Annotations

Because symptoms are often discordant with underlying disease activity, symptoms alone should not be used to make decisions about treatment changes.56 Relying on symptoms in isolation to guide food elimination or reintroduction is insufficient and can result in false identification of food triggers and unnecessarily prolonged dietary restriction.

:/

Initial standard empiric diet strategies include the 6-food (SFED), 4-food (4FED), 2-food (2FED), 1-food (1FED) elimination diets. The most well studied and prototypic of these is the SFED – avoidance of all animal milk products, wheat, soy, eggs, nuts/treenuts, and seafood (finfish and shellfish) –yielding pooled response rates of ~70% in both children and adults.

These skills include nutrition label reading to avoid contamination, cross-contact, and accidental ingestion. Because the threshold level of EoE food trigger is unknown, a strict avoidance of the food allergen group and all sources of cross-contamination is recommended during the initial phases of diet to clearly identify the specific EoE triggers. A wheat-free diet should also exclude gluten containing grains (e.g. oats, barley, rye) due to risk of cross contamination.

makes sense

The evidence that EoE is a food-mediated allergic disease includes i) almost all patients respond to an elemental diet and many respond to a diet in which dairy, wheat, eggs and/or soy are eliminated, ii) the presence of food-specific IgE and Th2 cells are consistent with a loss of tolerance to trigger foods and iii) many EoE patients have concomitant IgE-mediated food allergy and other allergic co-morbidities. This narrative review focuses on the hypothesis that EoE is a form of chronic food allergy. The goal is to describe similarities and differences in EoE and IgE-mediated food allergy, and to consider ways that these two increasingly common forms of food allergy are related to each other.

me_irl

Overall in the various studies throughout the world, milk is the most common allergen causing disease in about 2/3 of patients followed by egg and wheat in another ¼ of the patients.

Dosage appears to play a crucial role, as the meta-analysis indicated that histological remission rates were significantly higher with the use of double doses of PPIs compared to standard doses (51.7% vs. 28.3%, p < 0.005). The duration of treatment also seems to be important, with the EoE CONNECT database study suggesting that prolonging the initial treatment period from 8 to 12 weeks may increase the likelihood of achieving remission.

The traditional understanding of how PPIs might benefit patients with EoE has primarily focused on their ability to suppress gastric acid production. Gastroesophageal reflux, including acid reflux, can contribute to esophageal inflammation and potentially exacerbate EoE. By reducing gastric acid secretion, PPIs may alleviate this contributing factor, thereby reducing esophageal inflammation. Acid-peptic damage to the esophageal epithelium can increase its permeability, potentially allowing for greater penetration of allergens that trigger the immune response in EoE. Furthermore, acid exposure can enhance the expression of inflammatory mediators and adhesion molecules, potentially leading to the recruitment of eosinophils. Thus, the acid-suppressing effects of PPIs could indirectly benefit EoE by mitigating these processes.

However, accumulating evidence suggests that PPIs may also exert direct anti-inflammatory effects on the esophageal mucosa, independent of their acid-suppressing properties. In vitro studies have demonstrated that PPIs, such as omeprazole and lansoprazole, can inhibit the Th2 cytokine-stimulated secretion of eotaxin-3, a key chemokine responsible for the recruitment of eosinophils to the esophagus.

Current guidelines recognize PPIs as a reasonable first-line therapy for EoE due to their favorable safety profile and ease of administration. A typical initial trial of PPI therapy is 8 to 12 weeks in duration, followed by reassessment for symptomatic and histological remission.

Frequently, a cofactor, such as exercise, alcohol, stress, or nonsteroidal anti-inflammatory drugs are required to induce symptoms—this can create difficulties with the diagnosis since symptoms may be absent without the cofactor.

An interesting finding that was not discussed in this study is that LTP sensitization may occur by the inhalation or contact with cannabis LTP (Can s 3) even with passive smoke/exposure (for example, in young children), potentially leading to the development of LTP food allergy

Cow's milk (most common, affecting about 2/3 of patients)

About 30-50% of patients have one food causing disease, 30% have two, and the remaining 30% have 3 or more foods triggering EoE

might have to do 4-eliminative diet instead of one at a time

The main allergenic proteins in cow's milk are:

Casein

Whey proteins, particularly:

Beta-lactoglobulin

Alpha-lactalbumin

ige-mediated food allergies differ from other allergies like contact dermatitis or non-ige food reactions because they involve a specific immune pathway using immunoglobulin E antibodies that create rapid and potentially severe systemic reactions. this specific mechanism explains why ige food allergies can trigger anaphylaxis within minutes of exposure, while other allergic reactions typically develop more slowly and are rarely life-threatening

ige vs non-ige

Progression of PPI therapy from diagnostic tool to therapy for EoE. Initial belief that EoE was a consequence of GERD led to early interest in PPIs as a therapy for EoE. Next, it was hypothesized that PPI-responsive esophageal eosinophilia (PPI-REE) was a condition distinct from EoE. A lack of response to PPIs was subsequently viewed as an essential diagnostic criterion for EoE. Subsequently, characterizations of PPI-REE and EoE patients at the molecular level showed that the two conditions are virtually identical leading to the hypothesis that they are at different points along a continuum. Recent guidelines, enlightened by this observation, now view PPIs as a therapy rather than a diagnostic for EoE.

interesting

In the context of EoE, the allergic reactions are often considered to be primarily non-IgE-mediated, with symptoms developing in a delayed manner, typically hours or even days after the ingestion of the triggering food. On the other hand, hives are characteristically an IgE-mediated reaction, with symptoms appearing rapidly, usually within minutes to an hour after exposure to the allergen. Therefore, it is biologically plausible that an individual's body could react to the same allergen through both an IgE-mediated pathway, leading to the immediate onset of hives, and a non-IgE-mediated pathway, contributing to the delayed esophageal inflammation seen in EoE.

While studies have shown that a significant percentage of individuals with EoE may have positive skin prick test results for food allergens (nearly 70% in children and 50-60% in adults) , these positive results do not necessarily mean that the same foods are the ones triggering the inflammation in their esophagus. An individual with EoE might have a positive skin test to milk, indicating an IgE-mediated sensitivity, but the primary trigger for their esophageal eosinophilia could be wheat, which might not show up on a skin test. Therefore, a positive skin test result for a food allergen in a patient with EoE should be interpreted with caution and does not definitively confirm that the same food is causing their esophageal inflammation.

this connection actually gives you a potential advantage in your detective work. hives typically appear more quickly after exposure to a trigger (hours instead of days), which might help you narrow down suspects faster than just tracking your esophageal symptoms.