AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review.
AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review.
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美国胃肠病协会（AGA）关于萎缩性胃炎诊断与管理的临床实践更新：专家综述
DOI：
10.1053/j.gastro.2021.06.078
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发表时间：
2021-10
期刊：
影响因子：
29.4
通讯作者：
Li D
中科院分区：
文献类型：
--
作者：
Shah SC;Piazuelo MB;Kuipers EJ;Li D
本临床实践更新专家评审的目的是为临床医生提供萎缩性胃炎的诊断和治疗指导，萎缩性胃炎是一种常见的胃肿瘤前病症，主要关注慢性幽门螺杆菌感染（最常见的病因）或自身免疫引起的萎缩性胃炎。迄今为止，在美国，与萎缩性胃炎的诊断和治疗相关的最佳实践的临床指导仍然非常有限，这导致人们对这种癌前病症的认识较差，风险分层也不够理想。此外，文献中对萎缩性胃炎、自身免疫性胃炎、恶性贫血、胃肿瘤的定义存在异质性，导致临床实践和研究中的混乱。因此，本临床实践更新的主要目标是为临床医生提供萎缩性胃炎的诊断和治疗框架。通过关注萎缩性胃炎，本临床实践更新旨在补充 2020 年美国胃肠病学协会研究所关于胃肠化生管理的指南。这些最近的指南没有具体讨论萎缩性胃炎的诊断和治疗。然而，提供者应该认识到，胃组织病理学上肠化生的诊断意味着萎缩性胃炎的诊断，因为肠化生发生在下面的萎缩粘膜中，尽管组织病理学报告中通常没有明确指出这一点。然而，萎缩性胃炎代表了胃癌发病机制多步级联中具有明显组织病理学改变的重要阶段。本文提出的最佳实践建议声明是根据已发表文献的现有证据和基于共识的专家意见结合而成的。没有对证据的强度或质量进行正式评级。这些声明旨在为在美国执业的临床医生提供实用建议。萎缩性胃炎被定义为在主要由幽门螺杆菌感染或自身免疫引起的慢性炎症的情况下，胃腺体丧失，伴或不伴化生。无论病因如何，萎缩性胃炎的诊断均应通过组织病理学确诊。提供者应该意识到，胃组织学上肠化生的存在几乎总是意味着萎缩性胃炎的诊断。胃肠病学家和病理学家之间应协调努力，以提高记录萎缩性胃炎的范围和严重程度的一致性，特别是在存在明显萎缩的情况下。提供者应认识到萎缩性胃炎的典型内镜特征，包括胃粘膜苍白、由于胃粘膜变薄而导致脉管系统可见度增加、胃皱襞消失，以及如果伴有肠化生，则出现浅蓝色嵴和白色不透明区域。由于这些粘膜变化通常很微妙，因此应采用优化胃粘膜评估的技术。当出现萎缩性胃炎的内镜特征时，提供者应通过内镜评估其程度。提供者应从疑似萎缩/化生区域获取活检，以进行组织病理学确认和风险分层；至少应从身体和窦/切迹获取活组织检查并将其放置在单独标记的罐子中。另外还应从任何其他粘膜异常中获取有针对性的活检。对于组织学符合自身免疫性胃炎的患者，提供者应考虑检查抗壁细胞抗体和抗内在因子抗体以协助诊断。提供者还应评估是否因维生素 B-12 和铁缺乏而导致贫血。所有萎缩性胃炎患者均应接受幽门螺杆菌感染评估。如果呈阳性，应进行幽门螺杆菌治疗，并使用非血清学检测方式确认成功根除。萎缩性胃炎患者的最佳内镜监测间隔尚无明确定义，应根据个体风险评估和共同决策来决定。对于患有晚期萎缩性胃炎的个体，应考虑每 3 年进行一次内窥镜监测，根据解剖范围和组织学分级进行定义。自身免疫性胃炎患者的最佳监测间隔尚不清楚。应根据个体化评估和共同决策来考虑间隔内镜监测。医疗服务提供者应认识到恶性贫血是自身免疫性胃炎的晚期表现，其特点是维生素 B-12 缺乏和大细胞性贫血。新诊断为恶性贫血且近期未接受内镜检查的患者应接受内镜检查和局部活检，以确认胃体为主的萎缩性胃炎，进行风险分层，并排除常见的胃肿瘤，包括神经内分泌肿瘤。患有自身免疫性胃炎的个体应通过上消化道内镜检查筛查 1 型胃神经内分泌肿瘤。小的神经内分泌肿瘤应通过内镜切除，然后每 1-2 年进行一次内窥镜监测，具体取决于神经内分泌肿瘤的负担。提供者应评估萎缩性胃炎患者的铁和维生素 B-12 缺乏情况，无论病因如何，尤其是胃体为主的情况。同样，对于不明原因的铁或维生素 B-12 缺乏的患者，在鉴别诊断和适当的诊断评估中应考虑萎缩性胃炎。在患有自身免疫性胃炎的患者中，提供者应该认识到伴随的自身免疫性疾病，特别是自身免疫性甲状腺疾病，是常见的。应进行自身免疫性甲状腺疾病筛查。
The purpose of this Clinical Practice Update Expert Review is to provide clinicians with guidance on the diagnosis and management of atrophic gastritis, a common preneoplastic condition of the stomach, with a primary focus on atrophic gastritis due to chronic Helicobacter pylori infection—the most common etiology—or due to autoimmunity. To date, clinical guidance for best practices related to the diagnosis and management of atrophic gastritis remains very limited in the United States, which leads to poor recognition of this preneoplastic condition and suboptimal risk stratification. In addition, there is heterogeneity in the definitions of atrophic gastritis, autoimmune gastritis, pernicious anemia, and gastric neoplasia in the literature, which has led to confusion in clinical practice and research. Accordingly, the primary objective of this Clinical Practice Update is to provide clinicians with a framework for the diagnosis and management of atrophic gastritis. By focusing on atrophic gastritis, this Clinical Practice Update is intended to complement the 2020 American Gastroenterological Association Institute guidelines on the management of gastric intestinal metaplasia. These recent guidelines did not specifically discuss the diagnosis and management of atrophic gastritis. Providers should recognize, however, that a diagnosis of intestinal metaplasia on gastric histopathology implies the diagnosis of atrophic gastritis because intestinal metaplasia occurs in underlying atrophic mucosa, although this is often not distinctly noted on histopathologic reports. Nevertheless, atrophic gastritis represents an important stage with distinct histopathologic alterations in the multistep cascade of gastric cancer pathogenesis. The Best Practice Advice statements presented herein were developed from a combination of available evidence from published literature and consensus-based expert opinion. No formal rating of the strength or quality of the evidence was carried out. These statements are meant to provide practical advice to clinicians practicing in the United States. Atrophic gastritis is defined as the loss of gastric glands, with or without metaplasia, in the setting of chronic inflammation mainly due to Helicobacter pylori infection or autoimmunity. Regardless of the etiology, the diagnosis of atrophic gastritis should be confirmed by histopathology. Providers should be aware that the presence of intestinal metaplasia on gastric histology almost invariably implies the diagnosis of atrophic gastritis. There should be a coordinated effort between gastroenterologists and pathologists to improve the consistency of documenting the extent and severity of atrophic gastritis, particularly if marked atrophy is present. Providers should recognize typical endoscopic features of atrophic gastritis, which include pale appearance of gastric mucosa, increased visibility of vasculature due to thinning of the gastric mucosa, and loss of gastric folds, and, if with concomitant intestinal metaplasia, light blue crests and white opaque fields. Because these mucosal changes are often subtle, techniques to optimize evaluation of the gastric mucosa should be performed. When endoscopic features of atrophic gastritis are present, providers should assess the extent endoscopically. Providers should obtain biopsies from the suspected atrophic/metaplastic areas for histopathological confirmation and risk stratification; at a minimum, biopsies from the body and antrum/incisura should be obtained and placed in separately labeled jars. Targeted biopsies should additionally be obtained from any other mucosal abnormalities. In patients with histology compatible with autoimmune gastritis, providers should consider checking antiparietal cell antibodies and anti-intrinsic factor antibodies to assist with the diagnosis. Providers should also evaluate for anemia due to vitamin B-12 and iron deficiencies. All individuals with atrophic gastritis should be assessed for H pylori infection. If positive, treatment of H pylori should be administered and successful eradication should be confirmed using non-serological testing modalities. The optimal endoscopic surveillance interval for patients with atrophic gastritis is not well-defined and should be decided based on individual risk assessment and shared decision making. A surveillance endoscopy every 3 years should be considered in individuals with advanced atrophic gastritis, defined based on anatomic extent and histologic grade. The optimal surveillance interval for individuals with autoimmune gastritis is unclear. Interval endoscopic surveillance should be considered based on individualized assessment and shared decision making. Providers should recognize pernicious anemia as a late-stage manifestation of autoimmune gastritis that is characterized by vitamin B-12 deficiency and macrocytic anemia. Patients with a new diagnosis of pernicious anemia who have not had a recent endoscopy should undergo endoscopy with topographical biopsies to confirm corpus-predominant atrophic gastritis for risk stratification and to rule out prevalent gastric neoplasia, including neuroendocrine tumors. Individuals with autoimmune gastritis should be screened for type 1 gastric neuroendocrine tumors with upper endoscopy. Small neuroendocrine tumors should be removed endoscopically, followed by surveillance endoscopy every 1–2 years, depending on the burden of neuroendocrine tumors. Providers should evaluate for iron and vitamin B-12 deficiencies in patients with atrophic gastritis irrespective of etiology, especially if corpus-predominant. Likewise, in patients with unexplained iron or vitamin B-12 deficiency, atrophic gastritis should be considered in the differential diagnosis and appropriate diagnostic evaluation pursued. In patients with autoimmune gastritis, providers should recognize that concomitant autoimmune disorders, particularly autoimmune thyroid disease, are common. Screening for autoimmune thyroid disease should be performed.
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