Eosinophilic esophagitis (EoE) is a chronic immune-mediated condition marked by eosinophilic infiltration of the esophageal mucosa and symptoms of esophageal dysfunction. 1 EoE diagnosis is confirmed by identifying 15 or more intraepithelial eosinophils per high-power field in esophageal mucosal biopsies in a symptomatic patient. 1 The incidence and prevalence of EoE have increased 1; which may be attributed to an increased awareness of the condition, and potentially an increase in environmental factors interacting with genetic and epigenetic changes. 1, 2 Previously identified environmental factors linked to an increased risk of developing EoE are early antibiotic use, early acid suppressant use, cesarean delivery, living in cold or arid regions, and/or lack of Helicobacter pylori (H. pylori) exposure. 3, 4 EoE is known to predominantly affect those in industrialized nations and of higher socioeconomic status. 5 No studies have examined the environmental and socioeconomic risk factors associated with EoE in the diverse pediatric population in South Florida. Therefore, this study aims to address this gap and identify environmental and socioeconomic risk factors linked to pediatric EoE among a predominantly Non-Mexican Hispanic cohort. This study was approved by the Institutional Review Board (IRB) of Nicklaus Children's Hospital (NCH) in Miami, Florida (IRB approval number: 20235540). A case-control study based on a survey was conducted at a single tertiary care center in South Florida: NCH in Miami, Florida. A retrospective chart review was first performed to identify eligible case and control subjects. Cases were defined as patients under the age of 21 who presented with any esophageal dysfunction, growth faltering, or abdominal pain and met diagnostic criteria for EoE confirmed by histologic findings of 15 eosinophils or more per high-power field in esophageal mucosal biopsies. 1 Controls were defined as patients under the age of 21 who were evaluated for a history of abdominal pain and/or failure to thrive with normal esophageal histologic findings from an upper endoscopy. Once identified, participants who agreed to join the study provided consent and completed a 64-question anonymous Research Electronic Data Capture (REDcap) survey, based on environmental factors previously linked to EoE 3, 4 and general socioeconomic factors. Thus, case/control selection was based on chart review, while survey responses provided the exposure data analyzed. Data collection was conducted from January 15, 2024 to December 10, 2024. The study data was summarized using descriptive statistics. Proportions and chi-square tests were applied to analyze categorical variables. Student's t tests were employed to compare continuous variables. To compare exposure rates between case and control groups, odds ratios (OR) with 95% confidence intervals (CIs) were calculated. Univariate and multivariable logistic regression models were developed to adjust for potential confounders, first adjusting for age, sex, and race, then adjusting for parental education separately. Statistical significance was determined with a p-value < 0. 05. All statistical analyses were conducted using Microsoft Excel and IBM SPSS version 29. 0. 2. 0 (20) software. Out of 300 contacted individuals, 220 were reached, and 196 (89%) completed the survey (97 cases and 99 controls). The mean age for EoE cases and controls was 11. 2 and 10. 4 years, respectively. Notably, a very high proportion of participants identified as Hispanic (Cases: 76. 3%, controls: 87. 9%), while most also identified as White (Cases: 83. 3%, controls: 89. 9%). Male predominance was noted among EoE cases (Cases: 81. 4%, controls: 50. 5%), consistent with existing literature. Atopic comorbidities were more frequent in EoE cases, especially food allergies (69. 1%, p < 0. 0001). The majority reported a home address within South Florida (Cases: 98%, controls: 99%). See Supporting Information: Table 1. Significant negative associations were observed for the following factors: public insurance versus private insurance (OR 0. 372; 95% CI 0. 197–0. 707), household annual income below 70, 000 (OR 0. 479; 95% CI 0. 239–0. 956), parental education at or below high school (Mothers: OR 0. 198; 95% CI 0. 102–0. 386; fathers: OR 0. 498; 95% CI 0. 276–0. 899), and history of H. pylori infection (OR 0. 159; 95% CI 0. 053–0. 485). After adjusting for age, gender, and race, these associations remained statistically significant except for household income below 70, 000, which became non-significant (aOR 0. 531; 95% CI 0. 246–1. 145). When parental education was included as a separate adjustment, the association between public versus private insurance also lost statistical significance (aOR 0. 667; 95% CI 0. 326–1. 367). A single significant positive association with EoE was initially observed for a history of cow's milk protein allergy (CMPA) (OR 1. 906; 95% CI 1. 036–3. 508) ; however, this association lost significance after adjustment for age, gender, and race (aOR 1. 702; 95% CI 0. 858–3. 377) and for parental education (aOR 1. 878, 95% CI 0. 946–3. 728). Of all the environmental and socioeconomic factors studied, only two negative associations remained statistically significant after full adjustment: history of H. pylori infection (adjusted for age, sex, and race: aOR 0. 154, 95% CI 0. 048–0. 49; and separately for parental education: aOR 0. 177, 95% CI 0. 055–0. 565) and parental education at or below high school (Mothers: aOR 0. 19, 95% CI 0. 092–0. 393; fathers: aOR 0. 43, 95% CI 0. 23–0. 829, adjusted for age, sex, and race only). Several other perinatal, infancy, infectious, and household factors were evaluated and presented in Table 1 and Figure 1. Prior epidemiologic studies investigating environmental and socioeconomic factors associated with EoE have included limited representation of Hispanic children. This underrepresentation may stem from the geographic locations of previous studies, which lacked substantial Hispanic populations. To address this gap, our study evaluated environmental and socioeconomic factors linked to pediatric EoE among patients residing in South Florida—a region with the largest Latino/Hispanic population in the state. 6 The demographic profile of South Florida was reflected in our cohort (Supporting Information: Table S1). As expected, male subjects predominated among EoE cases. Additionally, we observed a significant prevalence of atopic comorbidities in these cases, potentially related to the shared Th2-mediated pathogenic pathway—commonly referred to as the “atopic march”—between EoE and other atopic conditions. 7 After adjusting for confounders, our study identified two significant negative associations with the development of EoE: low parental education and a history of H. pylori infection. Our findings suggest that socioeconomic factors may influence the prevalence of EoE among Hispanic children in South Florida. Consistent with Lanz et al. , who reported higher EoE prevalence in the highest median income Miami-Dade zip codes, our findings indicate greater diagnoses among higher socioeconomic groups. 8 One possible explanation is underdiagnosis in disadvantaged populations, potentially related to reduced access to comprehensive evaluation. In such settings, families may delay seeking care until symptoms become more severe and disruptive. 9 Supporting this, Mehta et al. reported that EoE patients from socioeconomically disadvantaged backgrounds were less likely to undergo radiologic evaluations, suggesting disparities in access to care. However, other factors may also contribute, including physician referral patterns, dietary differences, or variations in environmental exposures. The factors behind socioeconomic discrepancies in EoE remain unclear and require additional investigation. Our study also supports a significant inverse relationship between H. pylori infection and EoE prevalence. This association may be attributed to the immunomodulatory effects of H. pylori, which could confer protection against allergic conditions such as EoE. 10 A Mendelian randomization study by Zhu et al. further supported this finding, identifying anti-H. pylori IgG antibodies as a key factor associated with reduced EoE risk. 11 Additionally, H. pylori infection may alter the upper gastrointestinal microbiome, potentially influencing esophageal susceptibility to EoE. 10 Limitations of this study include its single-center design and modest sample size, which limit generalizability. The use of surveys introduces potential recall bias, particularly for early-life exposures such as antibiotic use or CMPA. Some participants declined to answer certain questions, resulting in missing data that may bias the strength of reported associations. Strengths of the study include the use of esophageal biopsy results for both case and control groups, enhancing diagnostic accuracy. Additionally, the cohort was matched for age and race, minimizing confounding from these variables. Notably, this study includes a large pediatric Hispanic cohort, a population that has been underrepresented in prior EoE research. In this study, where 82% of participants identified as Hispanic, EoE remained more prevalent among individuals identifying as White, male, and having food allergies—consistent with previous epidemiologic findings. Our results also suggest potential associations between socioeconomic status, infections such as H. pylori, and EoE development. After adjusting for confounders, only two associations remained statistically significant: a negative association between EoE and H. pylori infection, and between EoE and parental education level at or below high school. While these findings contribute to the growing evidence on environmental and socioeconomic influences in pediatric EoE—particularly within the Hispanic community—they should be interpreted with caution due to the limited number of significant associations. Future multi-center studies with larger cohorts and prospective designs in South Florida are needed to validate these results. Additionally, further research should explore the interplay between genetics, microbiome, physician referral practices, dietary patterns, and environmental exposures in the development of pediatric EoE. The authors declare no conflict of interest. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
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Elizabeth Torres Claudio
Christian Martinez
Natalie Flexman Jennings
Journal of Pediatric Gastroenterology and Nutrition
Miami Children's Hospital
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Claudio et al. (Tue,) studied this question.
www.synapsesocial.com/papers/69a75a9ec6e9836116a20aed — DOI: https://doi.org/10.1002/jpn3.70356
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