COMMENTARY

Eosinophilic Esophagitis: Three New Studies to Know

David A. Johnson, MD

Disclosures

July 13, 2016

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Hello. I am Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.

Eosinophilic esophagitis (EoE) continues to be explosive in the medical literature. This reflects, to a large extent, our lack of understanding about so many facets of this disease that we now see not uncommonly, particularly among the adult population and not just the pediatric population. There are three articles on EoE that came out recently that I thought were most notable to raise to your attention.[1,2,3]

Helicobacter pylori Infection and Risk for Eosinophilic Esophagitis

The first article found that Helicobacter pylori infection was associated with a reduced risk of developing EoE.[1] We know that the prevalence of H pylori infection has decreased considerably in industrialized nations over the past three decades. This has been attributed to improved hygiene with less antigenic exposure, and a corresponding increase in many atopic diseases, such as asthma and dermatitis. Altogether, this suggests that H pylori exposure may in fact affect immune system development. EoE is an antigen-mediated allergic disease of the esophagus, but the correlation with H pylori has not been previously evaluated in patients with well-defined disease.

This was a case/control study from Germany. The investigators evaluated H pylori serology in 58 patients (81% were male, as expected) with EoE diagnosed on the basis of well-characterized consensus recommendations. These cases were compared with 116 age- and sex-matched controls.

Among cases, the seroprevalence of H pylori infection was 5.2% when only participants with current infection were included and 13.8% when participants who were previously treated (8.6% of participants) were included. Among controls, the cumulative seroprevalence of H pylori infection was 37.9%. There was a statistically significant odds ratio of 0.24 for the association between EoE and H pylori infection. In this study, H pylori infection seemed to be protective against EoE.

This study adds further support to the potential protective role of H pylori in immune-mediated allergic diseases, which in this case was EoE or "asthma of the esophagus." The rise in allergic conditions has been attributed to a possible impairment in the T-helper (Th) cell balance, in particular Th1 and Th2 immune responses. Basically, the Th1 response is involved in cellular immunity, which helps fight viruses and other intracellular pathogens. The Th2 response is involved in humoral immunity, where antibody production is upregulated to some type of infectious organism. Both of these pathways can interact with each other and affect the upregulation or downregulation of the immune system.

It is thought that the rise in the allergic conditions that we are talking about may reflect an impaired balance between these Th1 and Th2 immune responses, possibly resulting from a higher standard of hygiene. Infection with H pylori induces more of a Th1 response, and these cytokines would inhibit the Th2 or humoral-mediated response, which is a major pathway for EoE. This imbalance can result in a higher likelihood for these Th2 or humoral immunity-type allergic diseases.

I think this study provides pathophysiologic evidence suggesting that the relevance of therapeutic consequences needs to be evaluated. This is particularly applicable in our rush to eradicate H pylori where we should be thinking about how this infection may potentially be protective. Instead of trying to shoot to kill, we may want to start raising science to save the bug.

Does Allergy Testing Predict Food Triggers in Eosinophilic Esophagitis?

The second article that came out is also related to allergic conditions in the context of EoE.[2] The recommendation is that we should do allergy testing in patients with EoE to try to identify allergens that we could target in our management. We have all been taught that the six-food elimination diet is really the way to go if we are going to start to withdraw things. A lot of times, it has been questioned whether could we test for specific food triggers rather than comprehensively eliminating such things as milk, soy, wheat, shellfish or seafood, peanuts and tree nuts, and eggs.

This very interesting and comprehensive study looked at a variety of different modalities to do allergy testing and found that we cannot rely on any specific testing modality other than the histologic response when we withdraw these foods and then reintroduce them. The investigators looked at participants with well-characterized EoE in a cohort that responded to the six-food elimination diet, which was about 50% of the participants. They did a comprehensive battery of allergy testing. They looked at skin-prick and skin-patch testing; serum food and aeroallergen-specific immunoglobulin (Ig) E levels; basophil activation testing, which is something that is used in patients who may have had an anaphylactic reaction; and serum food-specific IgG antibody levels. None of these predicted response when they sequentially reintroduced the foods, and there was no correlation with histologic assessment.

As you start to introduce these patients back to foods that were previously withdrawn, you need to rely on histologic assessment. That is the key message. Allergy testing does not seem to have any role as it relates to predicting food triggers.

Correlation of Symptoms With Endoscopic and Histologic Remission

The final article is a recent observational study from Switzerland.[3] The investigators looked at the relevance of symptoms in EoE. For example, when we start to withdraw foods, can we rely on clinical symptoms rather than endoscopic and histologic evidence of remission?

The short answer is no, because the correlation between clinical endoscopic and histologic remission was just not good at all in this study. Symptoms are an important parameter for response for EoE, but they cannot be used alone as a reliable determinant of the disease activity in response to therapy. We must look at histologic endpoints—at least that is my bias—because with subclinical EoE, we just do not know if it may lead to some form of a more formidable permanent injury as it relates to stricture formation. Despite clinical symptom improvement, the plan should be to go back and assess for histologic resolution of the eosinophilic infiltrate in the esophagus.

Hopefully, these three recently published articles give you some guidance and new information for managing EoE, along with some points to discuss with your patients. I am sure there are a lot more data to come.

I am Dr David Johnson. Thank you again for listening. See you next time.

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