a cut off of 15 eosinophils per high powered field. So when you have those two requirements met, you can make a diagnosis of eosinophil gittis. It's interesting to note that patients with eoe have a higher prevalence of asthma rhinitis and eczema than control groups. And there's a male predominant. So it occurs more in males and females. And treatment of the disease includes symptom alleviation, control of inflammation as well as control of fibrosis. And we'll talk about all those things in this session. So, interestingly, this is a study from Sweden where they looked at the increased incidence of eosinophilic esophagitis. This was a study done a while back. So what they noticed was that there was a 20 fold increase in EOE from 1997 to 2012 and a uh 25 fold increase in e esophageal eosinophilia. And it wasn't just due to them looking for it because during that same time, there was only a twofold increase in the number of uh of their biopsy rate. So there was something clearly going on, not just looking for it. Uh That was uh that there was an increase in the incidence here in this population looking globally. Uh This is a more recent study uh where they looked at the pool prevalence of EOE and show that it's been gradually increasing from this 19 seventies. Uh to 2022. So it went up from uh about eight cases, 100,000 inhabitant years to 74 cases per 100,000 inhabitant years. And in this study, they found that it was more common in high income countries. Uh Again, they noticed the more frequent frequency in male population and also seemed to be more pop uh prevalent in uh North America compared to Europe and Asia, looking at data from emergency departments in the United States. Uh They also noted that there was an increase from 2009 to uh 2019 in the eoe associated emergency department visits, it tripled over the time frame and in the future, it's projected to double again by 2030. So this is definitely an increase gonna be an increased burden on our uh ed department and in just medical care in general to take care of these patients and prevent complications. So, what's going on in eosinophilic esophagitis? Well, there, the I the thought is that there are irritants either inhaled or ingested that that cause uh activation of cytokines uh in the wall of the esophagus. These alarming uh stimulate or activate th two cells within the wall of the esophagus. And this results in a cytokine cascade involving a number of uh interleukins and TGF beta that result in uh recruitment of inflammatory cells and production of other cytokines within the esophageal wall and mucosa that lead to injury. In addition, there's probably induction of transcripts in various cells within the esophagus, epithelial cells, uh fibroblasts, et cetera that eventually cause inflammation and remodeling of the esophageal lumen. So, what are eosinophils? Well, they're bone marrow derived cells that can be activated through chemo tracts, cytokines and other mechanisms. And they provo provide a defense mechanism primarily by releasing cytotoxic Granules. Uh This can result in proinflammatory sequela tissue damage and remodeling. It can also have immuno regulatory um effects on various other immune cells. Uh These can affect any body compartment in organ and they're seen in a number of diseases that I've uh listed here. So, in terms of the immunology of eosinophilic esophagitis, I mentioned this is a type two allergic response. It's a th two mediated response. Well, it's important to understand that it is not an antibody mediated response. It's not an IgE mediated immune response that we see in food allergies that can cause, you know, I I inflammation of the lips or the difficulty breathing. Uh it's a different immune mechanism. And though we use eosinophils as a marker of inflammation and part of the diagnosis of making eoe it's not clear that they are important in the damage that we see in this disease. And that's been shown very nicely in several uh several uh uh immunotherapies that have been attempted to be used in the treatment of eosinophilic esophagitis. So, several monoclonal antibodies that have been tried because they deplete eosinophils from the body include Benoy zum methyl and resol. Uh these work on the il five cytokine or block the il five alpha receptor. And in this mechanism, they deplete eosinophils from uh the tissue. And even though you, you would have thought that this would have been a great drug to treat eosinophilic esophagitis. But in fact, when we looked at uh the effect on dysphasia symptoms, they didn't have an effect. So though they did deplete eosinophils, they didn't have an effect on dysphasia. And this was shown in a recent paper from the New England Journal of Medicine uh where they showed a very uh robust uh histologic response with over 85% of the patients uh having a histologic response with less than six eosinophils per high powered field compared to placebo. But when they looked at dysphasia symptoms through a question questionnaire, there was no difference between the Ben Benny, excuse me, Beli Zuma group and the uh control group. So you depleted the eosinophils, but you didn't have an effect on the dysphasia. So how do we make the diagnosis of eoe? Well, I mentioned that you have to have symptoms of esophageal dysfunction. So, dysphagia as well as uh eosinophilic infiltration in the esophagus. So a lot of times this will come to attention by uh patients having a food bolus impaction or them describing issues with dys dysphagia. And then on biopsies, we see the high eosinophil count again, you have to exclude other causes. And then your suspicion should be increased in patients who have had long-standing e esophageal symptoms may have had a family history of Eoin hylic esophagitis or have other at topic conditions like asthma, rhinitis and eczema. Again, you need to rule out other potential causes. Uh gastroesophageal reflux disease can cause the presence of eosinophils in the esophagus. Um And so it is possible for patients to have both gastroesophageal reflux disease and uh eoe uh and normally, uh we don't see eosinophils in the esophagus. They can be found normally in other parts of the G I tract, but they aren't found in the esophagus. Uh There are some conditions like I've listed here, reflux is a common reason to have eosinophils in the esophagus. So, what are the symptoms that we're looking for? Well, in adults pretty much solid food dysphagia, they may complain of chest pain in Children. It's a lot more difficult. Uh They may have heartburn symptoms, nausea and vomiting. They may regurgitate, uh they may refuse food or failure to thrive. So there's a lot more uh symptoms that occur in Children compared to adults. Regardless, we've had a difficulty in making the diagnosis that has persisted for over 30 years. So this was a study done in Switzerland where they compared diagnostic delay uh in, during different times. So, regardless of whether it was 1993 or in 2021 there's still a third of the patients have a diagnostic delay of more than 10 years. Um And like it shows here, it really has not changed over the past 30 years. And what's the issue with this diagnostic delay? Well, it's the sequela of the disease and the progression to fibrosis. So, again, this is a chronic disease. It's uh mediated by a type two inflammatory response in the es esophageal mucosa. There's a disruption of the epithelial barrier and dysregulation of gene expression that causes epithelial remodeling. And this remodeling of the epithelium drives the esophageal dysfunction and your disease symptoms. And over time, you go from a more inflammatory picture to a more fibrotic picture. And that's shown in some of the studies that I'm gonna show you next. So this is an older study where they look at uh how diagnostic delay results in more fibrotic disease or the presence of strictures. And what you can see is as the diagnostic de uh delay progresses, you're having more fibrotic issues uh and less uh of the inflammatory uh issues. And this, this graph looks at patients without strictures and you can see that as time progresses and you have untrue eoe uh you have fewer and fewer patients that are without stricture. So as this disease is left untreated or there's a delay in diagnosis, there's a mo a higher propensity to have more fibrotic disease remodeling and that those patients are more likely to present with uh dysphasia symptoms. This is another study more recent, again, showing that duration of delay increases the uh prevalence of fibrotic uh features um over time and, you know, the granddaddy of them all or what we're really trying to prevent is uh a food bowl of Impaction. And unfortunately, the scenario usually is that a patient, you know, goes to dinner, eat their food, uh dinner is about six or seven in the evening. By about eight o'clock, they're realizing that this food, they've tried to go to the bathroom to regurgitate it up or drink water to have it go down. And by eight or 830 they realize this isn't gonna go down and they need to go to the emergency department. They get to the emergency department around nine or 10 are seen by 11 o'clock and uh and it's determined that uh they need G I and uh that piece of food needs to either be extracted or pushed gently into the stomach. This usually happens around midnight or one in the morning. During that whole time, the patient is anxious. They're sitting at the bedside with a bucket trying to spit out their saliva because they can't even swallow their se secretion. So it's a very traumatic experience. It seems to happen very, we get called in early in the morning. So we're trying to really prevent this. The interesting thing is that even though this is a chronic inflammatory process, uh there's not been any association with esophageal malignancy. So uh this is a study that was done where they looked at the um the the odds ratio of developing esophageal cancer with various diseases. And so it's, it, it's not surprising that patients with Barry Barrett's esophagus have a higher odds ratio of developing esophageal cancer. Uh GD is next likely but eoe there was no difference between the control group. So uh it is at least something you can tell the patients that even though there is chronic inflammation uh and serious consequences of food bull in impaction can occur. There's been no to date no uh association with esophageal malignancy. So, how do we assess eoe? Well, I always tell patients that, you know, we look at their symptoms, we look at how things look endoscopically and we look at how things look uh on biopsy. And really anytime we make a treatment change, uh or uh a dietary change or any anything like that, we wanna assess these three parameters. How are the symptoms? How are the endoscope? How do the things look endoscopically and how do things look on biopsy? And I'm gonna talk about each of these things. So we mentioned that, you know, there's a diagnostic delay with this disease and you know why that is? Well, I think with these patients, they probably developed adaptive behaviors um to uh overcome the issues that they have with their eoe. So it's not just enough to ask about dysphasia. Uh Here's an acronym that can help with trying to elucidate some of those uh dysphasia problems impact is the acronym. So, eyes for imbibing flu fluids with meals to lubricate food. So, are they drinking a lot of water? Which in our case, patient, uh they mentioned that uh m is for modifying food. Do they really cut up their food? Do they um uh you know, make it into smaller pieces? Um So that's something that you can ask prolonged meal times. Are they the last person to finish? Um uh A is avoidance of certain textured food. So, you know, again, just asking about dysphagia isn't enough. But if you ask, can you eat a bagel or just a piece of bread? You know, they may say, oh, I don't have problems with swallowing, but then when you delve further, they're like Darryl, there's no way I could eat a bagel or a piece of bread by itself. Um Do they chew excessively and turning away pills? Do they have problems with pills? So those are things that you can ask to further uh delve into dysphagia issues that may bring up issues because as I mentioned, a lot of times they've developed adaptive behaviors to compensate for their eoe uh then we look at things uh uh endoscopically, obviously. So uh we have developed, there has been developed an eoe endoscopic reference code. It's another acronym, er EFS. Uh and, and, and it uh stands for Edema Rings, Exudate furrows and strictures. So all of these things um you can see or look for endoscopically that help with making the diagnosis and a picture is worth 1000 words. So here uh is for those of you who don't look at endos endoscopies, uh regularly, a normal endoscopy, you can see a nice vascular pattern here. Uh in patients with eoe, you can see edema. So this loss of these vascular patterns, uh these are pretty prominent rings, but they can be more subtle than this. Um exudate. These can be um boi of eosinophils and then these furrows which look like these tracks going down the esophagus and then, you know, strictures, which is a narrowing. And generally speaking, you know, this, these things would suggest eosinophilic esophagitis. And obviously, when one is doing an endoscopy, you would try to, if you see these exudates, you would biopsy in this area. If you see these furrows, you would biopsy in this area and we'll talk about dilation for strictures. Uh So then the third thing we look at, so we talked about symptoms, we talked about endoscopic findings. Then we look at the eosinophil count. This is where we have our pathologists. Uh So we send a tissue sample to the pathologist and they will be, they will stain this and they will look for these eosinophils uh and count them and give a peak eosinophil count. So once we've made the diagnosis with based on symptoms and uh biopsies uh then we can offer patients uh treatment. So how, what, what are the treatment options uh that are available? Uh We're gonna talk about diet. We're gonna talk about proton pump inhibitors, topical steroids and one biologic that it's a that's available to Pilum. And I think this is a, you know, great opportunity to involve the patients and obviously you'll need to involve patients in decision making on how to approach this. Um You know, which option you're gonna use for which patient will depend on. Uh As we'll talk about efficacy of the different treatments, ease of administration, the cost of the medication to the patient or if it's covered by insurance, uh patient pre preferences, some of these medicines are twice a day dosing. Uh diet elimination involves a strong willpower on the patient's part. Some patients have it. Some don't severity of the disease. Um are resources available to help them if they want to do uh dietary um therapies and then do they have other comorbid conditions? Do they have asthma? Do they have other at topic conditions? That would make sense uh to use to start with a biologic. So we'll talk about how I go through this and how you can discuss this with the patient in terms of uh decision making and treatment options. So in terms of diet, I think the important thing to understand as we talked about is that this isn't an IgE mediated disease. So skin testing and allergy testing for uh food triggers has limited utility is probably not that effective. In my experience, I've only had like one or two patients, um, that this worked in where they figured out what the, uh, that they were allergic to actually was fish. And then we eliminated fish and they did very well. But there is a lot of data to show that um elimination diet uh can be an effective treatment. Uh for instance, um patients put on elemental diet. So this is a diet where they consume a formula without any intact protein. So it's made of amino acids, fats, sugars, and other nutrients that are readily absorbed. When they've done studies looking at uh remission, uh they were able to achieve remission in over 90% of the patients. The problem with this, that it's extremely costly. It's inconvenient, it's not palatable and um patients may develop food allergies once uh foods are reintroduced. So it does show us that um eliminating foods can be a useful therapy but it's not. Um it's an in this is an inconvenient method. So, um one of the things that has come out of this is trying to uh eliminate certain foods. And one of the first to be start, one of the first diets to be started was a six food elimination diet. So the six food groups that are uh generally considered in when we, when you're doing elimination diets are milk or dairy wheats eggs, soy, peanuts or tree nuts and fish and shellfish. And there have been several studies looking at these six food elimination diets and they've been shown to, you know, induce histologic response in almost 70% of patients. And in general, it's been shown that dairy and wheat and eggs are most commonly implicated. Um, the issue with this therapy. The great thing is, it's, it's great for patients that don't want to use medicines. Um and that are strong willed that can do this. But the problems are you do need repeat uh endoscopies to figure this out. Um dietary adherence is difficult. Um And long term dietary restrictions can be challenging for patients. So generally how one would do this is you would eliminate the six foods, you would do this for 8 to 10 weeks and then you would assess symptoms, do the endoscopy, assess how things look endoscopically, take biopsies. And if everything is normal with no eosinophil count, then you'd start adding one of the foods back and then you'd repeat the endoscopy in 8 to 10 weeks. And you can see that there can be a lot of endoscopies that need to be done more recently. There's been a study that was published in 2023 in Lancet uh that compared one food elimination diet to six food elimination diet and they showed that they achieved similar remission rates and com you know, comparable uh improvement in his histologic and endoscopic features in adults. Um, and, and in this one food, they eliminated animal milk. And so maybe that's the first starting point that you can do. Um, and to, uh, in, if, if the patient states, you know, they don't want to use medications and they want to try elimination diet, uh, if they, if, if diet isn't, uh, gonna be something that's gonna work for the patient. Um, there are medications that we use. So proton pump inhibitors initially uh to make the diagnosis. Um, a trial of PPIs was previously required to exclude what was called PP I responsive esophageal eosinophilia. But now it's uh considered a first line therapeutic uh agent rather than a diagnostic agent for eoe. Uh it has a pretty favorable safety profile. It's not very expensive and it's readily available. Um It's thought to work by obviously reducing acid exposure that can facilitate uh epithelia improved epithelial barrier function. It also uh does have some anti-inflammatory effects, uh probably by blockading uh Eakin three expression uh that prevents migration of some, some of these uh immune cells into the esophagus. Generally, uh patients are on 20 or 40 mg depending uh twice a day, but depending on the PP I and I would do at least an eight week trial before determining if it's not working. So you put them on it eight weeks, 8 to 10 weeks later, you'll reassess their symptoms and how things look endoscopically. Uh It's been shown to reverse endoscopic features of fibrosis. Um when the histologic remission is achieved, uh the main limitation is its efficacy. Um Generally speaking, maybe 40 to 50% of patients will go into remission just on A PP I. Um if PPIs don't work, uh topical steroids uh is another option in the treatment of ein esophagitis. The idea here is to get contact of the steroid with the esophageal mucosa. In the past, we repurposed uh asthma medication. So we used uh fluticasone spray or Budesonide rescues. Uh and um the Budesonide rescues had to be mixed with a thickening agent like splenda or honey or agave nectar. Um And studies had shown that fluticasone and budesonide didn't really show any difference in terms of histologic and clinical response. Uh Obvious issues with this is patients could develop candidiasis. Very rarely. There were issues with adrenal insufficiency. But the problem with this is it's difficult to use. This is a a complex uh instructions that are needed whether you use the liquid respules, the meter dose inhaler, right? You have to coordinate depressing and putting it into the mouth and swallowing it rather than getting it into the lungs. Uh cost could be an issue because insurance didn't cover it. This was an off label use of this. And then anytime you talk about steroids, patients have concerns about long term risk. Now, um recently, there has been an oral rehydration, uh an oral uh suspension form of budesonide that has been FDA approved for the treatment of eoe. And so here's some data uh from the study. Uh This is basically a, it's a uh budesonide that comes in a packet that you squeeze and shake and it becomes a viscous solution that the patient swallows. And what you saw, what they saw was that there was a great histologic response in patients who took the Budesonide uh oral suspension solution compared to placebo in terms of less than six eosinophils per high powered field. And there was a statistical significant difference in dispace symptoms uh on patients on the Budesonide compared to the placebo group. So this is, this was FDA approved for patients older than 11. Uh It was 2 mg dose twice a day for 12 weeks. Obviously, I mentioned this is a chronic disease. Um So uh if patients stop this, likely they're gonna the disease will come back. So further studies need to be done to see is can we cut this back to once a day or lower dose or you know, using this more long term? What, what are the issues? So, again, going back to the immunopathology of eoe, we, we talked about the six group food groups that uh trigger a disease. Again, dairy, wheat, eggs, soy, fish, seafood and uh nuts. Again, if there's impairment in the barrier function, these whatever the antigen is on, these can trigger these alarming that trigger uh uh th two immune response that results in a number of cytokines being secreted that causes the migration of a number of different immune cells, including eosinophils, mass cells and basophils. This creates a no that affects the fibroblasts and the smooth muscle cells. It probably affects their transcriptome um as well as inflammatory changes. And this results in fibrosis and dis motility within the esophagus. And as we've begun to understand the players in this, um various specific targets have been developed to affect these different cytokines in an attempt to see if we can very specifically uh use uh targets for these players to treat eosinophilic esophagitis. And this is uh uh uh uh table of several biologics that have been tried or successfully used in the treatment of eosinophilic esophagitis that I'll talk about. Uh Dupilumab has been FDA approved. We'll talk about that for the treatment of eoe I showed you some data on Belis eppo lium also affects IO five with similar results of decreasing Eoin ils but not affecting uh dysphasia. Um And there's other uh drugs uh or antibodies that are uh in various stages of trials. Uh We are gonna be a site to look at uh further studies of D Diyab. Um We were involved in a trial of se uh send, send AAB which is an il 13 target and we are gonna start a trial uh with uh this TS LP uh antibody also rut. So, Dupilumab is an il four receptor alpha inhibitor. So Il four receptor, uh alpha is part of the Il four and Il 13 receptor. So, this uh monoclonal antibody blocks, both Il four and Il 13 function and it was FDA approved for the treatment of eoe in May of 2022. So this is some of the data from that. Again. Uh this looked at two different dosing of the antibodies. So, uh they did a weekly dosing and a once every two week dosing. And you can see from the above that the weekly dosing and the every two week dosing were very good at histologic remission in terms of decreasing the eosinophil count compared to placebo. But what's interesting is when you look at the dysphasia symptoms, weekly dosing was good compared to placebo uh with, with significant improvement in dysphasia symptoms. But every two week dosing um was not different from placebo. So this, the FDA approved uh 300 mg per week, uh weekly dosing uh given sub Q. And so again, this goes to the fact that you can have good uh histological remission without um affecting the dysphasia symptoms per se. So how might one incorporate biologics into the management of eoe? Well, if they're refractory to PP I therapy or topical steroids, uh this would be uh the, the patient that you would do this if they've had side effects from other medications, I've had some patients that don't tolerate PPIs or don't tolerate um the topical steroids. Um obviously if a patient is, is, is um uh worried about side effects, that's gonna be a problem. And um if some of these therapies like B ID dosing of the uh medication can be difficult for patient adherence. And uh a once a week uh injectable would be uh much easier for them to abide by. Uh I mentioned before, obviously, if they have other at topic uh comorbidities, if they have asthma or they have uh dermatitis or some other things that uh Dupilumab is indicated for, um then that might be a uh a time to use that medication as you can treat both things at the same time. Uh One thing I wanted to mention is the role of esophageal dilation. Uh Generally speaking, I will um perform this after initiating um anti-inflammatory therapy. Um Again, the dilation doesn't do anything to improve the inflammatory process. It's gonna obviously help with the fibrosis. Um And in general, it's pretty effective in clinical improvement. Uh You see it in 95% of the patients, serious complications are rare. If you do it correctly. You uh obviously want want to uh you don't want to dilate too quickly. Uh Generally speaking, we will bring these patients back for several dilations to get things uh up to, you know, we, we wanted get them to at least 15 millimeters. Uh if we can, and we'll usually do them three millimeters at a setting. Um Some serious complications like I said are rare, uh, can have bleeding, uh, perforation, hospitalization or chest discomfort is quite common. And usually if we're going to do dilation or I tell the patients beforehand, uh, please make sure you have like liquid um acetaminophen available so that, uh, if you do have some pain, um, you can take that on a regular basis until that subsides because what we're trying to do is actually make a controlled tear in the esophagus to open it up. And so uh it's not uncommon to have some chest discomfort after the procedure and it's always good to make sure uh the patient is aware um that this is a possibility. So, going back to the case, um you know, the primary care physician was astute and sent them for uh endoscopy um on endoscopy, uh they saw mucosal edema, small amount of exudate some subtle rings and longitudinal referrals, but no strictures that gives an er score of four. Um and pathology, they took biopsies again. So when I take biopsies, I tend to take biopsies from two parts of the esophagus near the ge junction, as well as from the proximal esophagus. I usually take at least uh three passes uh from both sides um to get a good uh representation because the esophagus is a long tube and the biopsies are small and you know, a movement of 2 to 3 centimeters in one direction or higher may change what the um eosinophil peak eosinophil count would be. So we wanna try to get as good a representation of both those sites as we can. Uh So based on the symptoms that the patient was having and based on the uh biopsy findings, um the diagnosis of uh eosinophilic esophagitis was made. And so kind of thinking through um once the diagnosis is made, how, you know, you would offer therapeutics to the patient. Generally speaking, I will offer uh PPI I like them to try, uh PP I twice a day, uh, for 8 to 10 weeks. And then we can see how things go if the patient says I don't wanna be on any medications we can offer dietary therapy. I think there are options for six food, four food, two food, one food elimination diet. Again, what I tell the patients are that every time we make a change, we wanna look at how things look symptom wise, how things look endoscopically and how things look on biopsy. We talked about allergy directed. I, I don't think that that's very useful. Uh, a lot of times patients are referred to us from allergist, but I would just send them, you know, if we're, if we're gonna try to manipulate diet, it's best to use the six or two or one food elimination diet. And we talked elemental diet does show us that food plays a role and eliminating food can, uh, be an, uh, therapy, but it's not a long term. Uh, therapy. So diet is one way and then if medical treatment is gonna be pursued, if PPIs aren't working, we'll try the topical steroids. There is the uh FDA approved Budesonide. Uh we have been using uh Budesonide Respi or the meter dose inhaler. Uh issues will be caused or insurance coverage. Um And then there is a biologic therapy uh dupilumab, it's a once a week sub QE injection um that can be used and has been shown to decrease uh Eoin count as well as um help with symptoms with this. When one does endoscopy, um esophageal uh dilations can be performed if there is evidence of fibrosis or remodeling of the esophagus. Um that can be done in addition or in addition to the medical therapy or diet therapy and one can move back and forth with these things depending on what the situation uh of the patient and what they can and cannot uh do. Uh the idea is to get them into remission. So, histologic remission as well as symptoms. Uh Once um you have achieved remission, you know, the question is uh what, what's the follow up that needs to be done? There's no clear data. I try to follow up with my patients at least once a year in clinic. Uh Obviously, if they have any issues where dysphasia comes back, then we would schedule them for an endoscopy and biopsies to see um what's going on. I don't think there's any fixed time frame if patient is doing well, that you need to repeat uh endoscopies. But uh some data suggests every two or three years to rook, make sure uh, something uh, underlying isn't brewing. Uh The reason for that is that symptoms aren't 100%. There can be underlying uh inflammation that's taking place even though the patient uh, doesn't have any symptoms. So that's another place where you discuss with the patient about, you know, how often we need to repeat endoscopies. But obviously, if they have any symptoms of dysphagia, uh that come back up, you'd wanna rook sooner, uh, to make sure, um, things look, ok, endoscopically and on biopsy. Um, yeah, if a patient is non responsive, obviously, you wanna make sure that they're adherent to the therapy. Uh, taking medicines twice a day can be difficult, uh, especially with the topical steroids. I try to, you know, tell patients, I, you know, I want you to rinse your mouth out and spit it out, but I don't want you to eat or drink anything for at least half an hour to an hour after taking the medication. Uh, because I wanna increase contact time of that medication with the esophagus. I also tell them to try to lie down if they can for the evening dose. That's not a problem if they're gonna go to bed after taking the medication, but the morning dose, obviously that can be difficult. So, um, but taking something twice a day trying to increase contact time that can be hard for the patient. Um Are there inadvertent antigen exposure? So, particularly if someone is uh using diet elimination diet, um that would be uh it would be important in these situations or very nice to be able to refer them to dieticians who can help them or are versed in these elimination diets? And are there things that they're eating where there could be contamination? Uh could there be uh an infection or a stricture present? Right. So, we talked about with steroid therapy, there's possibility for can esophageal candidiasis. You'd wanna make sure that they don't have candidiasis, did a stricture develop that could be dilated and then, you know, if all of these things have been checked, you know, is eoe truly the uh correct diagnosis. So, uh this brings us to, you know, thinking about a multidisciplinary approach to the treatment of eosinophilic esophagitis. Um obviously, uh the primary care physician or a pediatrician needs to have that uh uh thought that this dysphasia could represent eoe uh they may actually present with dermatitis or asthma to a pulmonologist and uh getting that history of dysphasia. Um you know, and then directing them to the gastroenterologist for further evaluation is important. And then obviously at the ed physician, uh this will usually come to presentation as a food bolus impaction. So making sure that patients um who do come in with a food bolus impaction um, I would say, you know, if one can obtain biopsies and put them on A PP I and then refer them to the, for fo for follow up with the gastroenterologist to, uh, determine if this is eoe, I think there's roles for allergist. I mean, we did talk that, um, you know, skin testing for food allergies is not the way to approach, uh, using food, uh, elimination as, uh, um, a therapy, you know, six food elimination diet, four food, two food is the way to go. But you know, being able to do that is um uh uh you know, it's good to have dieticians who are first, we do have dieticians available that we can refer patients within our group to um discuss um six food, four food, two food, one food elimination diet and help with that elimination. I think uh there's a big role for pathologists. We just in this, we just discussed about the peak eosinophil count um for patients. But I think there's more sophisticated ways of looking at this. There is a uh eoe logic scoring system that has been developed that looks at more than just the peak eosinophil count. Um It looks at um basal zone hyperplasia, dilated intercellular spaces, thickening of the lamin appro all of these can be put into a scoring system. And actually, there's been some data and papers published that these scoring systems can differentiate, differentiate, treated from untreated individuals and may also be useful in predicting patients that can respond to PP I. So there's a lot of uh work that could be done with the pathologist, just aside from looking at the peak eosinophil count. Uh The other thing I'll say is that these patients have had this disease for a long time. They have had a lot of, um they've had a lot of compensatory mechanisms to allow them to um swallow. Um you know, over time, um you know, they will have nervousness about swallowing. And so in patients um who uh you've dilated, who have been on medicine, they're in histologic remission. Um Endoscopically, everything looks fine but still are having complaints. Uh You, you know, you may wanna involve uh psychologists for cognitive behavioral therapy or other things uh to help and there's data to suggest that there can be issues uh there as well um in patients with EOE. Um So, let's see. Uh That's what I have for today. I think we have time for questions. I've also put in my contact information, that's my email. And then Jackie Statler is uh the clinical coordinator who works with me. So if you have any uh questions about EOE or have any concerns or patients that you are interested in getting further work up uh for eoe uh reach out to her, we can get them in pretty quickly and that's her uh direct office number. Great. Thanks so much. There is a question. Um First Thanks for a great presentation. So, pyrosis is not a symptom of asthenopia esophagitis nor is nausea. So, in, in, in, in patients in, in pediatric patients, all bets are off. So, for sure they can have nausea and vomiting as a symptom. It's not usually the symptom in adults. Usually they're gonna have solid food, um, dysphasia. Um, uh, and, um, sometimes they'll complain of chest pain, but primarily in adults it's gonna be solid food dysphasia. We check chat. Thank you. Fantastic presentation. So again, if you all do have questions, um that, you know, I mean, sometimes you don't think of those right away and then you think later on in the day. Oh yeah, so feel free. I'm gonna send out an email. You can always email me. Um you know, and I can also put in that email, doctor's email address and Jackie's email address. So, yeah, like you mentioned earlier, I see patients at South County and West County and clinic and um, you know, we, uh you know, we do endoscopies at both those places as well. So I think for a lot of these cases, if you have that concern, um you know, you can reach out to us, we can get them quickly seen uh for with endoscopy and get the biopsies done, then we really have all the information that we need to, you know, make that clinical pathologic diagnosis and uh then we can um set up follow up uh appointments by in person or telehealth to go over all the findings um and make decisions uh that way. Um And if a patient is concerned about doing the endoscopy first, we can always see them again in, in clinic or even by telehealth as well to discuss that and then move forward with um making the diagnosis and um treatment. Great. Thank you so much. No problem. Thanks for your time. Yeah, have a great rest of your day and then everybody else if you want to take a quick break and then we will come back um at our next speaker is at 2 p.m. So if you could just make sure you're back at two pm, that'd be great. Thanks so much. Created by Presenters Sandeep Kumar Tripathy, MD, PhD Gastroenterology View full profile
