No H. pylori, no adenocarcinoma for patients with autoimmune gastritis.
No H. pylori, no adenocarcinoma for patients with autoimmune gastritis.
复制标题
没有H pylori，自身免疫性胃炎患者无腺癌。
DOI：
10.1136/gutjnl-2022-328068
复制
发表时间：
2023-01
期刊：
影响因子：
24.5
通讯作者：
Goldenring, James
中科院分区：
文献类型：
--
作者：
Goldenring, James
Previous studies have noted that atrophic gastritis is the pathological finding most correlated with the development of gastric adenocarcinoma. 1 Worldwide, the most common cause of atrophic gastritis is chronic infection with Helicobacter pylori. This general loss of acid-secreting parietal cells is associated with the development in the corpus of metaplastic lineages including pyloric metaplasia (also known as spasmolytic polypeptide-expressing metaplasia (SPEM) or pseudopyloric metaplasia) and intestinal metaplasia as direct sequelae of atrophy. The intestinal metaplasia lineages can develop in both the corpus and the antrum. In contrast with H. pylori infection, direct destruction of parietal cells through the production of anti-parietal cell antibodies (most prominently antibodies against the H/K-ATPase) in patients with autoimmune gastritis induces profound atrophy in the corpus, sparing the antrum. While it has been known that autoimmune gastritis is associated with a higher incidence of enterochromaffin-like (ECL) cell carcinoids in the stomach, 2 the risk of adenocarcinoma has been controversial. 3–5 Many studies have failed to discriminate between cancer arising from H. pylori infection and that emanating from the primary results of autoimmune gastritis. This has led to confusion in how these patients should be followed up with endoscopy, especially in younger patients. In Gut, Massimo Rugge and colleagues present the results of an important study which clarifies the relationship of autoimmune gastritis with gastric adenocarcinoma versus carcinoid. 6 This study, which followed up prospectively 211 patients with autoimmune gastritis, but without H. pylori infection, definitively demonstrates that autoimmune gastritis, on its own, is not a significant precursor for gastric adenocarcinoma. Rather, as reported previously, Rugge et al demonstrate that autoimmune gastritis leads to an increased incidence of ECL cell carcinoids in the stomach. These studies provide the most definitive data to date that, in the absence of H. pylori infection, the risk of adenocarcinoma is not significant for patients with autoimmune gastritis. If atrophic gastritis with extensive loss of parietal cells is considered as precarcinogenic, why do patients with H. pylori-negative autoimmune gastritis fail to demonstrate increases in adenocarcinoma? The answers may lie in the precancerous milieu and its influence on gastric lineages. The present investigation reports that pyloric or pseudopyloric metaplasia was far more commonly observed in patients with autoimmune gastritis than intestinal metaplasia. This finding is supported by previous investigations. 7 8 Since pyloric metaplasia/SPEM is considered a direct response to significant gastric mucosal injury, 9 these lineages would be considered predominantly reparative. Increasing evidence suggests that pyloric metaplasia gives rise to intestinal metaplasia in the corpus of the stomach (figure 1). Glands with intestinal metaplasia can be further subclassified as either incomplete intestinal metaplasia (containing both intestinal lineages and SPEM lineages) or complete intestinal metaplasia (containing absorptive and Paneth cell lineages). Incomplete intestinal metaplasia is considered the lesion with the highest risk of progression to adenocarcinoma. 10 The present study does not report whether the intestinal metaplasia observed in patients with autoimmune gastritis was complete or incomplete intestinal metaplasia. Nevertheless, a previous study of 20 hours of patients with H. pylori-negative autoimmune thyroiditis/gastritis found only complete intestinal metaplasia in these patients, compared with patients with gastric adenocarcinoma …
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DOI：
10.14309/ajg.0000000000001622
发表时间：
2022-03-01
期刊：
The American journal of gastroenterology
影响因子：
--
作者：
Song M;Camargo MC;Derkach A;Rabkin CS;Engels EA
通讯作者：
Engels EA
DOI：
10.1007/s00428-021-03033-5
发表时间：
2021-07
期刊：
Virchows Archiv : an international journal of pathology
影响因子：
--
作者：
Wada Y;Nakajima S;Kushima R;Takemura S;Mori N;Hasegawa H;Nakayama T;Mukaisho KI;Yoshida A;Umano S;Yamamoto K;Sugihara H;Murakami K
通讯作者：
Murakami K
影响因子：
29.4
作者：
Petersen, Christine P.;Weis, Victoria G.;Goldenring, James R.
通讯作者：
Goldenring, James R.
影响因子：
29.4
作者：
BORCH, K;RENVALL, H;LIEDBERG, G
通讯作者：
LIEDBERG, G
影响因子：
29.4
作者：
Shah SC;Piazuelo MB;Kuipers EJ;Li D
通讯作者：
Li D