Eosinophilic Esophagitis (EoE) Treatment in Dallas, TX

What Is Eosinophilic Esophagitis (EoE)?

Eosinophilic esophagitis (EoE) is a chronic, immune-mediated inflammatory disease of the esophagus characterized by an abnormal accumulation of eosinophils — a type of white blood cell normally involved in allergic and parasitic immune responses — in the esophageal tissue. Under normal conditions, eosinophils are not present in significant numbers in the esophagus. In EoE, the esophageal mucosa becomes infiltrated with large numbers of eosinophils in response to food allergens and, in some cases, environmental allergens, leading to inflammation, tissue damage, and symptoms of esophageal dysfunction.

EoE has emerged as one of the most important esophageal conditions recognized in the past two decades. Once considered rare, it is now the leading cause of dysphagia (difficulty swallowing) and food impaction in children and young adults, and the second most common cause of chronic esophagitis after GERD. According to the American Gastroenterological Association (AGA), the prevalence of EoE has increased dramatically since the condition was first described in the early 1990s, now affecting an estimated 1 in 2,000 adults and up to 1 in 1,500 children in the United States. Whether this increase reflects true rising incidence or improved recognition and diagnostic awareness is debated, though most experts believe both factors contribute.

At Texas Gut Health in Sachse, TX, Dr. Jaison John provides comprehensive evaluation and individualized treatment for patients with EoE throughout the Dallas-Fort Worth area. Dr. John completed his gastroenterology fellowship at UT Medical Branch, where he served as Chief Fellow, and his internal medicine residency at UT Austin Dell Medical School, where he served as Chief Resident. He holds dual board certifications from the American Board of Internal Medicine in both internal medicine and gastroenterology. His expertise in upper endoscopy and esophageal dilation is essential for the diagnosis and management of EoE.

Understanding the Immune Response in EoE

EoE is fundamentally an allergic disease of the esophagus. The condition is driven by a type 2 helper T-cell (Th2) immune response, similar to the immune pathways involved in asthma, eczema, and allergic rhinitis. When a susceptible individual is exposed to a triggering allergen (most commonly a food protein), the esophageal epithelium produces cytokines — particularly thymic stromal lymphopoietin (TSLP), interleukin-13 (IL-13), and eotaxin-3 — that recruit eosinophils to the esophageal tissue. These eosinophils release toxic granule proteins and pro-inflammatory mediators that damage the esophageal epithelium, disrupt the mucosal barrier, and stimulate fibroblast activation. Over time, this chronic inflammation leads to tissue remodeling: the esophageal wall becomes thickened, stiff, and narrowed due to subepithelial fibrosis.

This understanding of EoE as a Th2-mediated allergic disease has been instrumental in developing targeted therapies, including dupilumab (a monoclonal antibody that blocks IL-4 and IL-13 signaling), which received FDA approval for EoE in 2022.

Symptoms of Eosinophilic Esophagitis

The symptoms of EoE vary by age and can be subtle, often leading to significant diagnostic delays. Studies show that the average delay between symptom onset and EoE diagnosis is 4 to 6 years in adults.

Adult Symptoms

• Dysphagia (difficulty swallowing) — Dysphagia, particularly for solid foods, is the most common symptom of EoE in adults, reported by 70% to 80% of patients. Patients may describe food "sticking" or "getting hung up" in the chest during swallowing. Dysphagia in EoE results from both active eosinophilic inflammation (which causes mucosal edema and reduced esophageal compliance) and chronic fibrosis/stricture formation.
• Food impaction — Food impaction — when a bolus of food becomes lodged in the esophagus and cannot pass — is the most dramatic presentation of EoE and often the event that leads to diagnosis. Food impaction may require emergent endoscopic removal. EoE is the most common cause of food impaction in adults.
• Chest pain — Non-cardiac chest pain is reported by up to 30% of adults with EoE. The pain may mimic GERD or cardiac chest pain and can occur with or without swallowing.
• Heartburn unresponsive to PPIs — Some patients with EoE present with heartburn-like symptoms that do not respond to standard GERD treatment. This "PPI-refractory heartburn" should prompt consideration of EoE, particularly in younger patients with atopic conditions.
• Adaptive eating behaviors — Many adults with EoE unconsciously develop compensatory strategies to manage their swallowing difficulty: eating extremely slowly, cutting food into very small pieces, drinking large volumes of liquid with meals, avoiding certain textures (such as bread, meat, and rice), and choosing soft foods. These behaviors often become so ingrained that patients do not recognize them as abnormal until specifically asked.

Pediatric Symptoms

In children, EoE symptoms are more varied and age-dependent. Infants and toddlers may present with feeding difficulties, food refusal, vomiting, and failure to thrive. Older children may report abdominal pain, nausea, vomiting, and difficulty swallowing. Adolescents tend to present more like adults, with dysphagia and food impaction as primary symptoms.

Causes & Risk Factors

EoE results from a complex interplay of genetic susceptibility, environmental exposures, and allergen-driven immune activation. While the exact cause is not fully understood, research has identified several important contributors.

Allergen Triggers

• Food allergens — Food proteins are the primary triggers for EoE in the majority of patients. The most commonly implicated foods in adults are milk (dairy), wheat, eggs, soy, nuts/tree nuts, and seafood/shellfish. These six food groups form the basis of the traditional six-food elimination diet (SFED) used in EoE management. Importantly, the food triggers for EoE are typically mediated through a delayed, non-IgE immune pathway, which is why standard allergy skin prick testing and serum IgE blood testing are generally unreliable for identifying EoE triggers.
• Environmental allergens — Aeroallergens (pollen, mold, dust mites, pet dander) may also contribute to EoE in some patients. Seasonal variation in EoE symptoms has been observed, with some patients experiencing worsening during peak pollen seasons. However, environmental allergens are considered a less prominent trigger than food allergens in most patients.

Genetic and Familial Factors

• Genetic predisposition — Genome-wide association studies have identified several genetic risk loci for EoE, most notably variants in the TSLP (thymic stromal lymphopoietin) and eotaxin-3 (CCL26) genes. These genes play central roles in the Th2 inflammatory pathway that drives EoE.
• Family history — EoE has a strong familial component. First-degree relatives of EoE patients have a significantly increased risk (estimated at 2% to 6%, compared to 0.05% in the general population). Concordance rates in twin studies are approximately 40%.

Atopic Association

• Atopic conditions — Approximately 50% to 80% of patients with EoE have concurrent atopic conditions such as asthma, allergic rhinitis (hay fever), eczema (atopic dermatitis), and food allergies. This strong atopic association underscores the allergic nature of EoE and is a key clinical clue to the diagnosis.

Demographic Risk Factors

• Male sex — EoE is approximately three times more common in males than females.
• Age — EoE can occur at any age but is most commonly diagnosed in children and young adults (peak incidence in the 20s and 30s).
• Caucasian race — EoE is disproportionately common in Caucasian populations, though it occurs in all racial and ethnic groups.

How EoE Is Diagnosed

EoE can only be definitively diagnosed through upper endoscopy (EGD) with esophageal biopsies. No blood test, imaging study, or symptom questionnaire alone can confirm the diagnosis.

Upper Endoscopy with Biopsies

During an upper endoscopy, Dr. John examines the esophagus for endoscopic features characteristic of EoE. These features are described using the EoE Endoscopic Reference Score (EREFS) and include:

• Rings (trachealization) — Concentric rings that give the esophagus a corrugated or "ringed" appearance, resembling the trachea. Rings can be fixed (fibrotic) or transient (inflammatory).
• White exudates (plaques) — Small white spots or plaques on the esophageal surface, representing eosinophilic microabscesses.
• Linear furrows (vertical lines) — Longitudinal grooves or lines running along the length of the esophagus, reflecting mucosal edema.
• Edema (decreased vascularity) — The esophageal mucosa appears pale and swollen, with reduced visibility of the normal submucosal vascular pattern.
• Strictures (narrowing) — Esophageal narrowing due to chronic fibrosis, particularly in the proximal or mid esophagus.
• Crepe-paper mucosa — Fragile, tissue-paper-like mucosa that tears easily during endoscopy, indicating advanced disease.

Multiple biopsies are taken from at least two different levels of the esophagus (proximal and distal), with a minimum of 2 to 4 biopsies from each level, as eosinophilic inflammation can be patchy. The AGA/ACG guidelines recommend obtaining at least 6 biopsies total for optimal diagnostic sensitivity. Biopsies are also taken from the stomach and duodenum to exclude other causes of eosinophilia.

Histologic Criteria

The histologic hallmark of EoE is the presence of 15 or more eosinophils per high-power field (eos/hpf) in esophageal biopsy specimens. Additional histologic findings may include eosinophilic microabscesses, basal zone hyperplasia, dilated intercellular spaces, and lamina propria fibrosis. These findings, in the appropriate clinical context (symptoms of esophageal dysfunction) and after exclusion of other causes of esophageal eosinophilia, establish the diagnosis of EoE.

Excluding Other Causes

Several other conditions can cause eosinophils to accumulate in the esophagus, including GERD, eosinophilic gastrointestinal diseases (EGID), Crohn's disease, infections, drug hypersensitivity reactions, hypereosinophilic syndrome, and achalasia. A thorough clinical evaluation is necessary to distinguish EoE from these conditions.

Treatment Options

The goals of EoE treatment are to relieve symptoms, reduce esophageal eosinophilic inflammation to histologic remission (fewer than 15 eos/hpf, ideally fewer than 6 eos/hpf), prevent complications (particularly fibrostenotic stricture formation), and maintain remission long term. The AGA and ACG guidelines recommend a shared decision-making approach, taking into account the patient's preferences, disease severity, and treatment response.

Proton Pump Inhibitors (PPIs)

PPIs are often the first-line pharmacologic treatment for EoE. While initially thought to simply rule out GERD, it is now understood that PPIs have direct anti-inflammatory effects on the esophageal epithelium beyond acid suppression, including downregulation of eotaxin-3 and restoration of barrier function. Approximately 30% to 50% of patients with EoE achieve both symptomatic and histologic remission with PPI therapy alone (standard or high-dose, taken twice daily for 8 weeks). Patients who respond to PPIs are now classified as having PPI-responsive EoE, which is considered part of the EoE spectrum rather than a separate condition.

Topical Swallowed Corticosteroids

For patients who do not achieve adequate response with PPIs, topical swallowed corticosteroids are the next-line pharmacologic therapy and are among the most effective treatments for EoE. These medications are swallowed (not inhaled) so that they coat the esophageal lining and deliver anti-inflammatory therapy directly to the affected tissue.

• Budesonide oral suspension (BOS) — An FDA-approved viscous budesonide formulation specifically designed for EoE (approved in 2024 under the brand name Eohilia). The viscous suspension adheres to the esophageal mucosa more effectively than aerosolized formulations. Alternatively, budesonide respules can be mixed with a viscous vehicle (such as sucralose) to create a slurry that is swallowed.
• Fluticasone — Fluticasone propionate from a metered-dose inhaler is actuated into the mouth (without using a spacer) and swallowed, delivering the medication to the esophageal surface. This is an off-label use but is supported by clinical trial data and guideline recommendations.

Patients should avoid eating, drinking, or rinsing the mouth for 30 minutes after taking topical steroids to maximize esophageal contact time. Oral candidiasis (thrush) is the most common side effect, occurring in approximately 5% to 10% of patients. Systemic steroid absorption is minimal with topical esophageal delivery.

Biologic Therapy (Dupilumab)

Dupilumab (Dupixent) is a monoclonal antibody that blocks interleukin-4 (IL-4) and interleukin-13 (IL-13), two key cytokines driving the Th2 inflammatory pathway in EoE. In 2022, dupilumab became the first FDA-approved biologic therapy for EoE in patients aged 12 years and older weighing at least 40 kg. Clinical trials demonstrated that dupilumab significantly reduced esophageal eosinophil counts, improved histologic and endoscopic disease features, and relieved dysphagia symptoms. Dupilumab is administered as a subcutaneous injection (typically weekly) and is an important option for patients with moderate to severe EoE who are refractory to or intolerant of PPIs and topical corticosteroids.

Dietary Elimination Therapy

Dietary elimination is a non-pharmacologic approach that removes the offending food allergens from the diet to eliminate the antigenic trigger driving esophageal inflammation. Several dietary strategies are used:

• Empiric elimination diets — The traditional six-food elimination diet (SFED) removes the six most common EoE trigger foods: milk, wheat, eggs, soy, nuts/tree nuts, and seafood/shellfish. After 6 to 8 weeks of elimination, endoscopy with biopsies is repeated to assess histologic response. Foods are then reintroduced one at a time, with endoscopy after each reintroduction to identify the specific trigger(s). This approach achieves histologic remission in approximately 70% to 75% of patients but is burdensome due to the number of endoscopies required.
• Step-up (two-food) elimination — A newer, less restrictive approach that begins by eliminating only milk and wheat (the two most common triggers, together accounting for approximately 50% to 60% of EoE cases). If remission is not achieved, additional food groups are eliminated stepwise. This approach reduces dietary burden and the number of endoscopies while maintaining good efficacy.
• Targeted elimination — Removal of specific foods identified through allergy testing or dietary history. However, because standard allergy testing poorly predicts EoE triggers, this approach has limited success and is not routinely recommended as a primary strategy.
• Elemental diet — A liquid amino acid-based formula that eliminates all intact food proteins. While highly effective (achieving remission in over 90% of patients), the elemental diet is poorly tolerated by adults due to taste and the elimination of all normal food. It is used primarily as a short-term rescue strategy or in severe, refractory cases.

Esophageal Dilation

For patients with significant esophageal strictures or narrowing causing dysphagia despite medical or dietary therapy, esophageal dilation is a safe and effective mechanical treatment. During upper endoscopy, Dr. John uses through-the-scope balloon dilators or graduated bougie dilators to gently stretch the narrowed esophagus. Dilation provides rapid improvement in swallowing symptoms but does not treat the underlying eosinophilic inflammation, so it should always be combined with pharmacologic or dietary therapy. Dilation in EoE is safe when performed carefully, with perforation rates well under 1% in experienced hands.

Maintenance Therapy

Because EoE is a chronic condition that typically recurs when treatment is stopped, long-term maintenance therapy is recommended for most patients. This may include ongoing PPI or topical steroid therapy (at the lowest effective dose), continued dietary avoidance of identified trigger foods, or ongoing biologic therapy. Regular endoscopic monitoring is performed to confirm that histologic remission is maintained.

Frequently Asked Questions