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. 2025 Jun 4;31(10):2895–2906. doi: 10.1093/ibd/izaf095

The Association of Inflammatory Bowel Disease and Eosinophilic Esophagitis: A Systematic Review and Meta-analysis

Russell Yanofsky 1, Rohit Jogendran 2, Tedi Hoxha 3, Avani Pathak 4,5, Ani Orchanian-Cheff 6, Tarun Chhibba 7, Alexa N Sasson 8, Parul Tandon 9,✉
PMCID: PMC12558585  PMID: 40468892

Abstract

Background

The association between inflammatory bowel disease (IBD) and eosinophilic esophagitis (EoE) remains unclear. We aimed to perform a systematic review and meta-analysis on the association between EoE, IBD, and other immune-mediated inflammatory diseases.

Methods

A systematic literature search was conducted in Ovid MEDLINE, Ovid Embase, and the Cochrane Central Register of Controlled Trials (Ovid) from inception to July 2023. The primary outcome was to compare the frequency of an EoE diagnosis in IBD and other immune-mediated inflammatory disease processes versus control populations. Where pooled analysis was possible, we reported odds ratios (ORs) with 95% confidence intervals (CIs). I2 values were used to report heterogeneity, with values >50% suggesting substantial heterogeneity.

Results

We identified 2612 eligible studies, of which 38 studies were included. A diagnosis of EoE was significantly greater in patients with IBD compared to the general population (OR 3.9; 95% CI, 2.6-5.9 [I2 = 99.5%]). There was no significant increase in EoE in patients with ulcerative colitis compared to Crohn’s disease (OR 1.0; 95% CI, 0.7-1.3 [I2 = 88.7%]). EoE was also significantly increased in patients with atopic dermatitis (OR 2.4; 95% CI, 1.9-3.1 3 [I2 = 70.4%]) compared to those without atopic dermatitis.

Conclusions

Both IBD and atopic dermatitis were associated with an increased odds of EoE diagnosis. Further research is needed to determine the underlying mechanisms behind these potential associations.

Keywords: inflammatory bowel disease, ulcerative colitis, Crohn's disease, eosinophilic esophagitis

Key Messages.

What is already known?

  • Inflammatory bowel disease (IBD) and eosinophilic esophagitis (EoE) are chronic inflammatory conditions of the gastrointestinal tract.

What is new here?

  • The totality of evidence suggests that IBD is associated with increased odds of EoE.

How can this study help patient care?

  • Treating clinicians should have a low threshold to consider endoscopic evaluation and esophageal biopsies in IBD patients with upper gastrointestinal symptoms.

Introduction

Inflammatory bowel disease (IBD) and eosinophilic esophagitis (EoE) are chronic inflammatory conditions of the gastrointestinal tract.1 There is an increasing global incidence and prevalence worldwide of both disease entities, particularly in industrialized countries.2 Although distinct conditions, IBD and EoE share several similarities, as both are driven by the interaction between underlying genetic and environmental influences.2 In addition, both have complex pathogeneses with overlapping features, including the presence of T helper (TH) cells, increased expression of mast cells, eosinophils, and similar cytokines such as interleukin (IL)-13.1

IBD and EoE have also been linked to other immune-mediated inflammatory conditions such as celiac disease and atopic dermatitis (AD), though the mechanisms remain unclear.3–7 IBD is thought to be related to overlapping pathogenic pathways, including immune dysregulation, common genetic mutations, and altered gut microbiota.8 EoE is considered part of the allergic marche as an immunoglobulin-E (IgE)-mediated condition and has been associated with AD, allergic rhinitis, asthma, and IgE-mediated food allergy.9 However, the etiology behind its connection to other immune-mediated inflammatory diseases is less certain.10

Emerging evidence has indeed supported an association of co-existence of IBD and EoE, but there have been conflicting reports.11,12 In addition, limited studies have examined whether the co-existence of these 2 conditions influences the natural history and prognosis of IBD.13,14 Therefore, we aimed to perform a systematic review and meta-analysis, evaluating the incidence and association of IBD with EoE. We also assessed whether other immune-mediated inflammatory conditions are associated with EoE to provide a more comprehensive assessment.

Materials and Methods

This systematic review and meta-analysis aimed to determine the event rate of subjects diagnosed with both IBD and EoE and whether a diagnosis of IBD inferred a greater risk of EoE than the general population. Similarly, we aimed to determine the event rate of other concomitant immune-mediated inflammatory conditions and EoE. We also explored the clinical characteristics of IBD and EoE compared to IBD or EoE alone to better understand the natural history of this patient population. The study was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement guidelines and was registered a priori on PROSPERO (CRD42023444121).15

Search Strategy and Eligibility Criteria

A comprehensive search strategy was developed using a combination of database-specific subject headings and text words for the main concepts of EoE, IBD, and immune-mediated inflammatory diseases. Databases searched included Ovid MEDLINE, Ovid Embase, Cochrane Database of Systematic Reviews (Ovid), and Cochrane Central Register of Controlled Trials. These databases were searched from inception to July 2023 (see Supplementary Appendix 1 for full search strategy). To complement our database search, we also screened the reference lists of included studies and review articles to identify any additional eligible studies.

We included all immune-mediated inflammatory conditions included under the main concepts of immune-mediated inflammatory disease (Supplementary Appendix 1) except for celiac disease, as this has been previously studied.5 Furthermore, we included publications in the English language and those that were conducted enrolling human participants. Full texts and abstracts of clinical trials, cohort studies, and case series, which evaluated the incidence of EoE in an IBD population and a given immune-mediated inflammatory disease population, were identified. Any studies enrolling both adult and pediatric patients were included. Exclusion criteria included non-English studies, systematic review/meta-analyses, research in progress, dissertations/theses, books, and case series or case reports with fewer than 5 patients. We also excluded studies evaluating the incidence of IBD and immune-mediated inflammatory diseases in EoE populations, as the purpose of the study was to focus on the influence of IBD and immune-mediated inflammatory diseases on the development of EoE only.

Study Selection

Five reviewers (R.Y., R.J., T.H., A.P., and P.T.) independently performed the initial title and abstract screen and selected abstracts that met the inclusion criteria for full-text review. The same reviewers then independently reviewed the full-length manuscripts (or abstracts when applicable), and those that met the inclusion criteria were included in the final qualitative and quantitative review. Discrepancies were resolved by consensus agreement (R.Y. and/or P.T.).

Outcome Definitions

The primary outcome was to determine whether an IBD diagnosis increased the odds of concomitant EoE compared to the general population. We further explored whether IBD subtypes, including ulcerative colitis (UC) or Crohn’s disease (CD) increased the odds of concomitantly being diagnosed with EoE. The secondary outcome was to determine whether a diagnosis of other immune-mediated inflammatory diseases increased the odds of concomitant EoE. We also explored whether concomitant IBD impacted the prognosis and natural history of IBD or EoE. Cases of IBD, EoE, and other immune-mediated inflammatory conditions were determined by individual studies. Our search strategy explored all other immune-mediated diseases and their association with EoE, such as rheumatoid arthritis, systemic lupus erythematosus, and Sjogren’s syndrome. Apart from studies assessing AD, there were limited studies identified and insufficient information to perform meaningful analysis. Therefore, our analyses only focused on AD.

Data Collection

Five reviewers (R.Y., R.J., T.H., A.P., and P.T.) independently completed data extraction using a standardized data collection sheet. Data collected included the following: (1) study characteristics including primary author, year of publication, type of study (full text vs. abstract), study design (case–control, prospective cohort, retrospective cohort, case series, cross-sectional), study population (adult, pediatric, or both), and the study location; (2) sample sizes including the total population, the total IBD or immune-mediated inflammatory disease population, the total non-IBD or non-immune-mediated inflammatory disease population, the total EoE population within the IBD or immune-mediated disease population and the total EoE population within the non-IBD or immune-mediated inflammatory disease population; (3) demographic information; and (4) disease characteristics, when available, age at study inclusion, age at diagnosis of IBD or immune-mediated inflammatory disease studied, sex, race, smoking status, other coexisting immune-mediated inflammatory diseases, and disease characteristics including the duration of the IBD or immune-mediated inflammatory disease studied, the IBD phenotype as per the Montreal Classification of CD and UC, previous surgery, and previous medical therapy for IBD and EoE.

Data Analysis

Analyses were performed using OpenMeta version 10.10. Where pooled analysis was not possible, we aimed to systematically synthesize the available literature. Where pooled analysis was possible, we reported a meta-analysis and odds ratios (ORs) with 95% confidence intervals (CIs). Forest plots were generated for the primary outcomes and secondary analyses. In a sensitivity analysis to investigate the impact of heterogeneity, we removed 1 study at a time, non-cohort studies, and outliers from the meta-analyses. All P-values were 2-sided and a value less than 0.05 was considered statistically significant. The I2 assessed between study heterogeneity with a value greater than 50% suggestive of substantial heterogeneity.

Quality Assessment

Four authors (R.Y., R.J., T.H., and A.P.) completed the study quality assessment. Cohort, case–control, and cross-sectional studies were assessed using the Newcastle–Ottawa Scale (NOS) for cohort, case–control, and cross-sectional studies, respectively.16 The scale is comprised of 8 questions, 4 of which assess selection criteria (score 0-4), 2 assess comparability (score 0-2), and 3 assess outcomes (score 0-3). Low-quality studies are defined as having an NOS score of less than 7. Using this criteria, 11 studies had a score ≥7 and 21 studies had a score <7 (Supplementary Appendix 2). The quality of studies was also determined using the GRADE definitions of quality of evidence, ranging from very low to high quality of evidence.17

Results

We identified 2612 eligible studies (Figure 1). After excluding duplicates, 2347 studies were screened at the title and abstract level. One hundred sixty-eight studies including published manuscripts and abstracts were considered for full-text review. Thirty-three studies were included in the systematic review.3,11–14,18–45 We included 10 full-text studies3,12–14,18–21,28 and 14 abstracts22–27,29–36 that evaluated IBD and EoE (Table 1). Furthermore, we included 6 full-text studies37–42 and 6 abstracts43–45 that evaluated AD and EoE (Table 1).

Figure 1.

Figure 1.

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Results of search strategy and review process for identification of studies to include into systematic review and meta-analysis. D, atopic dermatitis; IBD, inflammatory bowel disease. *Studies included in review refer to both articles and abstracts.

Table 1.

Background information on studies evaluating the association of IBD, AD, and EoE that were identified for inclusion in the systematic review.

Study Immune-mediated inflammatory disease Study type Abstract/article Country Adult or pediatric study Total population (n)
Mintz, 202113 IBD Retrospective Case-control Article USA Adult 285
Moore, 20213 IBD Retrospective Case-control Article USA Pediatric 217
Urquhart, 202114 IBD Retrospective Cohort Article USA Adult 69
Limketkai, 201918 IBD Prospective Cohort Article USA Adult + Pediatric 133 308 339
Aloi, 202319 IBD Retrospective Case-control Article Italy Pediatric 3090
Fan, 201912 IBD Retrospective Cohort Article USA Adult 5435
Sonnenberg 202011 IBD Case-control Article USA Adult 14 1451
Talathi, 201920 IBD Case-series Article USA Adult 6
Splawski, 202221 IBD Retrospective Cohort Article USA Pediatric 661
Barrie, 201328 IBD Prospective Cohort Article USA Adult + Pediatric 1176
Alaber, 202023 IBD Retrospective Cohort Abstract USA NR 64 417 480
Alaber, 201922 IBD Retrospective Cohort Abstract USA Adult + Pediatric 36 857 870
Altun, 202124 IBD Retrospective Cohort Abstract USA Pediatric 233
Amer, 201525 IBD Case-series Abstract USA Adult 6
Asfari, 201726 IBD Cross-sectional Abstract USA Adult 6 145 845
Barfield, 201227 IBD Retrospective Cohort Abstract NR Pediatric 73
Eid, 202129 IBD Retrospective Cohort Abstract USA Pediatric 541
Eid, 202130 IBD Retrospective Cohort Abstract USA Pediatric 464
Gersten, 201031 IBD Retrospective Cohort Abstract NR Pediatric 81
Leung, 201932 IBD Retrospective Cohort Abstract NR Adult NR
Liu, 201633 IBD Retrospective Cohort Abstract NR Adult 72
Mansoor, 201934 IBD Retrospective Cohort Abstract USA Adult + Pediatric 38 233 220
Spencer, 202135 IBD Retrospective Cohort Abstract USA Pediatric 2033
Sunkesula, 202036 IBD Retrospective Cohort Abstract USA NR 64 292 570
Chen, 202337 AD Cross-sectional Article USA Adult 240 635
Hill, 201838 AD, IgE-FA asthma, allergic rhinitis Retrospective Cohort Article USA Pediatric 130 435
Huang, 202139 AD Retrospective Cohort Article USA Pediatric 203 533
Paller, 202240 AD Retrospective Cohort Article USA Pediatric 489 552
Arratibel, 202241 AD Retrospective Cohort Article USA NR 215
Brailean, 202342 AD, asthma, CRSwNP, ABPA, EGPA, EG/EGE Retrospective Cohort Article USA Both 1 326 646
Deng, 202243 AD Retrospective Cohort Abstract USA Pediatric 82 402
Roque, 202044 AD Retrospective Cohort Abstract NR NR 110
Silverberg, 202145 AD Cross-sectional Abstract Multinational (18 countries) Pediatric 7465
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Abbreviations: ABPA, allergic bronchopulmonary aspergillosis; AD, atopic dermatitis; CRSwNP, chronic rhinosinusitis with nasal polyps; EG/EGE, eosinophilic gastritis/eosinophilic gastroenteritis; EGPA, eosinophilic granulomatosis with polyangiitis; IBD, inflammatory bowel disease; IgE-FA, immunoglobulin-E-mediated food allergy; n, number; NR, not reported; SD, standard deviation.

IBD and EoE

Of the studies evaluating IBD and EoE, there were 4 case–control studies,3,11,13,19 17 cohort studies,12,14,18,21–24,27–36 1 cross-sectional study,26 and 2 case series20,25 (Table 1). The majority of the studies were conducted in the United States. Nine studies included an adult population, 8 studies included a pediatric population, and 4 included both. The reported prevalence of patients with IBD who were also diagnosed with EOE ranged from 0% to 8.8%.22,28 Meta-analysis to evaluate the association of IBD and EoE was possible for 6 of the 24 studies only, as these studies compared the incidence of EoE in the IBD population to EoE in the general population. In the 6 studies included, the pooled odds of being diagnosed with EoE were significantly increased in those with IBD (n = 6462/1 547 960) compared to those without IBD (n = 191 123/278 269 416) (pooled OR 3.9; 95% CI, 2.6-5.9 [I2 = 99.5%]) (Figure 2).11,18,23,26,34,36 Given the significant I2, sensitivity analysis was performed with the removal of each study, removal of the 2 non-cohort studies included,11,26 and removal of the 2 outlier studies.11,36 The heterogeneity and overall effect estimates remained consistent in these sensitivity analyses (Figure S1). There was no difference in the odds of EoE in patients with UC (N = 1881/428 904) compared to CD (N = 2972/481 614) (OR 1.0; 95% CI, 0.7-1.3 [I2 = 88.7 %]) in 8 studies that evaluated the incidence of EoE in IBD subtypes (Figure 3).3,11,13,18,19,22,24,36

Figure 2.

Figure 2.

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Comparison of A (Event = Number of patients with concomitant IBD and EoE/total IBD population) to B (Event = Number of patients with EoE only [no IBD]/total general [non-IBD] population). EoE, eosinophilic esophagitis; IBD, inflammatory bowel disease.

Figure 3.

Figure 3.

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Comparison of A (Event = Number of patients with concomitant CD and EoE/number of CD population) to B (Event = Number of patients with concomitant UC and EoE/number of UC population). CD, Crohn’s disease; EoE, eosinophilic esophagitis; UC, ulcerative colitis.

Patient characteristics with combined IBD and EoE can be found in Tables 2 and 3. The IBD/EoE cohort appeared to be predominantly male and White, with a mean age at IBD diagnosis ranging from 11.3 to 22.3 years old (Table 1).3,13 The majority of patients were initially diagnosed with IBD, followed by EoE.12,14 Several studies also described patients having other atopic conditions, including asthma, allergic rhinitis, or AD (Table 1).3,18,19,21 Limketkai et al. found that concurrent IBD and EoE were associated with a 1.4- to 2.4-fold increased risk of immune-mediated conditions compared to EoE alone, including celiac disease and IBD-associated rheumatological conditions (eg, inflammatory arthropathy), but did not increase the risk of Th2-mediated conditions such as AD and asthma, which was increased by having EoE alone.18 Similarly, Moore et al. demonstrated that EoE alone was associated with an increased risk of asthma, eczema, allergic rhinitis, and IgE-mediated food allergy compared to IBD alone.3

Table 2.

Demographic characteristics of studies evaluating the association of IBD and EoE that were identified for inclusion in the systematic review.

Study Immune-mediated inflammatory disease Mean age at study inclusion, (y, SD) Mean age at IBD diagnosis (y, SD) Mean duration of IBD (y) Female IBD-EOE (n) Caucasian IBD-EOE (n) Smoking IBD-EOE (n) Concomitant immune-mediated inflammatory disease (n)
Mintz, 202113 IBD NR 22.3 (14) 13.6 (7.3) 11/67 61/67 12/67 NR
Moore, 20213 IBD NR 11.3 (4.3) NR 11/67 54/67 NR Asthma: 18/67
Eczema: 6/67
Allergic rhinitis: 24/67
IgE-mediated food allergy: 24/67
Urquhart, 202114 IBD Median age (IQR) 35 (20-30) NR NR 16/48 NR NR NR
Limketkai, 201918 IBD NR Reported by CD and UC
CD years: 33.4 (16.4)
UC: 41.3 (16.2)		 NR NR NR NR Reported by CD and UC
CD: Celiac 66
IBD-associated rheumatological conditions: 349
Eczema: 67
Asthma: 495
UC:
Celiac: 21
IBD-associated rheumatological conditions: 184
Eczema: 28
Asthma: 241
Aloi, 202319 IBD NR 11.66 (2.76) NR 1/33 NR NR Celiac disease: 0/11
IgE-mediated food allergy: 4/11
Asthma: 2/11
Eczema: 2/11
Allergic rhinitis: 4/11
Fan, 201912 IBD NR NR NR NR NR NR NR
Sonnenberg 202011 IBD 47.7 NR NR 4665/8666 NR NR NR
Talathi, 201920 IBD NR 11.33 NR 1/6 5/6 NR NR
Splawski, 202221 IBD NR Reported by CD and UC
CD: 11.92 (2.93)
UC: 11.94 (4.15)		 NR 6/30 NR NR CD:
Eczema: 3
Asthma: 4
Food allergy: 5
Environmental allergy: 6
UC:
Eczema: 3
Asthma: 3
Food Allergy: 13
Environmental allergies: 9
Barrie, 201328 IBD NR NR NR NA NA NA NR
Alaber, 202023 IBD NR NR NR NR NR NR NR
Alaber, 201922 IBD NR NR NR NR NR NR NR
Altun, 202124 IBD NR NR NR NR NR NR NR
Amer, 201525 IBD Median age 53 (IQR 36-74) NR NR 1/6 6/6 NR NR
Asfari, 201726 IBD 75 (20.6) NR NR NR NR NR NR
Barfield, 201227 IBD NR NR NR NR NR NR NR
Eid, 202129 IBD NR NR NR NR NR NR NR
Eid, 202130 IBD NR NR NR NR NR NR NR
Gersten, 201031 IBD NR NR NR NR NR NR NR
Leung, 201932 IBD 52 (15.9) NR NR 6/7 7/7 NR Allergic rhinitis: 3/7
Primary sclerosing cholangitis: 1/7
Rheumatoid arthritis: 1/7
Liu, 201633 IBD NR NR NR NR NR NR NR
Mansoor, 201934 IBD NR NR NR NR NR NR NR
Spencer, 202135 IBD NR NR NR 1/25 24/25 NR AD: 10/25
Allergic rhinitis: 12/25
Food allergy: 14/25
Sunkesula, 202036 IBD NR NR NR NR NR NR NR
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Abbreviations: AD, atopic dermatitis; CD, Crohn’s disease; EoE, eosinophilic esophagitis; IBD, inflammatory bowel disease; IQR, interquartile range; n, number; NA, not applicable; NR, not reported; SD, standard deviation; UC, ulcerative colitis.

Table 3.

Clinical characteristics of studies evaluating the association of IBD and EoE that were identified for inclusion in the systematic review.

Study UC-EOE/total UC population (n) CD-EOE/total CD population (n) IBD-EOE location (n) CD-EOE phenotype (n) UC-EOE phenotype (n) Prior IBD-related surgery (n) IBD treatment (n) EOE treatment (n)
Mintz, 202113 39/12 717 56/158
 L1: 10/56
L2: 16/56
L3: 28/56
L4: 2/56
Perianal: 13/56
 B1: 32/56
B2: 10/56
B3 13/56		 E1: 4/39
E2: 11/39
E3: 24/39
 18/95
 5-ASA: 52/67
IM: 22/67
MTX: 11/67
Anti-TNF 35/67
Vedolizumab: 12/67
Any biologic: 37/67
Corticosteroids: 42/67
*Patients with IBD before EoE		 Diet: 15/67
PPI: 39/67
Swallowed Steroid: 27/67
Endoscopic dilation: 7/67
Moore, 20213 17/51 45/138
 L1: 33
L2: 37
L3: NR
L4: 27
Perianal: 1
Did not differentiate L1/L2 from L3. 45 patients in total		 B1: 36/45
B2: 3/45
B3: 6/45		 NR NR 5-ASA: 23/32
IM: 6/32
MTX: 7/32
Anti-TNF: 12/32
Vedolizumab: 1/32
Ustekinumab: 1/32
Tacrolimus: 1/32		 NR
Urquhart, 202114 28 UC-EOE
Did not include UC without EOE		 39 CD-EOE
Did not include CD without EOE
 L1: 12/39
L2: 6/39
L3: 18/39
L4: 5/39
Perianal: 5/39		 NR E1: 4/28
E2: 9/28
E3: 15/28		 NR 5-ASA: 48/69
Budesonide: 24/69
Corticosteroids: 46/69
IM: 49/69
MTX: NR
Anti-TNF: 57/69
Vedolizumab: 9/69
Ustekinumab: 4/69		 Diet: 4/69
PPI: 54/69
Swallowed Steroids: 41/69
Oral corticosteroid: 4/69
Endoscopic dilation: 16/69
Limketkai, 201918 1267/328 375 2239/376 822 NR NR NR NR NR NR
Aloi, 202319 3
Did not include UC without EOE		 8
Did not include CD without EOE
 L1: 1/8
L2: 0/8
L3: 7/8
L4: 1/8
Perianal: 2/8		 B1: 5/11
B2: 1/11
B3: 2/11		 E1: 1/3
E2: 0/3
E3: 0/3
E4: 2/3		 NR 5-ASA: 4/11
IM: 5/11
Corticosteroids: 8/11
Anti-TNF: 7/11
Other biologics: 0/11		 Diet: 2/11
PPI: 8/11
Swallowed steroids: 4/11
Endoscopic dilation: 0/11
Fan, 201912 4/7 2/7 L1: 2/7
L2: 0/7
L3: 0/7
L4: 0/7
Perianal: 1/7		 B1: 0/7
B2: 1/7
B3: 1/7		 NR 2/7 Anti-TNF: 3/7
No other treatment reported		 NR
Sonnenberg 202011 65/3860 26/3330 NR NR NR NR NR NR
Talathi, 201920 NA NA NR NR NR NR Sulfasalazine: 1/6
IM: 1/6
Anti-TNF: 4/6
 NR
Splawski, 202221 17/114 13/228 NA NA NA NA NA NA
Barrie, 201328 0/48 NA—Excluded CD NA NA NA NA NA NA
Alaber, 202023 NA NA NR NR NR NR NR NR
Alaber, 201922 NR NR NR NR NR NR NR NR
Altun, 202124 3/95 6/126 NR NR NR NR NR Oral prednisone: 2/6
Oral budesonide: 2/6
Topical fluticasone: 1/6
PPI: 1/6
Amer, 201525 0/0 6/6 L1: 4/6
L2: 0/6
L3: 2/6
L4: 0/6
Perianal: 1/6		 B1: 2/6
B2: 4/6
B3: 1/6		 Not applicable NR Anti-TNF: 4/6
Budesonide: 2/6		 NR
Asfari, 201726 NR NR NR NR NR NR NR NR
Barfield, 201227 2/73 NA—Excluded CD NR NR NR NR NR NR
Eid, 202129 NR NR NR NR NR NR NR NR
Eid, 202130 NR NR NR NR NR NR NR NR
Gersten, 201031 2/24 NA—Excluded CD NR NA NR NR NR NR
Leung, 201932 3/NR 4/NR NR NR NR NR No therapy: 2/7
Mesalamine: 2/7
Anti-TNF + 6-MP: 1/7
Ustekinumab: 1/7		 PPI: 4/7
Elimination diet: 2/7
Swallowed fluticasone: 1/7
Liu, 201633 NR NR NR NR NR NR Specific medications NR but 11/22 patients were managed with anti-TNF, azathioprine, methotrexate, 6-mercaptopurine
 NR
Mansoor, 201934 NA—Excluded UC 539/165 980 NR NR NR NR NR NR
Spencer, 202135 21/25 4/25 NR NR NR NR NR
*11/25 diagnosed with IBD before EOE. Of these, almost 50% on anti-TNF. 11/25 diagnosed with IBD and EOE concurrently		 NR
Sunkesula, 202036 470/962 700
Extrapolated from prevalence of 488/100 000		 579/100 780
Extrapolated from prevalence of 575/100 000		 NR NR NR NR NR NR
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Abbreviations: CD, Crohn’s disease; EoE, eosinophilic esophagitis; IBD, inflammatory bowel disease; n, number; NA, not applicable (based on study design); NR, not reported; UC, ulcerative colitis; y, years.

Most patients with overlapping CD and EoE had ileal or ileocolonic IBD,3,12–14,19,25 with ileocolonic disease involvement ranging from 0% to 87.5%.12,19 Upper gastrointestinal involvement of IBD was generally rare. However, Moore et al. reported that 60% of patients with CD and EoE experienced gastrointestinal involvement of their CD, but only 6.7% of these patients had esophageal IBD.3 Patients with CD and EoE typically had an inflammatory (B1) phenotype, and the prevalence of stricturing and fistulizing complications ranged from 6.7% to 17.8% and 14.3 to 46.2%, respectively, in cohort studies.3,13,14 Only 3 studies reported on the disease location of UC in those with concurrent EoE, with 53.5%-66.7% having pancolitis.13,14,19 A single study by Mintz et al. compared UC disease location in overlapping IBD and EoE to IBD alone and reported no differences between the 2 groups.13

When assessing the clinical features of EoE in patients with IBD, common endoscopic findings included edema, furrows, and exudates. The presence of more advanced disease findings, such as rings and fibrostenotic disease, varied among studies. In particular, Mintz et al. observed that patients diagnosed with IBD prior to EoE developed more esophageal rings (50.0% vs. 23.1%, P = .02) compared to when the EoE diagnosis preceded IBD. There was also a numerical imbalance in the number of patients who developed strictures in patients with IBD diagnosed prior to EoE (15.6%) compared to patients with EoE diagnosed prior to IBD (n = 7.7%), though this was not statistically significant.13 In contrast, Moore et al. and Aloi et al. observed no difference in fibrostenotic EoE between concomitant IBD and EoE compared to IBD alone.3,19 There was heterogeneity in the initial clinical presentation of EoE, with conflicting findings on whether the combined IBD and EoE phenotype presents more frequently with dysphagia compared to patients with EoE alone.13,23,30,33

We also examined the treatment of IBD in patients with combined IBD and EoE, finding that the use of antitumor necrosis factor (anti-TNF) therapy ranged from 14.2% to 82.6%,14,32 with very few patients being treated with other advanced therapies, such as vedolizumab and ustekinumab.19 In evaluating the development of EoE in relation to advanced therapies, Moore et al. performed a case–control study of patients with IBD who developed EoE compared to patients who did not develop EoE.3 The authors observed that anti-TNF was protective against the development of EoE.3 Conversely, Fan et al. found that 71% of patients were started on an anti-TNF before developing EoE.12 Treatment outcomes in the combined IBD and EoE population also varied. Mintz et al. observed no differences in medical or surgical therapy for patients with concomitant IBD and EoE compared to patients with IBD alone.13 In contrast, Limketkai et al. found that concurrent IBD and EoE were associated with a greater composite risk of IBD-related complications, including corticosteroid use, biological therapy, hospitalization, and abdominal surgery.18 In a study by Urquhart et al., roughly one-third of patients with combined IBD and EoE required surgical intervention and/or hospitalization for IBD-related complications.14 In contrast, Talathi et al. observed that IBD alone was associated with a higher risk of hospitalization compared to patients with EoE alone and patients with combined IBD and EoE.19

For the treatment of EoE, most patients were treated with proton pump inhibitors, while other treatment approaches included diet, swallowed topical corticosteroids, and occasionally oral systemic corticosteroids. None of the patients received biologic treatments, such as dupilumab, for their EoE. Endoscopic dilatation of esophageal strictures ranged from 0% to 23.1%.14,19 Concurrent IBD and EoE were associated with a lower risk of food bolus impaction and esophageal stricture dilatation compared to EoE alone.18

Other Immune-Mediated Inflammatory Diseases and EoE

Our search identified only a select number of immune-mediated inflammatory diseases that have been evaluated in relation to EoE. AD was the most frequently studied immune-mediated inflammatory disease, with 9 studies identified (Table 1).37–45 Patient demographics and characteristics can be found in Tables S1 and S2. Meta-analysis was performed on 3 studies that evaluated the incidence of EoE in the AD population compared to the incidence of EoE in the general population. In these 3 studies, the pooled odds of EoE was significantly increased in patients with AD (n = 623/270 107) compared to those without AD (n = 991/531 632) (OR 2.4; 95% CI, 1.9-3.1 3 [I2 = 70.4 %], Figure 4).37,38,40

Figure 4.

Figure 4.

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Comparison of A (Event = Number of patients with concomitant AD and EoE/total AD population) to B (Event = Number of patients with EoE only [no AD]/total general [non-AD] population). AD, atopic dermatitis; EoE, eosinophilic esophagitis.

Discussion

In this study, we demonstrate that a diagnosis of IBD inferred a greater than 3.5-fold increase in the odds of concomitant EoE compared to the general population. Although not directly compared, this observation was greater than the odds of EoE in those with concomitant AD. Taken together, these findings may support shared pathophysiological processes underlying IBD and EoE.

Both IBD and EoE are driven by multifactorial inflammatory signaling pathways, with overlapping features in their pathophysiology.2 Both conditions involve genes related to immune function, epithelial barrier integrity, and cytokine signaling.2 They also share polymorphisms in genes of immune-signaling transcription factors, interleukins, and proteins involved in the mucosal barrier.2 Additionally, immune cells including the TH2 cells, mast cells, and eosinophils are implicated in both diseases.46–51

Given the limited understanding of the relationship between IBD and EoE, we reviewed clinical characteristics including demographics, coexisting immune-mediated inflammatory comorbidities, and disease-specific factors to IBD and EoE. In our meta-analysis, we did not observe a significant association of patients with combined CD and EoE compared to patients with combined UC and EoE. Studies suggest that shared TH2 cytokines in UC and EoE may support an increased risk of EoE in UC compared to CD, which is classically thought to be driven by TH1 and TH17 inflammatory pathways.21 However, recent research indicates that type 2 inflammation may be seen in CD, and therefore, type 2 inflammation may not be disease-specific but rather a distinct state of intestinal inflammation.52 This could explain the conflicting findings observed between UC and CD with EoE, where some studies have instead observed a higher incidence of EoE in CD compared to UC.12,18 In addition, genetic predispositions to EoE and CD, supported by family clustering and twin studies, further highlight an underlying connection.53 Surveillance bias may also increase the likelihood of EoE in CD, given that patients with CD frequently undergo upper endoscopies compared to patients with UC to evaluate for upper gastrointestinal CD involvement.

Due to limited data, we were unable to perform further meta-analyses to determine IBD-related factors that may increase the odds of concomitant EoE, such as IBD phenotype, disease severity, and medication use. Overall, the population commonly consisted of young white males with coexisting atopic conditions, consistent with previous epidemiological studies of the EoE population.54 Limketkai et al. found that while IBD and EoE were independently associated with immune-mediated conditions, concomitant diagnosis of IBD and EoE was linked to a greater risk of TH1-mediated conditions, such as celiac disease and IBD-related rheumatologic disorders, rather than TH2-mediated conditions, such as AD and asthma.18 In contrast, the risk of asthma and AD was greater among patients with EoE without concurrent IBD compared to CD or UC alone, suggesting that EoE may be the driver of TH2-mediated conditions in these cases.18

IBD was more often diagnosed prior to diagnosis of EoE. While surveillance bias may be a factor, studies have found that eosinophils were not significantly present on esophageal biopsies at the time of IBD diagnosis, suggesting that EoE likely develops later.3,12 Alterations in the immune profile caused by IBD or exposure to immunosuppressive therapy have been suggested as potential mechanisms that may explain the disease course in these patients, potentially increasing the risk of developing subsequent EoE.3,13 Indeed, several studies observed that patients with IBD were on anti-TNF therapy prior to EoE diagnosis.12,13,21 However, Moore et al. found that anti-TNF therapy was protective against developing EoE, speculating that it may be effective against eosinophilic intestinal disorders as has been shown in eosinophilic colitis.3 The effectiveness of advanced therapies for IBD in the treatment of EoE was also reported in one case report, whereby a patient with CD started on vedolizumab had endoscopic and histologic resolution of their EoE 6 months after treatment initiation.55 The limited use of newer advanced therapies in this population underscores the need for further research to understand their effects on EoE.

There were mixed findings regarding whether outcomes related to IBD, such as hospitalization, corticosteroid use, and need for surgery, worsened in patients with concomitant IBD and EoE. Urquhart et al. suggested that worsened outcomes could be attributed to heightened eosinophil-driven inflammation in the setting of coexisting EoE.14 There were also conflicting findings on EoE-related outcomes such as food bolus impaction and the need for dilatation. Limketkai et al. proposed that since IBD is frequently treated with systemic corticosteroids, this may simultaneously improve EoE disease activity, thus reducing complications and disease progression.18 In their study, the authors conducted an exploratory analysis that found corticosteroid use was linked to a statistically significant 53% reduction in the risk of food bolus impaction, as well as a nonsignificant decrease in the need for stricture dilatation.18 The group also proposed that better adherence to EoE treatment among IBD patients, who were already familiar with long-term treatment regimens, could contribute to a reduction in EoE-related complications.18

Few studies have examined the relationship between other immune-mediated inflammatory diseases and EoE, with the majority focusing on AD. We excluded celiac disease as recent systematic reviews and meta-analyses have evaluated the association of EoE and celiac disease.5,56 Our meta-analysis demonstrated a positive association between AD and EoE. It has been proposed that EoE is a late manifestation of the allergic marche, which refers to the natural progression of allergic manifestations that develop in infancy and childhood.38 The allergic marche is thought to occur as a consequence of predisposing genetic and environmental factors, and is linked by several pathophysiological processes including a heightened TH2 inflammatory response, production of allergen-specific IgE, and activation of granulocytes.38 One study identified overlapping mRNA expression profiles between EoE, allergic airway disease, and AD, with shared dysregulated genes.57 Notably, IL-13-stimulated epithelial transcripts were more commonly present in EoE compared to AD or allergic airway disease, underscoring differences in the pathophysiological processes of these diseases. IL-13 is pivotal in eosinophil recruitment and esophageal remodeling in EoE, and contributes to abnormal TH2 response in IBD, further supporting the stronger association of IBD with EoE compared to AD.1

Our study has several strengths. We employed a comprehensive literature search, which generated a large repository of potential studies for consideration of the association of IBD and EoE. By including concurrent diseases (apart from celiac disease), we provided a broader understanding of the relationship between IBD, EOE, and other immune-mediated inflammatory conditions. Our study is novel, as to our knowledge, this represents the first systematic review exploring the relationship of IBD and EoE to date. However, there are several limitations to our study. Appreciable heterogeneity was observed across the studies examined, likely due to the small sample sizes and variations in study populations and designs, leading to high I2 values in the meta-analysis conducted here. In particular, we identified 2 studies that may have contributed to the heterogeneity to some degree; however, their exclusion did not meaningfully change the I2 values (Figure S1).11,36 One of these studies demonstrated that EoE was significantly less common in IBD, attributing their discordant findings related to the makeup of the control arms across these studies, such as having a mixed adult and pediatric population.11 The second study was published in abstract format, and therefore, it is difficult to describe the differences in their findings.36 Findings from our meta-analyses are also likely subject to publication bias, as studies with significant results are more likely to be published compared to negative ones. As less than 10 studies were included in the meta-analysis, we were unable to assess the potential impact of publication bias using a funnel plot.58 In addition, there is a potential for misclassification bias of EoE, as eosinophils can be present in the esophagus in other conditions than EoE. This includes IBD, where they have been associated with a more severe clinical course.2 We also could not determine the true pooled incidence of EoE in IBD versus EoE or perform meta-analysis on other characteristics due to unreported or examined data. This highlights critical gaps in the literature and underscores the need for further research and standardization of study designs, particularly regarding assessing the effectiveness of therapies for IBD and EoE in co-diagnosed patients compared to patients with IBD or EoE alone.

In conclusion, this study demonstrated that IBD is significantly associated with EoE and that this relationship appears to be independent of IBD subtype (CD vs. UC). This relationship was also found to be greater than the association between AD and EoE. Further research is necessary to better understand the relationship of IBD and EoE, whether there are differences in their natural history and outcomes, and the pathophysiological mechanisms that may connect these two conditions. Until then, the treating clinician should explore upper gastrointestinal symptoms in patients with IBD and have a low threshold to consider performing endoscopic evaluation and esophageal biopsies, particularly in individuals with high-risk features.

Supplementary data

Supplementary data is available at Inflammatory Bowel Diseases online.

izaf095_Supplementary_Appendix_I
izaf095_supplementary_appendix_i.docx (50.1KB, docx)
izaf095_Supplementary_Appendix_II
izaf095_supplementary_appendix_ii.docx (196.4KB, docx)
izaf095_Supplementary_Figures_1
izaf095_supplementary_figures_1.docx (289.2KB, docx)
izaf095_Supplementary_Tables_1-2
izaf095_supplementary_tables_1-2.docx (41.8KB, docx)

Contributor Information

Russell Yanofsky, Division of Gastroenterology and Hepatology, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Rohit Jogendran, Department of Internal Medicine, University of Toronto, Toronto, Ontario, Canada.

Tedi Hoxha, Department of Internal Medicine, University of Toronto, Toronto, Ontario, Canada.

Avani Pathak, College of Osteopathic Medicine, Michigan State University, East Lansing, MI, USA; Library and Information Services, University Health Network, Toronto, Ontario, Canada.

Ani Orchanian-Cheff, Department of Internal Medicine, University of Toronto, Toronto, Ontario, Canada.

Tarun Chhibba, Division of Gastroenterology and Hepatology, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada.

Alexa N Sasson, Division of Gastroenterology and Hepatology, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Parul Tandon, Division of Gastroenterology and Hepatology, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Author Contributions

Concept for manuscript: R.Y., P.T. Search strategy development and literature search: A.O.C. Study inclusion and retrieval: R.Y., R.J., T.H., A.P., P.T. Quality analysis: R.Y., R.J., T.H., A.P. Draft of .anuscript: RY. Revisions and final edits: R.Y., R.J., T.H., A.P., T.C., A.S., P.T.

Funding

None declared.

Conflict of Interest

R.Y., R.J., T.H., A.P., A.O.C., T.C., A.S., and P.T.: None.

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Associated Data

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Supplementary Materials

izaf095_Supplementary_Appendix_I
izaf095_supplementary_appendix_i.docx (50.1KB, docx)
izaf095_Supplementary_Appendix_II
izaf095_supplementary_appendix_ii.docx (196.4KB, docx)
izaf095_Supplementary_Figures_1
izaf095_supplementary_figures_1.docx (289.2KB, docx)
izaf095_Supplementary_Tables_1-2
izaf095_supplementary_tables_1-2.docx (41.8KB, docx)

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