Division of Gastroenterology, National Center for Child Health and Development, Tokyo, Japan; Department of Pediatrics, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Department of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, Japan; Division of Allergy, National Center for Child Health and Development, Tokyo, Japan.
J Allergy Clin Immunol Pract. 2017 Nov-Dec;5(6):1639-1649.e2. doi: 10.1016/j.jaip.2017.03.030. Epub 2017 May 16.
Eosinophilic gastritis (EG) is clinicopathologically characterized by both marked gastric eosinophilia and clinical symptoms. The endoscopic findings in EG vary among patients, leading to clinical confusion. However, little is known about the relationship between precise endoscopic findings and the pathophysiological process responsible for EG.
We aimed to elucidate whether the gross endoscopic findings of EG can be classified into distinct gene expression profiles.
We enrolled pediatric patients who underwent gastrointestinal endoscopy for clinical symptoms suggestive of eosinophilic gastrointestinal disorder between 2011 and 2016. EG was diagnosed when gastric eosinophilia was greater than or equal to 30 eosinophils/hpf. The gene expression profiles of gastric biopsies were assessed using microarray technology.
Patients with EG and control subjects (n = 8, each) were examined. On the microarray, 1,999 genes were differentially expressed between EG and the controls (≥2-fold difference, adjusted P value < .05), including significant upregulation of eotaxin-3 (C-C chemokine ligand 26). The endoscopic findings of patients with EG fell roughly into 2 types, namely, ulcerative and nodular lesions. Despite identifying distinct patterns of gene expression, most differentially regulated genes overlapped between the 2 endoscopic finding types. Several gene ontology terms were enriched in the substantially overlapped genes, but not in each of the distinct genes.
Our results strongly indicate that ulcerative and nodular lesions are a single disease, EG, or a variation thereof, in spite of morphological differences. Our findings may contribute to a better understanding of the pathogenesis of EG, as well as to more accurate diagnosis of this disease.
嗜酸性粒细胞性胃炎（EG）的临床病理特征为胃嗜酸性粒细胞明显增多和临床症状。EG 的内镜表现因患者而异，导致临床混淆。然而，对于 EG 确切的内镜表现与导致 EG 的病理生理过程之间的关系知之甚少。
我们旨在阐明 EG 的大体内镜表现是否可以分为不同的基因表达谱。
我们招募了 2011 年至 2016 年间因疑似嗜酸细胞性胃肠道疾病而行胃肠内镜检查的儿科患者。当胃嗜酸性粒细胞计数大于或等于 30 个/高倍视野时诊断为 EG。使用微阵列技术评估胃活检的基因表达谱。
检查了 8 例 EG 患者和 8 例对照者。在微阵列上，EG 与对照组之间有 1999 个基因表达差异（差异倍数≥2，调整 P 值<0.05），包括 eotaxin-3（C-C 趋化因子配体 26）的显著上调。EG 患者的内镜表现大致可分为溃疡和结节病变两种类型。尽管存在明显的基因表达模式，但在这两种内镜表现类型之间，大多数差异调节基因存在重叠。在大量重叠基因中富集了几个基因本体论术语，但不在每个独特基因中富集。
我们的结果强烈表明，溃疡和结节病变是一种单一的疾病，即 EG，或其变异，尽管存在形态学差异。我们的发现可能有助于更好地理解 EG 的发病机制，并更准确地诊断这种疾病。
