Autoimmune Metaplastic Atrophic Gastritis Research Articles

Gastric intestinal metaplasia and gastric cancer prevention: Watchful waiting.

Gastric intestinal metaplasia (GIM), a common histologic finding, is associated with increased risk of gastric cancer, and GIM associated with Helicobacter pylori infection is classified as an environmental metaplastic atrophic gastritis. Patients may be asymptomatic or present with various dyspeptic symptoms. Autoimmune metaplastic atrophic gastritis is a less common but important cause of chronic gastritis. The Correa cascade describes the evolution of precancerous mucosal changes that lead to development of GIM, with differentiation of 2 histologic types of GIM (complete and incomplete) and the consequences of each type. The risk of progression to malignancy is higher with incomplete GIM. It is also higher for those who immigrate from regions with a high incidence of H pylori infection to areas where the incidence is low. Guidelines regarding endoscopic management of GIM vary by geographic region.

Clinicopathologic Features of Autoimmune Metaplastic Atrophic Gastritis (AMAG) in an Underserved Community

Abstract Introduction/Objective Autoimmune metaplastic gastritis (AMAG), typically associated with pernicious anemia and subsequent risk of gastric neoplasia, is an entity often underrecognized in routine gastric biopsies and can lead to delay in the diagnosis and management of patients. In this study, we analyze the demographics and clinical features of AMAG in an inner city, underserved population with histopathologic and serologic correlation. Methods/Case Report We retrospectively collected data on patients diagnosed with or with probable AMAG over a 29-month period from Jan 2020-May 2022 and correlated the histopathology with demographics and clinical presentation. We retrieved prior biopsies on available cases. Results (if a Case Study enter NA) Our Data Demonstrates: -Almost equal prevalence of AMAG in African American and Caucasian patients, with a higher rate of incidence in older population (68% over the age of 60 years), and in female patients. -43.5% had antibody testing and only 25% of patients had testing for Gastrin levels, but the diagnosis of AMAG was frequently associated with a positive laboratory finding (78.7% and 74.3%, respectively) when performed. -57.8% had clinically documented anemia, among those, 88.9% had microcytic or normocytic anemia. Only 11.1% had macrocytic anemia -A history of prior biopsies demonstrating chronic gastritis was seen in 33% of patients. Conclusion Our study demonstrates that patients with AMAG come from diverse backgrounds and frequently lack laboratory findings typically associated with pernicious anemia at the time of diagnosis. As such, pathologists and gastroenterologists may benefit from a lower threshold when considering which patients to evaluate for AMAG. Complete laboratory evaluations were infrequent, which is a limitation, but this may be secondary to a lack of clinical knowledge regarding appropriate testing and an underserved patient population which lacks good continuity of care.

A Case of Autoimmune Metaplastic Atrophic Gastritis with Concurrent Pernicious Anemia and Coombs-Negative Hemolysis

Pernicious anemia is an autoimmune disease characterized by atrophic gastritis and vitamin B12 deficiency. Concurrent hemolytic anemia has been described, however its prevalence and mechanism are not well understood. Herein, we present the case of a 40-year-old female who presented with abdominal pain, fatigue, and a 50-lb weight loss over four months. She was found to have macrocytic anemia, leukopenia, moderate neutropenia, and severe vitamin B12 deficiency. Further laboratory testing (indirect hyperbilirubinemia, low haptoglobin, increased lactate dehydrogenase, low reticulocyte index) implied the presence of intravascular hemolysis with a poor bone marrow response. Peripheral blood smear showed hypersegmented neutrophils consistent with megaloblastic anemia and schistocytes suggestive of hemolysis. Notably, the direct Coombs test was negative.The patient’s serum was positive for anti-intrinsic factor and anti-parietal cell antibodies. Esophagogastroduodenoscopy revealed H. Pylori-negative, metaplastic atrophic gastritis with no evidence of malignancy. Thus, a diagnosis of pernicious anemia was confirmed in addition to hemolytic anemia. She was treated with intramuscular cyanocobalamin, resulting in improvement of symptoms, cytopenias, and hemolytic markers. Hemolysis is a rare complication of vitamin B12 deficiency, and multifactorial anemia must always be considered.

Incidence of Gastric Neoplasms Arising from Autoimmune Metaplastic Atrophic Gastritis: A Systematic Review and Case Reports.

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 Morphologic Spectrum of Gastric Type 1 Enterochromaffin–Like Cell Neuroendocrine Tumors

Although most well-differentiated gastric neuroendocrine tumors (gNETs) arise from enterochromaffin-like (ECL) cells in patients with autoimmune metaplastic atrophic gastritis (AMAG), the morphologic spectrum of these type 1 ECL-cell gNETs is not well defined. The extent of metaplastic progression in the background mucosa of AMAG patients with gNETs is likewise unclear. Here we report the histomorphology of 226 gNETs, including 214 type 1 gNETs (78 cases from 50 AMAG patients) pooled from a population with high AMAG prevalence. Most type 1 gNETs were ≤1.0 cm, of low grade, and multifocal, consistent with the results of previous reports. However, a high proportion (70/214, 33%) displayed unusual gNET morphologies not previously appreciated in AMAG patients. Unlike other type 1 gNETs with conventional neuroendocrine tumor morphologies, unconventional type 1 gNETs displayed cribriform networks of atrophic cells embedded within myxoid matrix (secretory-cribriform variant, 59%), sheets of deceptively bland discohesive cells resembling inflammatory infiltrates (lymphoplasmacytoid variant, 31%), or wreath-like arrangements of columnar cells wrapped around collagenous cores (pseudopapillary variant, 14%). Another unusual feature was that unconventional gNETs grew laterally within the mucosa (50/70, 71%) and were only rarely sampled from the submucosa (3/70, 4%). These features also differed from the conspicuous radial nodules (99/135, 73%) and frequent submucosal involvement (57/135, 42%) observed for conventional gNETs (P < .0001). Irrespective of morphology, type 1 gNETs were nearly always detected at first AMAG diagnosis (45/50, 90%) and tended to persist thereafter (34/43, 79%), despite similar clinical symptoms and laboratory values between AMAG patients with gNETs and those without. However, unlike AMAG patients without gNETs (n = 50), the background mucosa in patients with gNETs (n = 50) had already progressed to the morphologic equivalent of end-stage metaplasia (P < .0001). This included diffuse loss of parietal cells (92% vs 52%), complete intestinal metaplasia (82% vs 40%), and pancreatic metaplasia (56% vs 6%). Thus, type 1 ECL-cell gNETs are morphologically heterogeneous with a high prevalence of unconventional gNET morphologies. They tend to present silently at first AMAG diagnosis as multifocal lesions that persist within fields of mature metaplasia.

S3560 Who Knows When It All Began? A Case of Autoimmune Gastritis

Introduction: Gastritis is a common entity that manifests as erythema of the gastric mucosa seen on EGD. The most common cause of Gastritis is infection, specifically H pylori. Atrophic gastritis is suggested endoscopically by loss of rugal folds and appearance of the submucosal vessels. Autoimmune Metaplastic Atrophic Gastritis (AMAG) is a subtype and is suggested pathologically by full thickness chronic inflammation, oxyntic gland destruction, prominent eosinophils, metaplasia, or parietal cell pseudohypertrophy. Endoscopic surveillance remains controversial. Management strategies include eradication of H pylori infection. We present a case of AMAG assoc with Lupus. Case Description/Methods: A 45-year-old Caucasian female with history of Lupus presented with persistent, dull, aching epigastric pain aggravated by solid food intake and anemia. She had no previous history of H pylori, no previous use of antacids, NSAIDs, or digestive enzymes. When she was younger, she had iron deficiency anemia thought to be solely nutritional or related to heavy menses. Her Mother had Hashimoto's thyoiditis. Laboratory work up showed mild microcytic anemia Ferritin 253 ng/mL, Iron 143 ug/dL while on Iron supplementation. EGD showed loss of rugal folds with edematous change in fundus and body. Biopsy showed chronic gastritis with intestinal metaplasia. Repeat EGD in 1 year showed loss of rugal folds and pallor to the mucosa. Biospies were done according to mapping protocol for intestinal metaplasia of greater and lesser curvature of antrum, incisura and body showed atrophic/autoimmune gastritis. Gastrin level was 1419 pg/mL, Antiparietal cell Antibody 108.1 Units (>24 U being positive), and Intrinsic factor Ab was low 1.0 AU/mL (Cut off is 1.1 AU/mL). She was managed with Iron supplementation, assessment for other vitamin deficiencies (B12 and folate were normal), and with yearly surveillance EGDs with mapping due to presence of intestinal metaplasia (Figure). Discussion: The endoscopic findings in Atrophic Gastritis can be very subtle. It is important that endoscopists are aware of these findings in order to better identify this illness. Additionally regimented biopsies per protocol ensure that this diagnosis is not missed. Beyond eradication of H. pylori further surveillance measures remain controversial. These should be considered on a case by case basis taking family history, region, smoking history, age, comorbidities, obesity, and alcohol consumption into consideration. More research is required to make universal screening guidelines.Figure 1.: Stomach showing atrophic folds.

Gastric lesions in patients with autoimmune metaplastic atrophic gastritis: a retrospective study in a single center

Objectives 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. Patients and methods 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). Results 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. Conclusions 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.

Оценка коморбидного статуса и структурных изменений щитовидной железы у больных с хроническим метапластическим атрофическим гастритом: обзор и собственные исследования

Актуальность. Коморбидная патология остается распространенной, но недостаточно изученной проблемой. В настоящее время частота и характер соединенной патологии у больных с хроническим метапластическим атрофическим гастритом (ХМАГ) окончательно не выяснены, как и роль щитовидной железы (ЩЖ) в этиопатогенезе данного заболевания. Цель: оценить состояние коморбидности у больных с ХМАГ и изучить частоту и характер структурных изменений ЩЖ у данной категории больных, исследовать литературные данные по этой проблеме. Материалы и методы. В обследование включен 41 больной с ХМАГ в возрасте (60,1 ± 2,4) года, среди которых было 29 женщин и 12 мужчин. Больным проводилась гастроскопия (с NBI-режимом и забором биопсийного материала), ультразвуковое исследование ЩЖ, анкетирование с помощью Сumulative Illness Rating Scale (CIRS), а также по историям болезни изучались коморбидные заболевания желудочно-кишечного тракта (ЖКТ). Результаты. У 82,9 % больных с ХМАГ выявлены ультразвуковые диффузные изменения ЩЖ, причем у 48,8 % обследованных они выявлялись впервые, а у 37,8 % пациентов данные изменения сочетались с наличием узлов в ЩЖ. К тому же у 9,8 % больных выявлены ультразвуковые признаки аутоиммунного тиреоидита. У 97,6 % пациентов с ХМАГ наблюдалась полиморбидная патология, причем у 92,7 % больных — со стороны 3 систем и больше и только у 4,9 % — со стороны 2 систем. Установлена положительная корреляционная связь между возрастом больных и суммарным количеством баллов, набранных с помощью опросника коморбидности CIRS (r = 0,412, p = 0,04). По данным СIRS, наиболее часто у пациентов с ХМАГ сочеталась патология верхнего и нижнего отделов ЖКТ (97,7 и 53,7 % соответственно), патология костно-мышечного аппарата и кожных покровов (68,3 %), патология глаз, ушей, горла, носа и гортани (56,1 %), сосудистая патология (56,1 %), заболевания сердца (51,2 %) и эндокринно-метаболическая патология (34,1 %). Выводы. У 82,9 % больных с ХМАГ выявлены ультразвуковые структурные изменения ЩЖ. Перспективным направлением дальнейшего исследования, на наш взгляд, было бы изучение аутоиммунных процессов в желудке и ЩЖ (установление возможных взаимосвязей между аутоиммунным тиреоидитом и аутоиммунным гастритом), а также особенностей течения данных коморбидных заболеваний. Необходимо уделить внимание ХМАГ не только как заболеванию, которое является фактором риска развития рака желудка, но и как возможному маркеру наличия сопутствующей патологии щитовидной железы.

A Rare Case of Autoimmune Metaplastic Atrophic Gastritis

Autoimmune metaplastic atrophic gastritis is an important pathological finding associated with neoplasia and pernicious anemia. Defined guidelines on surveillance endoscopy for this diagnosis are lacking. We present a rare case of a patient with a known history of pernicious anemia that presented with blood-tinged sputum. The patient underwent endoscopic evaluation with random gastric biopsies that showed a two-month progression from diffuse inflammation to intestinal metaplasia in the background of autoimmune metaplastic atrophic gastritis (AMAG) on surveillance endoscopy. AMAG is an important finding that deserves close endoscopic surveillance as complications can include autoimmune conditions, pernicious anemia,gastric carcinoid, and gastric adenocarcinoma.

S2158 Fundic Gland Polyp Causes Massive Melena During Induction Chemotherapy With R-EPOCH for DLBCL

INTRODUCTION: Fundic Gland Polyps (FGPs) are hamartomatous cystic lesions in the gastric mucosa, and mostly occur sporadically. Bleeding from an FGP is very rare but has been reported in the setting of long-term PPI use and rare hematologic conditions. Overall, these polyps are considered quite benign. CASE DESCRIPTION/METHODS: A 71-year-old gentleman presented to the hospital in active tumor lysis and was subsequently diagnosed with Diffuse Large B Cell Lymphoma of the non-germinal center type, in a background of 3B follicular lymphoma. He was started on induction chemotherapy with the R-EPOCH regimen (without rituximab given unknown HBV status) and a day later, developed massive melena resulting in hemorrhagic shock. His chemotherapy regimen was stopped and he was resuscitated, requiring multiple transfusions. Once in stable condition, an EGD was performed which found only a benign FGP in a background of chronic atrophic gastritis as a source of the bleed (Figure 1). The pathology revealed pyloric and intestinal metaplasia, consistent with autoimmune gastritis (Figure 2), with no evidence of dysplasia or malignancy. Mesenteric angiography was subsequently performed to identify any other source of GI bleed for IR embolization, but no contrast extravasation was observed to suggest one. The patient's clinical status improved during the procedure, suggesting that the hemorrhage had ceased. DISCUSSION: The development of FGPs is a rare phenomenon. When they do form, they may form sporadically, or may be associated with hypergastrinemia seen in patients taking proton pump inhibitors, in those with Zollinger-Elison syndrome, and in those with autoimmune metaplastic atrophic gastritis (AMAU). Interestingly, our patient was found to have AMAU on pathology and there have been multiple reports of a bidirectional association between lymphocytic malignancies, like DLBCL, and autoimmune manifestations. Our patient's GI bleed was likely the result of a combination of factors, including his AMAU and his DVT prophylaxis (enoxaparin), but the most significant of these factors is the gastrointestinal side effects of his chemotherapeutic R-EPOCH (Rituximab, Etoposide, Prednisone, Oncovin, Cyclophosphamide and Doxorubicin Hydrochloride) regimen. Many of the drugs used in this regimen are known to cause mucositis, and prednisone in particular has been historically associated with GI bleeds due to mechanisms such as impaired wound healing. As seen in this case, when his chemotherapeutic regimen was stopped, his bleeding also ceased.Figure 1.: Endoscopic photograph of the fundic gland polyp.Figure 2.: The biopsy of the fundic gland polyp demonstrates cystically dilated glands arising in oxyntic-type mucosa.Figure 3.: The biopsy of the background fundic mucosa shows atrophic mucosa with loss of oxyntic glands, pseudopyloric metaplasia, and chronic inflammation in the lamina propria, compatible with autoimmune gastritis.

Risk factors and clinical correlates of neoplastic transformation in gastric hyperplastic polyps in Chinese patients

Gastric hyperplastic polyps (GHPs) have a potential risk of neoplastic transformation, but the responsible mechanisms have not yet been established. We conducted a study involving 55 patients (33 female) who had undergone endoscopic or surgical resection of GHPs. We compared 16 patients who had GHPs showing neoplastic transformation with 39 patients who had non-neoplastic GHPs. We analyzed differences in serology, gastroscopic manifestations and pathology between the two groups in order to establish risk factors that may be associated with neoplastic transformation. The mean age of the cohort was 61.73 ± 9.024 years. The prevalence of positive serum gastric parietal cell antibody (PCA) was 61.8%. 30 of the GHPs with neoplastic formation had a “strawberry-like” appearance with erosions of polyps (P = 0.000). A history of anaemia was a risk factor for GHPs which demonstrated neoplastic transformation (odds ratio [OR], 3.729; 95% confidence interval [CI], 1.099–12.649; P = 0.035). Although the differences were not significant, our data showed higher prevalences of positive serum PCA (P = 0.057), hypergastrinemia (P = 0.062) and female gender (P = 0.146) in the GHP patients who had neoplastic transformation. Multiple polyps in the corpus (P = 0.024) occurred more frequently in serum PCA positive patients. Hypergastrinemia occurred more frequently in Helicobacter pylori negative patients and of these 20/22 patients had a positive PCA (P = 0.007). GHPs are associated with autoimmune metaplastic atrophic gastritis (AMAG). AMAG is probably one of the risk factors for GHPs to undergo neoplastic transformation.

Autoimmune metaplastic atrophic gastritis and association with neuroendocrine tumors of the stomach.

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.

An Update on the Role of Immunohistochemistry in the Evaluation of Gastrointestinal Tract Disorders.

As in other organ systems, immunohistochemistry (IHC) serves as an ancillary diagnostic tool for a wide variety of neoplastic and non-neoplastic disorders, including infections, work-up of inflammatory conditions, and subtyping neoplasms of the gastrointestinal (GI) tract. In addition, IHC is also used to detect a variety of prognostic and predictive molecular biomarkers for carcinomas of the GI tract. The purpose of this review is to highlight the use of IHC in common diagnostic scenarios throughout the tubular GI tract. The clinical indication and guidelines for performing IHC for detecting Helicobacter pylori is discussed along with role of gastrin and neuroendocrine markers in the diagnosis of autoimmune metaplastic atrophic gastritis. The major portion of this review discusses the use of IHC in the diagnostic workup of malignant neoplasms of the GI tract, such as adenocarcinoma versus squamous cell carcinoma, workup of poorly differentiated malignant neoplasms, and evaluation of uncommon gastric neoplasms (alpha-feto protein-producing carcinomas) and switch/sucrose-nonfermenting complex-deficient carcinomas. Lastly, localization of neuroendocrine tumors of unknown origin to aid clinical management, as well as HPV-driven anal neoplasia and IHC in the workup of basaloid anal neoplasms are also reviewed.

Comparative study between autoimmune metaplastic atrophic gastritis (AMAG) and type 1 gastric neuroendocrine tumors (G-NETs) in Hospital Clinico San Carlos (HCSC), Madrid

Comparative study between autoimmune metaplastic atrophic gastritis (AMAG) and type 1 gastric neuroendocrine tumors (G-NETs) in Hospital Clinico San Carlos (HCSC), Madrid

MON-LB057 A Descriptive Study of Type 1 Gastric Neuroendocrine Tumors and Its Association with Autoinmune Metaplasic Atrophic Gastritis in Hospital Clinico San Carlos

INTRODUCTION Type 1 Gastric neuroendocrine tumors account for 70 to 80% of all gastric neuroendocrine tumors (G-NETs) and they are found more commonly in older adults, particularly women. They are associated with autoimmune metaplastic atrophic gastritis (AMAG) with or without pernicious anemia. Endoscopically, they are usually smaller than 1 cm and often multiple. These tumors present a non-aggressive evolution. Our aim is to describe different characteristics of type 1 G-NETs and to approach the presence of risk factors to develop G-NET in patients with AMAG. PATIENTS AND METHODS A descriptive and observational study of 16 patients diagnosed with AMAG (controls) and 31 patients diagnosed additionally with type 1 G-NET (cases). All of the 47 patients were retrieved from the Endocrinology Service of HCSC in the last 15 years. Variables between both groups were compared using the statistical program SPSS 23.0. RESULTS In the group of cases, 31.3% presented micronodular hyperplasia. 60.4% were grade 1 type 1 G-NET. 75.6% presented a single lesion. Median size was 0.4 cm (IQR 0.3-0.6). 41.9% of the lesions were located in the body of the stomach. Ki67 was ≤2% in 95.3% of the cases. Only 10.4% were treated with somatostatin analogs. Taking into account both groups: Mean age was 64.75 (SD 12.03) in controls and 63.47 (SD 11.35) in cases. 75% of controls and 62% of cases were female. The diagnosis of AMAG in controls was due to vitamin B12 deficiency in 68.8%. In cases, the diagnosis of G-NET was due to follow-up AMAG in 40.6%. We did not find differences between the personal and family history in both groups. 86.7% of controls and 71.8% of cases were non-smokers without reaching statistical significance. The presence of H. pylori was found in 18.8% of controls and in 3.1% of cases (p= 0.101). The median of vitamin B12 (normal range 180 -914 pg/ml) in controls was 186 (IQR 141.5-398.5) & 288 (IQR 204-386) in cases (p <0.05). There were no statistically significant differences in the levels of hemoglobin, ferritin or serum iron although the median values were lower in controls. Regarding autoimmunity, anti-parietal cell antibodies could protect the development of G-NET OR: 0.192 (0.038-0.956). We found a higher prevalence of intrinsic factor antibodies in controls (41.2% vs 21.7) that was not statistically significant (p=0.185). CONCLUSIONS In our sample, the presence of anti-parietal cell antibodies might be a protective factor against G-NET development. Vitamin B12 levels were significantly higher in cases than in controls. Further research confirming these data might help to establish the usefulness of Vitamin B12 levels in the early diagnosis of G-NET in patients with AMAG. Larger studies are necessary to assess whether the presence of intrinsic factor antibodies and H.Pylori infection are indeed associated with a lower risk of developing G-NETs in patients with AMAG. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. s presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

Hyperplastic polyps arising in autoimmune metaplastic atrophic gastritis patients: is this a distinct clinicopathological entity?

Objectives: 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.Patients and 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.

Pernicious Anemia: Early Detection of the Historical “Great Pretender"

Pernicious anemia (PA) is the late manifestation of autoimmune metaplastic atrophic gastritis (AMAG) characterized by the presence of anti-intrinsic factor with eventual decreased absorption of cyanocobalamin. Various clinical manifestations from subtle anemia to serious neurological symptoms gives PA notoriety as a “great pretender”. We present a case of an asymptomatic patient who was found to have severe gastritis with anemia leading to further evaluations revealing a chronic autoimmune disorder. A 52-year-old female with history of HTN, abnormal uterine bleeding, DM2 and anemia presented with abnormal labs. Colonoscopy completed 6 years ago for iron deficiency anemia found no etiology. Labs revealed Hb 6.0g/dl, Hct 17.5%, Plt 140,000/uL, MCV 114, RDW 27.2%, Iron 108μg/dL, ferritin 338ng/ml. Iron Saturation 32%, transferrin 258mg/dL, TIBC 335μg/dL, vitamin B12 <50pg/mL, Folate 22.8ng/mL, vitamin D 25-OH 13ng/mL. Fecal occult blood test was negative.EGD was performed to screen for (PA) and gastric malignancies which revealed frank blood in the gastric fundus, friable gastric mucosa, and erythematous mucosa in the pylorus. Pathology was consistent with autoimmune gastritis. Intrinsic factor antibody assay was positive. She was started on Cyanocobalamin injections, and continued on lifelong B12 supplementation. PA accounts for 20-50% of all cobalamin deficiencies in adults, and it is a complex disorder associated with hematological, gastric, immunological and neurological alterations. It has a prevalence 0.1% in the general population and is diagnosed in up to 15-25% of patients with AMAG. Disease progression includes symptoms ranging from fatigue and weakness, to atrophic glossitis, to more severe peripheral neuropa thies and subacute combined degeneration. Increase in MCV and hypersegmented neutrophils are usually the initial laboratory findings. This case illustrates the need to have early detection and timely treatment of PA induced vitamin B12 deficiency. Vitamin D displays immunomodulatory properties may be a risk factor. One case-control study revealed levels of vitamin D in autoimmune gastritis patients were significantly lower than in the general population. Evaluation by EGD and histopathology of AMAG is necessary due to its precancerous nature. Gastric carcinoid tumors have been observed in 4-9% of patients with AMAG and PA so continued surveillance should always remain a part of the patient's plan of care.2036_A Figure 1. Upper GI Bleed2036_B Figure 2. Gastritis2036_C Figure 3. Friable Gastric Mucosa

Su1233 - Gastric Hyperplastic Polyps in Patients with Autoimmune Metaplastic Atrophic Gastritis at a Large Tertiary Medical Center

Su1233 - Gastric Hyperplastic Polyps in Patients with Autoimmune Metaplastic Atrophic Gastritis at a Large Tertiary Medical Center

Tu1320 - The Prevalence and Incidence of Neoplasia in Patients with Autoimmune Metaplastic Atrophic Gastritis: A Renewed Case for Surveillance Endoscopy

Tu1320 - The Prevalence and Incidence of Neoplasia in Patients with Autoimmune Metaplastic Atrophic Gastritis: A Renewed Case for Surveillance Endoscopy

The incidence of neoplasia in patients with autoimmune metaplastic atrophic gastritis: a renewed call for surveillance.

BackgroundAutoimmune 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.MethodsA 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.ResultsThe 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.ConclusionsAMAG 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.