Beyond the Wheeze: Incidental Diagnosis of Eosinophilic Oesophagitis in a Young Child With Asthma‐Like Symptoms

1. Case Presentation

A 7‐year‐old male child with a normal birth history presented with chronic regurgitation and non‐bloody, non‐bilious emesis on breastmilk since birth. Symptoms were unrelieved by the Proton Pump Inhibitor (PPI) Lansoprazole, the trial of different formulae as well as maternal dietary restrictions. Differentials like pyloric stenosis and malrotation were ruled out by ultrasonography and upper GI series. He had no weight loss, diarrhoea, oliguria or respiratory distress.

Family history was significant for mild intermittent asthma in his mother and seasonal allergies in both parents. His 4‐year‐old sister had allergic colitis since the first year of her life and suffered from poor weight gain until 3 years of age.

At 7 months of age, the patient developed poor weight, requiring nutritional supplementation and occupational therapy for feeding. Over time, he developed atopy with multiple food allergies, a chronic maculopapular rash, and congestion, for which multiple dietary changes were advised with no clinical improvement.

He required two hospitalisations due to Failure to Thrive (FTT) and dehydration. His Gastroesophageal Reflux Disease (GERD) with emesis had progressively worsened with age, and he developed a chronic nocturnal dry cough, which was not relieved with PPIs; hence, he was referred to our centre at 12 months of age for further evaluation.

A Modified Barium Swallow study was normal, determining normal swallowing. Skin prick testing was performed using a standardised paediatric food and aeroallergen panel including milk, egg, wheat, soy, peanut, tree nuts, dust mite, pollens and moulds. Serum‐specific IgE testing was conducted for corresponding food allergens. Patch testing was performed using a standardised food allergen series. These revealed allergies to eggs, milk and penicillin. Molecular allergen diagnostics were not utilised. He was diagnosed as well with Allergic Rhinitis and Atopic dermatitis, partially responsive to topical steroids and oral antihistamines.

Initially, we started him on a diet restricting milk and eggs and counselled parents about food avoidances, label reading, cross‐contamination, food allergy resources and anaphylactic symptoms. Considering his family history of asthma, atopy and his cough, he started Albuterol as needed, which was found to be effective. Given his GERD symptoms, the PPI was continued, and he was also given antihistamines.

At 13 months of age, he presented to the Emergency department (ED) with an acute febrile illness and a maculopapular rash with hypoglycemia to 30 mg/dL and dehydration, where he was managed symptomatically.

At 14 months, while admitted to our hospital due to a 2‐day febrile illness and Upper respiratory tract infection (URI) symptoms he again had hypoglycemia to 66 mg/dL. He had an extensive workup over the course of two hospital admissions for his severe and prolonged hypoglycemia episodes and noted delayed linear growth velocity. Evaluation revealed Growth Hormone (GH) deficiency with a low Insulin like Growth Factor‐1 (IGF‐1) and a normal cortisol response. He was started on GH infusions after a normal Brain Magnetic Resonance Imaging (MRI). Genetic work‐up showed long‐chain fatty acid deficiency, and was managed with cornstarch supplementation.

At 16 months, his cough became productive with nighttime awakenings and unresponsive to inhaled corticosteroids. A sweat chloride test ordered was normal, ruling out Cystic Fibrosis. Bronchoscopy with bronchoalveolar lavage and an upper endoscopy were performed. Results revealed Tracheomalacia and Oesophageal Eosinophilia (30 eos/hpf mid, 20 eos/hpf distal oesophagus) consistent with possible Eosinophilic oesophagitis (EoE) but since the patient had stopped PPIs at the time of his scopes, GERD as the cause of his findings could not be ruled out. Celiac and infectious workup was negative. A pH probe showed normal results, making reflux a less likely cause of his symptoms.

Given that asthma is a common cause of chronic cough and considering the patient's history of atopy, Fluticasone and Salmeterol inhaled combination therapy were started and he was continued on antihistamines. PPIs were also restarted due to the presence of vomiting, with strict dietary restrictions, and he was closely followed.

At 22 months, he presented with chest congestion and exercise intolerance and was treated with oral steroids. A follow‐up endoscopy confirmed eosinophilic oesophagitis, with 14 eosinophils/hpf in the mid and 30 eosinophils/hpf in the distal oesophagus, accompanied by reactive changes (Figures 1 and 2).

FIGURE 1.

Biopsy of the distal oesophagus in 4× showing > 30 eosinophils/hpf (arrowhead) in the squamous mucosa with mild basal zone hyperplasia, with an intact lamina propria. The eosinophils are distributed throughout the epithelial layers, occasionally forming microabscesses.

FIGURE 2.

Biopsy of the mid oesophagus showing superficial non keratinising squamous epithelium with desquamation, intraepithelial eosinophils (14/hpf) and basal zone hyperplasia (arrowhead).

Dietary elimination initially targeted foods with documented sensitisation (milk and egg), with empirical addition of peanuts and tree nuts due to persistent symptoms and high allergenic potential. A stepwise approach was chosen over a Four‐food elimination diet given the patient's young age, nutritional vulnerability and prior restrictive diets, and he was also started on oral viscous budesonide 1 mg swallowed daily with continued PPIs. After 3 months of Budesonide, dietary restrictions, PPI and antihistamine therapy in addition to his fluticasone/salmeterol inhaled therapy, he attained histological remission of his EoE in a repeat upper gastroendoscopy.

After this, Budesonide was decreased to 0.5 mg daily along with continued PPI, and he maintained his histological remission.

Peripheral blood eosinophil counts were monitored serially, with an initial elevation of 768 cells/UI. decreasing to 450–400 cells/UI in correlation with treatment response, and subsequently remaining within the normal range.

Overall, his asthma symptoms improved in parallel with EoE control. At 6 years, due to persistent allergic rhinitis and eczema requiring intermittent steroids, therapy was transitioned to Dupilumab (200 mg biweekly) with continued PPI use. Follow up endoscopy 4 months later showed EoE in continued remission.

Now aged 7 years old, the child remains asymptomatic, with well‐controlled asthma, atopy and EoE on Dupilumab, inhaled budesonide/formoterol and antihistamines, with normal growth and nutrition. He has also been gaining weight without GI symptoms despite stopping use of PPI. He has been evaluated for nutritional deficiencies, renal function, osteopenia and Clostridium difficile , and results were normal. To aid interpretation of the complex clinical data, Table 1 summarises the treatment interventions and corresponding responses.

TABLE 1.

Review of course of pathology.

Age of the patient	Gross findings	Histo pathological findings	Treatment at the time of the scope	Control of asthma	Intervention based on endoscopy findings
16 months	Normal	30 eos/hpf in the mid oesophagus		Severe persistent asthma symptoms	Dietary changes
		20 eos/hpf in the distal oesophagus with reactive changes			Omeprazole 10 mg twice daily
		DIAGNOSED WITH POSSIBLE EOE
22 months	Mild linear furrowing in the middle and distal oesophagus	14 eos/hpf in the mid oesophagus	Famotidine and Omeprazole 20 mg once daily	Severe persistent asthma symptoms—chronic cough, exercise intolerance and congestion	Start of oral viscous budesonide 1 mg daily, continued omeprazole 20 mg once daily, and removed milk, eggs, peanuts and tree nuts from diet
		30 eos/hpf in the distal oesophagus with reactive changes
		CONFIRMED WITH EOE
27 months	Normal	4 eos/hpf in the mid oesophagus	Oral viscous budesonide 1 mg once daily	Improvement noticed in cough	Omeprazole 20 mg once daily
		0 eos/hpf in the distal oesophagus with reactive changes	Omeprazole 20 mg once daily		Tapered Oral viscous budesonide to 0.5 mg once daily
		ATTAINED REMISSION
2 years 5 months	Normal	7 eos/hpf in the mid oesophagus	Oral viscous budesonide 0.5 mg once daily	Night cough reduced and Improved activity and quality of life	No changes
		12 eos/hpf in the distal oesophagus with reactive changes	Omeprazole 20 mg once daily
4 years 5 months	Normal	2 eos/hpf in the mid oesophagus	Oral viscous budesonide 0.5 mg once daily	Asthma control test score 27 (consistent with well‐controlled asthma per parent/patient assessment)
		9 eos/hpf in the distal oesophagus	Omeprazole 20 mg once daily
		IN HISTOLOGICAL REMISSION	Fluticasone, Cetirizine, Albuterol
5 years 8 months	Normal	0 eos/hpf in the mid oesophagus	Stopped Oral Viscous Budesonide and Omeprazole	No asthma flares since starting Dupilumab, and no exercise intolerance noted. Significantly improved quality of life	No changes. Plan for repeat endoscopy in 2026
		< 3 eos/hpf in the distal oesophagus with reactive changes
		CONTINUED REMISSION	Started Dupilumab 200 mg once every 2 weeks

2. Discussion

Eosinophilic oesophagitis (EoE) is a chronic, antigen‐mediated immune disease of the oesophagus, characterised clinically by dysphagia, feeding intolerance, food impaction or abdominal pain, and pathologically by eosinophil predominant inflammation. It is a T cell‐mediated delayed type hypersensitivity reaction, associated with CD4+ G protein coupled receptor and IL‐5 and 13 [1].

The first EoE‐like case was reported in 1978, though EoE was not recognised as a distinct entity from GERD and other causes of oesophageal eosinophilia until the early 1990s [2, 3]. A global systematic review of 40 meta‐analyses in 2025 confirmed a continuing rise in both prevalence and incidence of EoE over the decades [4].

Studies do consistently demonstrate a strong association between EoE and allergic asthma, highlighting their shared allergic and type‐2 inflammatory mechanisms. Narrative reviews by Durrani et al. [2] and Capucilli et al. [3] report asthma prevalence ranging from 32% to 84% in children with EoE and 12%–68% overall, with both suggesting that EoE may either unmask or contribute to subclinical asthma‐like airway changes. Capucilli et al. [2, 3] further emphasised the allergic nature of EoE, linking it to atopic dermatitis, IgE‐ mediated food allergy and allergic rhinitis due to shared genetic and immune pathways. Supporting these findings, a systematic review and meta‐analysis by González‐Cervera et al. [5], that included over 53 542 EoE patients, found that asthma was significantly more common in EoE patients than in controls (OR, 3.01; 95% CI, 1.96‐4.62; I ² = 84.5%), reinforcing the strong epidemiological association between the two conditions [5].

Our patient exemplifies the diagnostic complexity of overlapping EoE and asthma. He had significant feeding intolerance and severe respiratory and allergic issues since birth, which were initially treated as GERD, asthma and atopy without complete symptomatic relief and worsening symptoms over time.

GERD is a significant differential, as it may be a trigger for asthma in some patients. Abnormal reflux, as measured by symptoms or by oesophageal pH monitoring, occurs in 25%–75% of children with persistent asthma, and the association increases with severity of either condition; however, whether or not this association is causal remains unclear [6]. Existing literature suggests that when patients are treated for GERD, they may see clinical improvement in their asthma as well [7].

Hence, GERD is an important differential for EoE, and their symptoms and histologic findings often overlap, making it difficult to clearly distinguish between them. It is important to determine the number and distribution of eosinophils in the oesophageal mucosa for differentiation. In children with GERD, the degree of eosinophilic inflammation tends to be less intense (< 15 eosinophils per high‐power field) and limited to the distal oesophagus, whereas in children with EoE, the inflammation tends to be more severe (> 15 eosinophils per high‐power field) and located in the middle or proximal oesophagus as well [8]. Most importantly, many patients with EoE have a history of atopy or peripheral eosinophilia and are more likely to fail to respond to antireflux treatment [8].

Given the child was already on other treatment modalities, Dupilumab was initiated at a biweekly dose with a plan for escalation to weekly dosing if the response was inadequate. Given the patient's favourable and sustained clinical and histological response, dose escalation was not required.

The clinical trajectory of our patient improved substantially after a targeted approach for EoE was initiated with dietary elimination, PPIs, topical steroids, and later Dupilumab injections. Currently, the patient continues limited avoidance of previously identified trigger foods while tolerating a broader diet without gastrointestinal symptoms.

This case highlights the importance of considering EoE in children with atypical or treatment‐refractory asthma, and the response in our patient is most likely due to a combined therapeutic effect rather than attributing to a single intervention. These interventions not only stabilised his pulmonary status but also are hopefully preventing complications such as oesophageal remodelling or strictures, feeding aversions and long‐term growth delays, in turn improving his quality of life.

Our case findings support the growing literature of co‐occurrence of EoE and Asthma, by documenting clinical and histological improvements in both EoE and Asthma symptoms following specific EoE targeted therapy [9, 10, 11]. The delay in diagnosis complements similar challenges seen in other reports, where EoE remained undiagnosed until endoscopic evaluation was performed. It also supports the theory that EoE is not merely a gastrointestinal disease but a systemic allergic disorder with long term complications, emphasising that asthma is controlled not just with inhalations but also with treatment of underlying oesophageal inflammation.

We advocate for early gastroendoscopic in addition to a bronchoscopic evaluation in children with difficult to control asthma, particularly when accompanied by GI symptoms or atopy, and for a multidisciplinary approach involving gastroenterology, pulmonology, allergy‐immunology and nutrition.

3. Learning Points

1. Chronic cough and wheeze in early childhood are not always pulmonary in origin; oesophageal inflammation from EoE can mimic or exacerbate lower airway disease through shared type 2 inflammatory pathways.

2. Eosinophilic esophagitis (EoE) should be considered in children with asthma‐like symptoms that are atypical, refractory or disproportionate to airway findings, particularly when accompanied by feeding intolerance, vomiting or poor growth.

3. Failure to respond to proton pump inhibitors and standard asthma therapy should prompt reconsideration of the diagnosis, rather than escalation of inhaled or systemic corticosteroids alone.

4. The coexistence of EoE, asthma, allergic rhinitis, atopic dermatitis and food allergy reflects a unified atopic phenotype, underscoring EoE as part of a systemic allergic disorder rather than an isolated gastrointestinal disease.

5. Endoscopic evaluation with oesophageal biopsies is essential for diagnosis, as clinical features and imaging alone cannot reliably distinguish EoE from gastroesophageal reflux disease in young children.

6. Targeted treatment of EoE (dietary elimination, topical corticosteroids and biologic therapy when indicated) may lead to parallel improvement in respiratory symptoms, supporting a bidirectional relationship between oesophageal and airway inflammation.

7. This case highlights the importance of a multidisciplinary approach, involving paediatric pulmonology, gastroenterology, allergy–immunology and how Delayed recognition of EoE may contribute to prolonged morbidity, including feeding aversion, failure to thrive, oesophageal remodelling and persistent respiratory symptoms.

Author Contributions

Sameena Tabassum: conceptualisation of research idea, data collection, review of literature, writing – original draft, supervision, synthesis of inferences and recommendations. Keslar Just: review of literature, data collection, writing – original draft, synthesis of inferences and recommendations. Mili Jyotsna: review of literature, writing – original draft, synthesis of inferences and recommendations. Anayansi Lasso‐Pirot: conceptualisation of research idea, review of literature, led and supervised the study, writing – review and editing.

Funding

The authors have nothing to report.

Ethics Statement

The authors declare that the research presented in this manuscript adheres to the ethical principles outlined by the Institutional Review Board of the University of Maryland School of Medicine. All procedures involving human participants were conducted in accordance with the ethical standards of the University of Maryland of School of Medicine, United States and the Declaration of Helsinki (1964), as revised in 2013.

Consent

Informed consent was taken from the patient's guardians.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.