Kathryn Peterson, MD, on Diagnosing and Treating Eosinophilic Gastritis

Dr Kathryn Peterson provides an overview of her presentation at the American Academy of Allergy, Asthma, and Immunology on eosinophilic gastric diseases other than EoE, including the challenges of diagnosis and options for treatment.

CLINICAL PRACTICE SUMMARY

Eosinophilic Gastrointestinal Disorders (non-EoE EGIDs): Diagnostic Challenges and Emerging Therapies

• Non-EoE EGIDs (eosinophilic gastritis/enteritis) are increasing in prevalence and often mimic functional GI disorders, presenting with nonspecific symptoms (abdominal pain, bloating, IBS-like features). A large Japanese cohort identified atopic comorbidities (allergic rhinitis/sinusitis, asthma, urticaria, trend with atopic dermatitis) as risk factors, supporting heightened bedside suspicion in patients with overlapping allergic disease.
• Diagnosis requires proactive biopsy despite normal endoscopy and variable disease course. In a Netherlands cohort (~n=70), ~20–25% had chronic disease and most others had relapsing–remitting symptoms, complicating detection timing. Notably, ~60% had normal-appearing endoscopy, necessitating routine biopsies (stomach, duodenum, colon). Histologic guidance suggests >30 eosinophils per high-power field (≥1 field) should raise strong suspicion for EGID.
• Therapeutic evidence is emerging but limited. A 2024 study supports elemental diet efficacy, and an NIH retrospective series (n≈12) found topical budesonide improved symptoms. A randomized controlled trial (n=41, 12 weeks) of dupilumab (IL-4Rα inhibitor; 600 mg load, then 300 mg q2w vs placebo) in eosinophilic gastritis showed reduced tissue eosinophils and trends toward symptom and remission improvement, with transcriptomic normalization; however, persistent symptoms may reflect comorbidities (e.g., alpha-tryptasemia, autonomic dysfunction).

Kathryn Peterson, MD, MS, is a Senior Associate Consultant and gastroenterologist at the Mayo Clinic in Jacksonville, Florida.

TRANSCRIPT:

Hi, I'm Kathryn Peterson. I'm an adult gastroenterologist at the Mayo Clinic in Jacksonville, Florida. And I just recently gave a lecture on human studies and clinical trials in EGIDs or eosinophilic gastrointestinal disorders at QuadAI 2026. And I'd like to just summarize and give you some clinical pearls from my presentation that maybe would be applicable to your practice.

One thing that I think is really important is that these non-EoE EGDs, and we're going to focus a little bit on this because there's a lot of data and everybody's pretty familiar with EOE. So I'm going to focus below the esophagus. But one thing that I think is really important is these are actually increasing. So we're increasingly recognizing these non-EOE EGDs. And so probably very similar to atopic disease in general, patients are developing these conditions more and more.

But what's hard about these conditions is they present with a myriad of symptoms and they can present as a functional bowel disease, irritable bowel. They can present as nonspecific abdominal pain or bloating. And so they're very hard to tease out unless we actually know what we're supposed to be looking for. And so some groups actually in the last year have been trying to figure this out. They've said, let's look to see if we can find risk factors for these diseases to help people that are at the bedside identify when a patient might have one of these conditions. And a group from Japan actually looked at this in a very large cohort of their non-EOE lower eosinophilic disorders. And what they actually found is that atopic disease did seem to increase the risk of their patients being diagnosed with eosinophilic gastritis or enteritis. And so things like allergic rhinitis or sinusitis, asthma, there was actually a trend towards atopic dermatitis.

Urticaria was actually much more common in patients that had these otherwise non-pecific GI symptoms. And so it's something to think about at the bedside when you actually have these patients present and then you're dealing with the fact that they have a lot of other allergic comorbidities, we should be thinking, do they have an underlying eosinophilic disorder? And they are hard to follow.

And so that is something we also have to take into consideration that once we identify that we have a symptom and we are suspicious of the disease, how do we actually diagnose them? And we have to realize that some of these patients, the natural history could be variable. And so in the Netherlands, they actually followed patients for a while and they followed about 70 patients with these conditions. And they identified that about a little over 20, 25% of them had chronic symptoms, chronic disease. And then a lot of the remaining ones actually had relapsing and remitting symptoms so that if you're not scoping them and trying to get biopsies at the right time or catching them at the right time, it can look like they don't have disease.

In addition, what they found—and this is really important for clinicians to talk to the allergists, the primary care to talk to the gastroenterologist—is that about 60% of these patients can actually have a normal-appearing endoscopy. So unless you know to have that suspicion and you know to have that conversation with the endoscopist that you need the biopsies no matter what, these patients can actually get missed. So this is really important information I think that is coming out because we don't want to have that delay in diagnosis because they can have increased complications and we want to have that increased kind of suspicion of disease so that we can have these conversations and make sure they get the biopsies done.

To do the biopsies is even more complicated. We know that we need to actually get multiple biopsies in the duodenum, in the stomach, and the colon, wherever we're looking for this disease. And they've come out actually now, at least with some relief for pathologists, because we have to now talk to pathologists about enumerating the number of eosinophils so that we have an idea if those patients have disease. And what we really want to look at if the pathologist cannot look at the 5 high-power fields, is at least have them evaluate one high power field, the one that has the most eosinophils in it. And if they have greater than 30 eosinophils in one high power field, there is literature now to suggest that you should have a highest suspicion that this could be an eosinophilic gastrointestinal disorder. And again, take everything else in context.

Understand that maybe you want this to have chronicity, maybe they need to have other atopic disease, but these are all things that are going to increase your suspicion of getting this actual condition diagnosed in your patients. So at least in the stomach, one biopsy with greater than 30, and they're going to come out sooner with other recommendations in the small bowel with a minimum count that should increase our suspicion. Well, it's great to do that, but now what we really need to do is what is the most recent data that actually helps us once we identify these patients? Once we finally say, actually, you don't have irritable bowel, you have an eosinophilic gastrointestinal disorder, how do we actually treat these patients?

Well, there was a study in 2024 that showed that elemental diet works, arguing that there is a food component to these diseases much like eosinophilic esophagitis. There's also recent data that came out of the NIH that showed that topical budesonide could be helpful. This was a retrospective trial on about 12 patients where they just looked back to see their response rate and they showed that it really could help symptoms even if it didn't completely resolve the eosinophilia.

And then we actually were really lucky this year that we had results published at Digestive Disease Week, and there's actually a paper, it's just not published yet, where they actually said, we have our first randomized controlled trial of dupilumab. Dupilumab is that antibody against IL-4 alpha receptor that actually inhibits signaling from IL-4 and IL-13. Dupilumab is approved for EoE. So the thought is because we know EoE and lower eosinophilic diseases tend to run hand in hand, maybe this would actually work on eosinophilic gastritis. So they studied patients with eosinophilic gastritis and wanted to look and randomize them.

Now, they randomized them to a different dose of dupilumab than what we're used to for EoE because at the time we only knew the atopic dermatitis dosing. So they randomized them to the 600 milligrams upfront and then 300 every two weeks versus placebo. And they randomized 41 patients to a one-to-one to either that dosing arm or a placebo arm and then followed them for 12 weeks. And what they found is that actually by 12 weeks, even with a different type of dosing, they had substantially different reductions. So they had a greater reduction in eosinophils in the tissues in the dupilumab arm. And they had trends towards improvement in the gastro eosinophil count, the mean count, the averaging of all the counts, the symptoms, there was a trend toward improvement, and then the proportions of patients actually going into remission. And they even showed that the transcriptome that was being studied with a microarray and the tissues was starting to normalize once these patients got dupilumab.

So I do think that once we're able to identify these diseases, there are going to be options out in the future. Being clinicians though, we have to realize that not everyone's going to respond to these. And so I think what's really important is understanding if your patient responded to these therapies is why. And some data is now coming out to explain maybe some continued symptoms. So a lot of your patients will come in, they'll have abdominal pain, nausea, vomiting, you get suspicious of an eosinophilic disorder, you diagnose it, you treat it, the eosinophils go away and they're no better. Well, what is going on? I think that what we need to realize is there's data now coming out that there's a lot of comorbid conditions that run hand in hand with eosinophilic gastrointestinal disorders. There are things like alpha-tryptasemia, there's autonomic dysfunction, there's hypermobility, and all of these in and of themselves can cause GI symptoms.

So it's really important to think about counseling your patients when they come in to say, "We're going to treat the disease. If you have concurrent diseases, those symptoms may not get better, but now we'll be able to hopefully identify and characterize which symptom is going with which condition." So I think in the general, in the future, we're going to have a lot more information about these disease states, hopefully a lot more information on other medications that we can use to treat them and hopefully better ways to identify and follow these patients. And that's my update for 2025. Thank you.