Departments of Pediatrics, Medical College, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Departments of Pathology, Medical College, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Helicobacter. 2022 Jun;27(3):e12885. doi: 10.1111/hel.12885. Epub 2022 Mar 20.
Helicobacter pylori infection is the leading cause of peptic ulcer and chronic gastritis and may initiate gastric carcinogenesis following the Correa cascade. Another lineage of metaplasia, spasmolytic peptide-expressing metaplasia (SPEM) has recently been found to be an alternative precursor to gastric cancer. To date, few reports have investigated gastric precancerous lesions among children with H. pylori infection. This study aimed to evaluate the histopathological pattern of H. pylori atrophic gastritis in children and the extent of precancerous lesions.
This study enrolled pediatric patients with H. pylori infection from 1998 to 2019. During esophagogastroduodenoscopy examinations, biopsy fragments were collected from the gastric antrum and corpus for rapid urease test, culture, and histology evaluation. The presence and degree of chronic inflammation, activity of gastritis, H. pylori density, atrophy, and intestinal metaplasia (IM) were assessed according to the modified Updated Sydney System. Trefoil factor 2 (TFF2) immunohistochemistry was also performed to assess SPEM in the gastric tissues collected from each case using rabbit anti-human TFF2 antibodies.
A total of 92 children with H. pylori infection and adequate gastric mucosa biopsies were enrolled. Esophagogastroduodenoscopy showed that 39 (42.4%) had duodenal ulcers, 11 (12.0%) had gastric ulcers, 41 (44.6%) had gastritis, and 1 (1.1%) had negative findings. Mild-to-moderate IM was identified in 4 patients (4.3%). SPEM was found in 8 patients (8.7%) with a significantly higher incidence among female patients (15.8% vs. 8.7%, p = .031). Gastric glandular atrophy presented in 28 patients (30.4%), and high-grade atrophy was more common in female patients (3.2% vs. 1.9%, p = .031).
The prevalence rates of atrophic gastritis in the children with H. pylori infection were 30.4% for gastric glandular atrophy, 4.3% for IM and 8.7% for SPEM. SPEM and high-grade atrophy were more common in female patients.
幽门螺杆菌感染是消化性溃疡和慢性胃炎的主要病因,并且可能会在 Correa 级联反应之后引发胃癌。最近发现另一种化生谱系——舒血管肠肽表达化生(SPEM)是胃癌的另一种前体。迄今为止,很少有研究报道儿童幽门螺杆菌感染者的胃癌前病变。本研究旨在评估儿童幽门螺杆菌萎缩性胃炎的组织病理学模式和癌前病变的程度。
本研究纳入了 1998 年至 2019 年期间患有幽门螺杆菌感染的儿科患者。在食管胃十二指肠镜检查期间,从胃窦和胃体采集活检标本进行快速尿素酶试验、培养和组织学评估。根据改良的悉尼系统评估慢性炎症、胃炎活动度、幽门螺杆菌密度、萎缩和肠化生(IM)的存在和程度。还使用兔抗人 TFF2 抗体对从每个病例中收集的胃组织进行三叶因子 2(TFF2)免疫组织化学染色,以评估 SPEM。
共纳入 92 例患有幽门螺杆菌感染且胃黏膜活检充足的儿童。食管胃十二指肠镜检查显示 39 例(42.4%)有十二指肠溃疡,11 例(12.0%)有胃溃疡,41 例(44.6%)有胃炎,1 例(1.1%)无异常发现。4 例(4.3%)存在轻度至中度 IM。8 例(8.7%)发现 SPEM,女性患者的发生率明显更高(15.8%比 8.7%,p=0.031)。28 例(30.4%)存在胃腺萎缩,高等级萎缩在女性中更常见(3.2%比 1.9%,p=0.031)。
幽门螺杆菌感染儿童的萎缩性胃炎发生率分别为胃腺萎缩 30.4%、IM 4.3%和 SPEM 8.7%。SPEM 和高等级萎缩在女性中更为常见。