Eosinophil Counts in Upper Digestive Mucosa of Western European Children: Variations With Age, Organs, Symptoms, <i>Helicobacter pylori</i> Status, and Pathological Findings

Kalach, Nicolas; Huvenne, H; Gosset, Pierre; Papadopoulos, Stephanos; Dehecq, E.; Decoster, A.; Creusy, Colette; Dupont, Christophe

doi:10.1097/mpg.0b013e3181e2ae00

Cited by 36 publications

(32 citation statements)

References 29 publications

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“…This study, too, was limited by small numbers, with only 8 patients with eosinophil counts ≥ 15 eos/hpf. 33 To our knowledge, there have been no prior investigations that also examined esophageal eosinophilia in relation to the manifestation of H. pylori in the stomach.…”

Section: Discussionmentioning

confidence: 99%

Inverse Association of Esophageal Eosinophilia With Helicobacter pylori Based on Analysis of a US Pathology Database

et al. 2011

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Background & Aims Eosinophilic esophagitis (EoE) is of increasing prevalence and thought to result from allergic processes. Helicobacter pylori has been inversely associated with allergic diseases, but there is no known relationship between H. pylori, EoE and esophageal eosinophilia. We investigated the association between esophageal eosinophilia and H. pylori infection. Methods We performed a cross-sectional study of data, collected from a United States pathology database, on 165,017 patients in the US who received esophageal and gastric biopsies from 2008 and 2010. Patients with and without H. pylori on gastric biopsy were compared and odds of esophageal eosinophilia were determined. Results From the data analyzed, 56,301 (34.1%) had normal esophageal biopsies, 5,767 (3.5%) had esophageal eosinophilia, and 11,170 (4.8%) had H. pylori infection. Esophageal eosinophilia was inversely associated with H. pylori (odds ration [OR]: 0.77, 95% confidence interval [CI]: 0.69–0.87). Compared to patients with normal esophageal biopsies, odds of H. pylori were reduced among patients with ≥15 eosinophils per high-power field (eos/hpf) (OR 0.79; 95% CI 0.70–0.88), ≥45 eos/hpf (OR 0.75; 0.61–0.93), ≥75 eos/hpf (OR 0.72; 0.62–0.83), and ≥90 eos/hpf (OR 0.52; 0.31–0.87) (p for trend <0.001). A similar dose-response trend was observed for increasing clinical suspicion for EoE and decreasing prevalence of H pylori. Additionally, severity of histologic effects of H. pylori was inversely associated with esophageal eosinophilia. All trends held in multivariate analysis. Conclusions In a large cross-sectional analysis, H. pylori infection was inversely associated with esophageal eosinophilia. This relationship could have implications for the pathogenesis and epidemiology of EoE.

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Section: Discussionmentioning

confidence: 99%

Inverse Association of Esophageal Eosinophilia With Helicobacter pylori Based on Analysis of a US Pathology Database

et al. 2011

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“…18 Recently, early environmental exposures, such as antibiotic exposure in the first year of life, 19 have been implicated. Indeed, birth season, climate, seasonality 20–24 and Helicobacter pylori exposure 25,26 modify disease susceptibility. Further, epigenetic regulation 27,28 may play a role in altered expression 29–31 associated with EoE.…”

Section: Introductionmentioning

confidence: 99%

Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis

Alexander

Martin

Collins

et al. 2014

Journal of Allergy and Clinical Immunology

236

183

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Background Eosinophilic esophagitis (EoE) is a chronic antigen-driven allergic inflammatory disease, likely involving the interplay of genetic and environmental factors, yet their respective contributions to heritability are unknown. Objective To quantify risk associated with genes and environment on familial clustering of EoE. Methods Family history was obtained from a hospital-based cohort of 914 EoE probands, (n=2192 first-degree “Nuclear-Family” relatives) and the new international registry of monozygotic and dizygotic twins/triplets (n=63 EoE “Twins” probands). Frequencies, recurrence risk ratios (RRRs), heritability and twin concordance were estimated. Environmental exposures were preliminarily examined. Results Analysis of the Nuclear-Family–based cohort revealed that the rate of EoE, in first-degree relatives of a proband, was 1.8% (unadjusted) and 2.3% (sex-adjusted). RRRs ranged from 10–64, depending on the family relationship, and were higher in brothers (64.0; p=0.04), fathers (42.9; p=0.004) and males (50.7; p<0.001) compared to sisters, mothers and females, respectively. Risk of EoE for other siblings was 2.4%. In the Nuclear-Families, combined gene and common environment heritability (hgc2) was 72.0±2.7% (p<0.001). In the Twins cohort, genetic heritability was 14.5±4.0% (p<0.001), and common family environment contributed 81.0±4% (p<0.001) to phenotypic variance. Proband-wise concordance in MZ co-twins was 57.9±9.5% compared to 36.4±9.3% in DZ (p=0.11). Greater birth-weight difference between twins (p=0.01), breastfeeding (p=0.15) and Fall birth season (p=0.02) were associated with twin discordance in disease status. Conclusions EoE recurrence risk ratios are increased 10–64-fold compared with the general population. EoE in relatives is 1.8–2.4%, depending upon relationship and sex. Nuclear-Family heritability appeared to be high (72.0%). However, Twins cohort analysis revealed a powerful role for common environment (81.0%) compared with additive genetic heritability (14.5%).

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“…Previous studies show that an H. pylori infection results in significantly higher tissue inflammatory cell densities, including lymphocytes, plasma cells, neutrophils, mast cells, and eosinophils. [52][53][54][55] Likewise, in the present study, eosinophil counts of the gastric antrum and body were significantly high in the order of the H. pylori infection group, AP-FGID group, and normal controls; however, duodenal eosinophil counts were not significantly different. Although the difference between mean duodenal eosinophil counts in patients with AP-FGID and that of normal controls was not statistically significant, it might be notable that duodenal eosinophil counts in AP-FGID patients in our study were still more than 10 cells/HPF in most cases, and duodenal eosinophilia have previous been defined as > 10 cells/HPF for children.…”

Section: Discussionmentioning

confidence: 74%

Analysis of Gastric and Duodenal Eosinophils in Children with Abdominal Pain Related Functional Gastrointestinal Disorders According to Rome III Criteria

Lee

Yang

Lee

2016

J Neurogastroenterol Motil

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Background/AimsAbdominal pain-related functional gastrointestinal disorder (AP-FGID) is common in children and adults. However, the mechanism of AP-FGID is not clearly known. Recently, micro-inflammation, especially eosinophilia in the gastrointestinal tract, was suggested in the pathophysiology of AP-FGID in adults. The aim of this study was to evaluate the association of gastric and duodenal eosinophilia with pediatric AP-FGID. MethodsIn total, 105 pediatric patients with AP-FGID were recruited and classified into 4 subgroups based on the Rome III criteria. Eosinophil counts in the gastric and duodenal tissues of children with AP-FGID were compared to those from normal pathology references or those of children with Helicobacter pylori infection. Tissue eosinophil counts were also compared among the 4 subtypes of AP-FGID. ResultsEosinophil counts in the gastric antrum and body were significantly higher in children with AP-FGID than normal reference values. Duodenal eosinophil counts were higher in children with AP-FGID, but not significantly when compared with normal reference values. There were no significant differences in eosinophil counts of the stomach or duodenum among the 4 subtypes of AP-FGID. Eosinophils counts in the gastric antrum and body were significantly higher in children with H. pylori infection than in those with AP-FGID. Duodenal eosinophilia was prominent in cases of H. pylori infection, but not statistically significant when compared with AP-FGID. ConclusionsOur study revealed that gastric eosinophilia is associated with AP-FGID in children, regardless of the subtype of functional abdominal pain. This suggests some contribution of gastrointestinal eosinophils in the development of pediatric AP-FGID.

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Eosinophil Counts in Upper Digestive Mucosa of Western European Children: Variations With Age, Organs, Symptoms, Helicobacter pylori Status, and Pathological Findings

Cited by 36 publications

References 29 publications

Inverse Association of Esophageal Eosinophilia With Helicobacter pylori Based on Analysis of a US Pathology Database

Inverse Association of Esophageal Eosinophilia With Helicobacter pylori Based on Analysis of a US Pathology Database

Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis

Analysis of Gastric and Duodenal Eosinophils in Children with Abdominal Pain Related Functional Gastrointestinal Disorders According to Rome III Criteria

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