报告1例经颈静脉肝内门体分流术（TIPS）后重度黄疸患者，首诊为特发性非硬化性门静脉高压（INCPH），术后进行性黄疸加重、恶性贫血，经血液学、影像学、病理学等检查，确诊为自身免疫性胃炎（AMGA）合并TIPS相关的机械性损伤所致黄疸。.

Autoimmune metaplastic atrophic gastritis (AMAG) is associated with an increased risk of gastric neoplasms. This study aimed to systematically analyze the incidence rate of gastric cancer (GC), low-grade dysplasia (LGD) and type-1 gastric neuroendocrine tumor (gNETs) development in AMAG adults. Studies on AMAG patients reporting the incidence of gastric neoplasms was identified through a systematic search in PUBMED and EMBASE. Study quality was assessed using the Joanna Briggs Institute quality assessment tool. Incidence rates of GC, LGD and type-1 gNETs were examined by meta-analysis. Thirteen studies met eligibility criteria. Incidence rate of gastric cancer calculated from the pooled data was 0.14% per person-year in both single-center studies and national registration studies. Meta-analysis showed a relative risk of 11.05 (95% CI: 6.39-19.11) for gastric cancer development in AMAG patients. The calculated pooled gastric LGD and type-1 gNETs incidence rates were 0.52% and 0.83% per person-year, respectively. As for experience from our center, we presented three distinctive cases of gastric neoplasm arising from the background of AMAG. This study underscores the potential for malignant transformation of precancerous lesions and reiterates the importance of careful esophagogastroduodenoscopy screening.

The presence of autoimmune metaplastic atrophic gastritis (AMAG) may lead to an increased risk of associated gastric neoplastic lesions. This study aims to investigate the prevalence of gastric neoplasia in AMAG patients and to explore the possibility of PGI/II ratio as a predictor for AMAG diagnosis.
Retrospective audit of 135 patients diagnosed with AMAG on endoscopic gastric biopsy between January 2017 and December 2020 at Beijing Friendship Hospital. The study was registered in Chinese Clinical Trial Registry (ChiCTR2000041163).
A total of 135 patients (the mean age 61.9 ± 10.9 years,109 female) had histologically confirmed AMAG. 31.1% (42/135) had AMAG without neoplasia on the initial biopsy; 37% (50/135) had multiple type 1 gastric neuroendocrine tumors (g-NETs), 36 grade 1 and 14 grade 2, the median diameter was 5 mm (range 1-25); 31.9% (43/135) had multiple gastric hyperplastic polyps (GHPs), including 15 cases of GHPs with neoplastic transformation, the median diameter was 14.5 mm (range 3-50). 3.7% (5/135) had single gastric low-grade dysplasia/adenoma, the median diameter was 5 mm (range 3-15). 5.9% (8/135) had single or double gastric high-grade dysplasia or adenocarcinoma, the median diameter was 15 mm (range 8-43). 40.7% (55/135) had pepsinogen (PG) I< 10 ng/ml, 45.9% (62/135) had PG I/II ratio ≤1 and each group had a median of PG I/II ratio <1.
Lower serum PG I level and PGI/II ratio may be a predictor to indicate the diagnosis of AMAG. It\'s necessary to perform regular endoscopic surveillance for AMAG patients to recognize associated gastric neoplasia timely.

Autoimmune gastritis (AIG) is a clinicopathologic diagnosis requiring characteristic histopathology and correlation with laboratory work-up. To better understand how the diagnosis of AIG is made and reported in the pathology community, we conducted an anonymous web-based survey which was circulated among a diverse group of pathologists. Excluding trainees there were 64 respondents: 25 academic gastrointestinal pathologists (AGI, 39%), 22 academic general pathologists (AGP, 34%), 17 private general pathologists (PP, 27%). Our survey results highlighted variations in work-up and sign-out practices. The type of metaplasia needed to diagnose AIG lacked consensus. There was variation in accurate interpretation of immunostains with a trend towards more accurate diagnosis of enterochromaffin-like (ECL) cell hyperplasia by AGI (92%) and AGP (95%) than PP (71%) (p = 0.07). G-cells in antrum on neuroendocrine immunostain, a mimicker of ECL cell hyperplasia, was more frequently misdiagnosed by PP/ AGP (44%), versus AGI (12%) (p = 0.02). A triple immunostain panel (H. pylori, neuroendocrine, gastrin) was used in the work-up of AIG by 72% of AGI versus 23% AGP and 12% PP (p = 0.000061). The less-specific term \"atrophic gastritis\" was used in the diagnostic line more by respondents with >10 years sign-out experience compared with others (p = 0.04). In conclusion, the survey results highlighted deficiencies in the interpretation of neuroendocrine immunostains which is crucial for AIG diagnosis, as well as variation in reporting practices and definitions. Uniform criteria and terminology are needed in this field to improve communication with clinicians, resulting in appropriate testing and follow-up.

Autoimmune gastritis is a well-known pathologic entity, but there are few studies that examine its clinical and histologic presentation in children. This is a single institution, retrospective study performed on patients diagnosed from 2011 through 2019. Patients were identified by their pathologic diagnosis within the laboratory information system. The electronic medical record and archived slides were reviewed. Twenty-two children (3 months to 18 years; median, 10.9 years) with autoimmune gastritis were diagnosed of a total of 14,257 nonconsultation gastric biopsies from unique patients (0.15% prevalence). Patients with autoimmune gastritis were diagnosed at an average age of 10.9 years and were mostly female (68.2% women, 31.8% men). The majority had extragastric immune disorders (13/22; 59.1%). All patients in the study had gastric body mucosa with enterochromaffin-like cell hyperplasia, atrophy, and histologic features of chronic injury. Most biopsies showed gastric body metaplasia (n = 19) or active gastric inflammation. However, antral atrophy was also observed in 12 patients, and antral metaplasia was identified in one patient; four patients had active chronic antral gastritis. All biopsies were negative for Helicobacter pylori. Pediatric autoimmune gastritis is a rare disorder that should be recognized because of its systemic effects with long-term morbidity. In addition, the possibility of tandem extragastric immune disorders should be considered when a diagnosis of pediatric autoimmune gastritis is established.

暂无摘要。

BACKGROUND: Pernicious anemia (PA) caused by vitamin B12 deficiency is associated with Autoimmune Metaplastic Atrophic Gastritis (AMAG). Patients with AMAG have threefold risk of the development of gastric cancer.
METHODS: We describe a case of a 66 year old man with a history of PA and atrophic antral-corpus gastritis. After endoscopic and chromoendoscopic evaluation the patient was treated with subtotal gastrectomy plus D2 lymphadenectomy. The tumor was diagnosed as Stage Ia; pT1a pN0 pM0 G2 with multiple foci of high grade dysplasia and intramucosal adenocarcinoma.
CONCLUSIONS: Multifocal Early Gastric Cancer can be a problem for minimally invasive treatment such as endoscopic excision. Surgical management where it is not possible Endoscopic Mucosal Resection or Submucosal Resection (EMR/ESD) should include D1 or more type of lymphadenectomy because of the risk of nodes metastases. The chromoendoscopic evaluation may be helpful in the preoperative work-up and during the follow-up period.
CONCLUSIONS: Multidisciplinary approach is very important to reduce the under-treatment risk in multifocal early gastric cancer. Further studies will be needed to evaluate the safety of Subtotal vs Total Gastrectomy in this kind of disease.

Autoimmune metaplastic atrophic gastritis (AMAG) previously called type A chronic gastritis is an immune-mediated chronic inflammatory disease characterized by the immune-mediated destruction of gastric parietal cells in the fundus and body of the stomach. AMAG is an uncommon disease that often presents with hematological manifestations and may lead to the development of gastric carcinoids. AMAG can be reliably diagnosed by antibody assays, functional serology, and histology. The understanding of the disease process is essential for the detection and management of hematological complications and gastric lesions. The prevalence of AMAG is on the rise and subsequently gastric carcinoids. However, this association is not well recognized in clinical practice, and management and diagnosis of AMAG and gastric carcinoids remain suboptimal. In the current review, we will discuss the pathophysiology, diagnosis and management of AMAG. A special focus is given to the association between AMAG and gastric carcinoids. We will also review the management options of type 1 gastric carcinoids.

BACKGROUND: Autoimmune metaplastic atrophic gastritis (AMAG) is an immune-mediated process that may lead to pernicious anemia (PA) and an increased risk of gastric cancer. Although some literature supports 3- or 5-year endoscopic surveillance for gastric cancer in patients with PA, no formal guidance exists for the general AMAG population. We sought to identify the prevalence and incidence rates of dysplasia or adenocarcinoma in patients with AMAG in order to clarify endoscopic best practices.
METHODS: A retrospective study of 150 patients diagnosed with AMAG on endoscopic gastric biopsy between 1/2010 and 11/2015 was performed at a tertiary medical center. Clinical and pathologic data were obtained in order to calculate the prevalence and the incidence rate of dysplasia or adenocarcinoma.
RESULTS: The cohort was predominantly female (82%) and white (61%), with median age 64 years. PA was present in 47% of patients. On index endoscopy, the prevalence of adenocarcinoma was 5.3%. A total of 59 patients with AMAG, but without neoplasia on initial biopsy, underwent subsequent endoscopic surveillance. Two patients, both of whom had confirmed PA, developed adenocarcinoma. The incidence rate of adenocarcinoma among this group was 14.2 cases per 1000 person-years, which far exceeds that of the general population (0.073 per 1000 person-years) based on Surveillance, Epidemiology, and End Results data.
CONCLUSIONS: AMAG is associated with a high prevalence and incidence of gastric cancer, and endoscopic surveillance should be considered. Prospective cohort studies and cost effectiveness analyses are needed to better estimate cancer risk and recommended endoscopic surveillance intervals in these patients.

OBJECTIVE: Gastric hyperplastic polyp (GHP) commonly arises in the abnormal surrounding mucosa, including autoimmune metaplastic atrophic gastritis (AMAG). We aimed to compare clinicopathological features in patients with GHPs associated with AMAG with those in patients with GHPs associated with non-AMAG.
METHODS: A total of 1170 patients with GHP(s) were enrolled, and their clinical and pathological data were analyzed, retrospectively.
RESULTS: The GHP patients were divided into 181 A-GHP (type A GHP, AMAG-associated GHP) participants, 312 B-GHP (type B GHP, Helicobacter pylori infection-associated GHP) participants, and 677 other GHP participants (non-A-GHP and non-B-GHP) based on pathological status of the surrounding non-polypoid mucosa. The A-GHP patients were older and predominantly female (p < .05). Gastroscopically, A-GHPs showed less distal and more multiple-region distribution in the stomach (p < .001). In addition, the A-GHPs were observed to be usually numerous (55.8%), larger (mean maximum diameter 12.3 mm), and more pedunculated or sub-pedunculated (45.3%) (p < .001). Histopathologically, the intestinal metaplasia, intraepithelial neoplasia, and carcinomatous transformation within GHPs were present in 24.3%, 9.9%, and 2.8% of AMAG patients, respectively, which were significantly higher than those in the B-GHPs and other GHPs (p < .05). However, the differences of intraepithelial neoplasia and adenocarcinoma in surrounding non-polypoid mucosa did not reach statistical significance (p > .05).
CONCLUSIONS: The GHP(s) arising in AMAG patients is a distinct subgroup of GHP(s) and was an important precancerous lesion. The biopsy from surrounding non-polypoid mucosa was essential to evaluate the underlying etiology of the GHPs, and endoscopists should pay attention to these.