Autoimmune Gastritis Patients Research Articles

Distinguishing Features of Autoimmune Gastritis Depending on Previous Helicobacter pylori Infection or Positivity to Anti-Parietal Cell Antibodies: Results From the Autoimmune gastRitis Italian netwOrk Study grOup (ARIOSO).

To describe the clinical features and the risk of developing gastric tumors in patients with autoimmune gastritis (AIG). This was a retrospective, longitudinal, multicenter study conducted at 8 Italian tertiary referral centers. We retrieved clinical data from all histologically proven patients with AIG. Differences between Helicobacter pylori -exposed vs H. pylori -naive and anti-parietal cell antibody (PCA)-positive vs PCA-negative patients were investigated. The rate of gastric adenocarcinoma and type 1 gastric neuroendocrine neoplasm (gNEN) was assessed. A multivariable model for factors associated with gNEN was fitted. A total of 1,598 patients with AIG (median age 58 years, interquartile range 46-68; F:M ratio 2.7:1) were included. H. pylori -naive patients were more likely to have a first-degree family history of AIG (14.7% vs 8.9%; P = 0.012), type 1 diabetes mellitus (4.9% vs 2.3%; P = 0.025), and pernicious anemia (30.9% vs 21.1%; P = 0.003). PCA-positive patients had significantly more associated autoimmune diseases (59.0% vs 42.9%; P < 0.001) and were more likely to have been diagnosed by a case-finding strategy (15.3% vs 2.6%; P < 0.001). Overall, 15 cases (0.9%) of gastric adenocarcinoma and 153 cases (9.6%) of gNEN occurred, with a global rate of 0.12 (95% confidence interval [CI] 0.07-0.20) and 1.22 (95% CI 1.03-1.42) per 100 person/year, respectively. Having a vitamin B12/iron deficiency manifestation at AIG diagnosis was associated with a 16.44 (95% CI 9.94-27.20 P < 0.001) hazard ratio of gNEN. The "pure" AIG pattern has typical features of an autoimmune disease and seems to be unrelated to H. pylori . In a tertiary referral setting, the risk of developing overt gastric adenocarcinoma is low, while patients with vitamin B12 deficiency complications at onset may benefit from a more intense endoscopic follow-up for early gNEN detection.

Long-Term Natural History of Autoimmune Gastritis: Results From a Prospective Monocentric Series.

The natural history of autoimmune gastritis (AIG) has been poorly described. In this study, we report the long-term natural history and clinical clustering of the full spectrum of AIG, from the potential to the complicated stage. Prospective single-center study conducted in a tertiary referral center. Patients with AIG at any stage (0 = potential; 1 = early; 2 = florid; 3 = severe; and 4 = complicated) were enrolled (January 2000-December 2022). The histopathological evolution, the clinical presentation, and the correlates of evolution of potential AIG were assessed. Four hundred ninety-eight patients with AIG (mean age 56.7 ± 15.2 years, F:M ratio 2.5:1) were included, of whom 93 experienced potential AIG. The maximum disease duration was 27 years (median 18, interquartile range 14-23), while the overall median follow-up was 52 months (interquartile range 12-95). Age was significantly lower in stage 0 compared with that in the other stages. Accidental histologic evidence and hematologic findings were the most common clusters of diagnosis. The overall median rate of progression was 7.29 per 100 persons/yr (95% confidence interval [CI] 6.19-8.59), while the stage-specific rates of progression were 10.85 (stage 0; 95% CI 7.75-15.18), 14.83 (stages 1-2; 95% CI 11.89-18.49), and 2.68 (stage 3; 95% CI 1.88-3.84). Newly onset neoplastic complications at follow-up occurred in 41/483 patients (8.5%; 23 neuroendocrine tumors and 18 epithelial dysplasia). No cases of adenocarcinoma were noticed. Male sex was associated with a greater likelihood of evolving from potential AIG to overt AIG. AIG is a progressive disorder, with a virtually absent risk of gastric adenocarcinoma. Patients with potential AIG should be monitored because they carry a high risk of evolving into overt AIG.

Atrophic Gastritis and Autoimmunity: Results from a Prospective, Multicenter Study.

Despite a global decrease, gastric cancer (GC) incidence appears to be increasing recently in young, particularly female, patients. The causal mechanism for this "new" type of GC is unknown, but a role for autoimmunity is suggested. A cascade of gastric precancerous lesions, beginning with chronic atrophic gastritis (CAG), precedes GC. To test the possible existence of autoimmunity in patients with CAG, we aimed to analyze the prevalence of several autoantibodies in patients with CAG as compared to control patients. Sera of 355 patients included in our previous prospective, multicenter study were tested for 19 autoantibodies (anti-nuclear antibodies, ANA, anti-parietal cell antibody, APCA, anti-intrinsic factor antibody, AIFA, and 16 myositis-associated antibodies). The results were compared between CAG patients (n = 154), including autoimmune gastritis patients (AIG, n = 45), non-autoimmune gastritis patients (NAIG, n = 109), and control patients (n = 201). ANA positivity was significantly higher in AIG than in NAIG or control patients (46.7%, 29%, and 27%, respectively, p = 0.04). Female gender was positively associated with ANA positivity (OR 0.51 (0.31-0.81), p = 0.005), while age and H. pylori infection status were not. Myositis-associated antibodies were found in 8.9% of AIG, 5.5% of NAIG, and 4.4% of control patients, without significant differences among the groups (p = 0.8). Higher APCA and AIFA positivity was confirmed in AIG, and was not associated with H. pylori infection, age, or gender in the multivariate analysis. ANA antibodies are significantly more prevalent in AIG than in control patients, but the clinical significance of this finding remains to be established. H. pylori infection does not affect autoantibody seropositivity (ANA, APCA, AIFA). The positivity of myositis-associated antibodies is not increased in patients with CAG as compared to control patients. Overall, our results do not support an overrepresentation of common autoantibodies in patients with CAG.

Gastric Th17 Cells Specific for H+/K+-ATPase and Serum IL-17 Signature in Gastric Autoimmunity.

Human gastric autoimmunity [autoimmune gastritis (AIG)] is characterized by inflammation of the gastric mucosa and parietal cell loss. The gastric parietal cell proton pump H+/K+-adenosine triphosphatase (H+/K+-ATPase) is the major autoantigen in AIG. Our work aimed to investigate the gastric H+/K+-ATPase-specific T helper 17 (Th17) responses in AIG and serum interleukin (IL)-17 cytokine subfamily in AIG patients, in healthy subjects [healthy controls (HCs)], and in patients with iron deficiency anemia (IDA) without AIG. We analyzed the activation of gastric lamina propria mononuclear cells (LPMCs) by H+/K+-ATPase and the IL-17A and IL-17F cytokine production in eight patients with AIG and four HCs. Furthermore, we compared serum levels of IL-17A, IL-17F, IL-21, IL-17E, IL-22, and IL-23 in 43 AIG patients, in 47 HCs, and in 20 IDA patients without AIG. Gastric LPMCs from all AIG patients, but not those from HCs, were activated by H+/K+-ATPase and were able to proliferate and produce high levels of IL-17A and IL-17F. AIG patients have significantly higher serum IL-17A, IL-17F, IL-21, and IL-17E (393.3 ± 410.02 pg/ml, 394.0 ± 378.03 pg/ml, 300.46 ± 303.45 pg/ml, 34.92 ± 32.56 pg/ml, respectively) than those in HCs (222.99 ± 361.24 pg/ml, 217.49 ± 312.1 pg/ml, 147.43 ± 259.17 pg/ml, 8.69 ± 8.98 pg/ml, respectively) and those in IDA patients without AIG (58.06 ± 107.49 pg/ml, 74.26 ± 178.50 pg/ml, 96.86 ± 177.46 pg/ml, 10.64 ± 17.70 pg/ml, respectively). Altogether, our results indicate that IL-17A and IL-17F are produced in vivo in the stomach of AIG patients following activation with H+/K+-ATPase and that serum IL-17A, IL-17F, IL-21, and IL-17E levels are significantly elevated in AIG patients but not in patients without AIG. These data suggest a Th17 signature in AIG and that IL-17A, IL-17F, IL-21, and IL-17E may represent a relevant tool for AIG management.

Increase of Deep Intraepithelial Lymphocytes in the Oxyntic Mucosa of Patients With Potential and Overt Autoimmune Gastritis.

Pathological correlates of potential autoimmune gastritis (AIG), defined by anti-parietal cell antibody (PCA) positivity in the absence of gastric atrophy, have never been described. We herein aimed to assess intraepithelial lymphocyte (IEL) infiltration in gastric corpus of AIG patients. From 2000 to 2021, among 53 potential AIG patients, we focused on nine (median age 61 years, IQR 53-82; four females) who subsequently developed overt AIG. IEL infiltration of the oxyntic mucosa was assessed before and after developing overt AIG by measuring deep and superficial CD3+ IEL. AIG patients with different degrees of corpus atrophy, healthy controls (HC), active H. pylori gastritis, celiac disease (CD), and Hashimoto’s thyroiditis patients were included as controls. Of note, deep, but not superficial, CD3+ IEL count was higher (p<0.001) in potential AIG compared to HC and H. pylori gastritis. Deep CD3+ IEL infiltration did not change before or after the evolution into atrophy (median 9.6, IQR 8.8-12.4, vs 11.3, IQR 9.4-12.9). No difference was found in deep CD3+ IEL infiltration among potential, mild, and severe AIG, and compared to Hashimoto’s thyroiditis or CD. A deep CD3+ IEL cut-off of >7/100 epithelial cells allowed discrimination of any AIG stage and severity (AUC=0.842). We conclude that an increased deep CD3+ IEL infiltration of the oxyntic mucosa could represent a marker of potential AIG. Prospective studies including a larger number of potential AIG patients are needed.

Time course and risk factors of evolution from potential to overt autoimmune gastritis.

The natural history of patients with potential autoimmune gastritis (AIG), defined by the presence of serum anti-parietal cell antibody (PCA) positivity and no gastric histopathological alterations, is unknown. We therefore aimed to assess the natural history and clinical correlates of potential autoimmune gastritis (AIG). In 2000-2019, we enrolled potential AIG patients by monitoring once a year (±6 months) histopathological evolution into overt AIG, defined as the occurrence of atrophy in the oxyntic mucosa. Factors affecting disease progression were assessed. Fifty-one potential AIG patients (median age 57 years, IQR 43-73, F:M ratio 1.7:1) were monitored for up to 15 years (median 6 years, IQR 3-8). Of them, 24 (47.1%) evolved into overt AIG in a median time of 2 years (IQR 2-4.5). Having a concomitant autoimmune disorder (HR 4.09, 95% CI 1.52-11.00; p=0.005), but not older age (HR 1.00, 95% CI 0.45-2.22; p=0.992) and female sex (HR 1.19, 95% CI 0.51-2.78; p=0.395), was associated with evolution into overt AIG. Roughly one in two potential AIG patients will evolve into overt AIG over a median time of two years, especially those with a concurrent autoimmune disorder.

Evaluation of screening tests for autoimmune gastritis in histopathologically confirmed Japanese patients, and re-evaluation of histopathological classification

BackgroundThe aims of the present study are to evaluate non-invasive screening tests for autoimmune gastritis (AIG) and re-evaluate histopathological classification.MethodsWe screened candidates of AIG in JCHO Shiga Hospital between May 2012 and January 2020. The screening criteria were as follows: endoscopic O-p atrophy with Updated Kimura–Takemoto classification, 3 + pepsinogen (PG) test, low serum vitamin B12 or elevated serum gastrin with positive anti-parietal cell (PC) or intrinsic factor antibodies. We evaluated the screening criteria in the patients who were histopathologically confirmed as AIG, and re-evaluated histopathological staging in clinical aspects.ResultsTwenty-two of 28 (78.6%) patients who met the screening criteria were histopathologically confirmed as AIG. Common clinical findings in the AIG patients were 10 × or greater anti-PC antibody, elevated serum gastrin greater than 172 pg/mL and endoscopic atrophy O-1 or greater. The areas under the curve of PG I, PG II and PG I/II ratio were 0.81, 0.29 and 0.98, respectively. Among histopathologically confirmed AIG patients, 4 and 18 patients were histopathologically classified into florid and end stages, respectively, while no patients into early stage. We could not find a significant difference between florid and end stages in the screening items studied.ConclusionsFlorid and end stages in histopathological classification are both advanced-stage AIG in clinical aspects. Our screening criteria without biopsy are applicable to screen clinically-advanced AIG with 78.6% positive predictive value. PG I and PG I/II ratio may be useful to screen AIG. However, we may need other criteria to screen early stage of AIG.

Decreased anti-parietal cell antibody titer in the advanced phase of autoimmune gastritis

Background Autoimmune gastritis (AIG) is histologically classified into three phases according to the severity of oxyntic mucosal atrophy: early, florid, and end phases. This study aimed to clarify the relationship between the AIG phase and the anti-parietal cell antibody titer. Methods Patients who underwent upper gastrointestinal endoscopy were retrospectively reviewed in this study. We enrolled patients who were histologically diagnosed with AIG and serologically tested for anti-parietal cell antibody (APCA). AIG patients were classified into three groups: early, florid, and end phase groups. Clinical characteristics, including APCA titers, were compared among these three groups. Results A total of 44 AIG patients were enrolled. There were two patients in the early phase, 11 in the florid phase, and 31 in the end phase. APCA-positive rates were 100% in the early phase, 90.9% in the florid phase, and 90.3% in the end phase. The mean APCA titer was 480 U in the early phase, 220 U in the florid phase, and 150 U in the end phase. There was a stepwise decrease in the APCA titer from the early phase to the end phase. The mean APCA titer for the end phase was significantly lower than that of the early phase or florid phase. Additionally, there was a stepwise decrease in serum gastrin levels from the early phase to the end phase. Conclusion AIG progresses from the early phase to the end phase, and the APCA titer shows a decrease. The negativity of APCA could occur, especially in the end phase.

Five Autoimmune Gastritis Patients with Positive Findings of Serum Anti-parietal Cell Antibodies

Autoimmune gastritis is a corpus-dominant type of gastritis with positive serum anti-parietal cell antibodies (APCA) and/or anti-intrinsic factor antibodies. Serum APCA and pepsinogen (PG) assays were performed in subjects with corpus-dominant gastritis detected by endoscopy. Serum APCA was positive in five patients. All these patients were postmenopausal women (four Koreans and one Caucasian from the Russian Federation) with a mean age of 59.0±3.2 years. They displayed low PG I levels ranging from 8.1 to 18.8 ng/mL (mean, 11.4±4.8 ng/mL) and low PG I/II ratios ranging from 0.7 to 2.4 (mean, 1.2±0.7). Three of the patients were being treated for autoimmune thyroiditis. Multiple gastric neuroendocrine tumors were observed in two Helicobacter pylori (H. pylori)-naive patients with high serum gastrin levels exceeding 700 pg/mL and serum chromogranin A levels exceeding 1,000 ng/mL. In the remaining three patients, intestinal metaplasia was observed in the biopsied specimens from the antrum, suggesting a history of H. pylori infection. Our findings indicate the value of positive serum APCA findings, low serum PG I levels, and low serum PG I/II ratios in confirming autoimmune gastritis in patients showing corpus-dominant atrophy, regardless of their H. pylori infection status.

Differences in image-enhanced endoscopic findings between Helicobacter pylori -associated and autoimmune gastritis.

Background and study aims The aim of this study was to elucidate the differences in image-enhanced endoscopy (IEE) findings between Helicobacter - pylori -associated and autoimmune gastritis. Patients and methods Seven H. pylori -naïve, 21 patients with H. pylori -associated gastritis and seven with autoimmune gastritis were enrolled. Mucosal atrophy in the corpus was evaluated using autofluorescence imaging and classified into small, medium and large. In a 2 × 2-cm area of the lesser curvature of the lower corpus, micromucosal pattern was evaluated by magnifying narrow band imaging and proportion of foveola (FV)- and groove (GR)-type mucosa was classified into FV > 80 %, FV 50 % to 80 %, GR 50 % to 80 %, and GR > 80 %, then a biopsy specimen was taken. Results Fifteen of 21 (71 %) H. pylori -associated gastritis patients exhibited medium-to-large atrophic mucosa at the corpus lesser curvature. All autoimmune gastritis patients had large atrophic mucosa throughout the corpus ( P < 0.001). All H. pylori -naïve patients had the FV > 80 % micromucosal pattern. Nineteen of 21 (90 %) H. pylori -associated gastritis patients had varying proportions of GR- and FV-type mucosae and five of seven (71 %) autoimmune gastritis patients showed FV > 80 % mucosa ( P < 0.001). Compared with patients who were H. pylori -naïve, patients with H. pylori -associated and autoimmune gastritis exhibited a higher grade of atrophy ( P < 0.001), but only patients with H. pylori -associated gastritis showed a higher grade of intestinal metaplasia ( P = 0.022). Large mucosal atrophy with FV > 80 % micromucosal pattern had sensitivity of 71 % (95 % CI: 29 %–96 %) and specificity of 100 % (95 % CI: 88 % to 100 %) for diagnosis of autoimmune gastritis. Conclusions IEE findings of the gastric corpus differed between H. pylori -associated and autoimmune gastritis, suggesting different pathogenesis of the two diseases.

Distinct Features of Autoimmune Gastritis in Patients with Open-Type Chronic Gastritis in Japan

In Asia, the incidences of Helicobacter pylori infection and gastric cancer are high, but their association with autoimmune gastritis (AIG) is unclear. This was a retrospective cohort study of patients endoscopically diagnosed with chronic gastritis between 2005 and 2017. AIG was diagnosed according to anti-parietal cell antibody positivity. Laboratory, histological findings, and gastric cancer incidence were compared between AIG and non-AIG patients. The AIG group had more females and a higher rate of thyroid disease. Serum levels of gastrin were significantly higher in AIG patients (mean 1412 and 353 pg/mL, p < 0.001). The endoscopic findings included a significantly higher percentage of corpus-dominant atrophy in AIG (31.67%) than in non-AIG (7.04%) patients (p < 0.001). Clusters of ECL cells were observed in 28% of AIG patients and 7% of non-AIG patients (p = 0.032). The cumulative incidence of gastric cancer at 5 and 10 years was 0% and 0.03% in the AIG group and 0.03% and 0.05% in the non-AIG group, and no significant difference in gastric cancer incidence was observed. Despite significant differences in gastrin levels between AIG and non-AIG patients, there was no evidence of an impact of AIG on the incidence of gastric cancer.

A Comparison of Baseline Clinical Characteristics of Autoimmune Gastritis Patients with and without Type-1 Gastric Carcinoid Tumor

Objectives : Autoimmune gastritis (AIG) is an antibody-mediated autoimmune disease and characterized by gastric parietal cell loss. Type-1 gastric carcinoid tumor (GCT) is a disease that mostly develops on the basis of AIG. The aim of this study is to determine similarities and differences of baseline clinical parameters between these two disorders.&#x0D; Methods: Patients diagnosed as AIG both without gastric carcinoid tumor (n:197) and with GCT (n:40) between 2004 and 2015 at Ankara University Faculty of Medicine, Department of Gastroenterology, were included in this analysis. Data of initial signs and symptoms, basal blood count-anemia parameters, laboratory investigations, serum gastrin levels, anti parietal cell antibody (APCA) status, serological helicobacter pylori (Hp) markers and serum chromogranine A (CgA) levels of patients were obtained, and baseline parameters of these disorders were compared&#x0D; Results: Patient groups were similar in age and gender. Hemoglobin, iron, total iron binding capacity (TIBC), ferritin, vitamin B12 levels, APCA and HpIgG positivity rates and concomitant autoimmune thyroid disease prevalence were also similar. Median gastrin level in AIG+GCT patients was significantly higher compared to the AIG without GCT (807 vs. 1307 pg/ml; p:0.006). ROC analysis revealed that a 1000 pg/ml threshold value for serum gastrin level is able to distinguish these two disorders with 65% sensitivity and 65% specificity rates (area under the curve: 0.65;p:0.006). The serum CgA level did not significantly differ between patient groups.&#x0D; Conclusion: High serum gastrin but not CgA levels may be useful in deciding which patients should be followed closely in AIG.

Gastric cancer in autoimmune gastritis: A case-control study from the German centers of the staR project on gastric cancer research.

ObjectivesPatients with autoimmune gastritis (AIG) are reported to have an increased risk of developing gastric cancer (GC). In this study, we assess the characteristics and outcomes of GC patients with AIG in a multicenter case-control study.MethodsBetween April 2013 and May 2017, patients with GC, including cancers of the esophagogastric junction (EGJ) Siewert type II and III, were recruited. Patients with histological characteristics of AIG were identified and matched in a 1:2 fashion for age and gender to GC patients with no AIG. Presenting symptoms were documented using a self-administered questionnaire.ResultsHistological assessment of gastric mucosa was available for 572/759 GC patients. Overall, 28 (4.9%) of GC patients had AIG (67 ± 9 years, female-to-male ratio 1.3:1). In patients with AIG, GC was more likely to be localized in the proximal (i.e. EGJ, fundus, corpus) stomach (odds ratio (OR) 2.7, 95% confidence interval (CI) 1.0–7.1). In GC patients with AIG, pernicious anemia was the leading clinical sign (OR 22.0, 95% CI 2.6–187.2), and the most common indication for esophagogastroduodenoscopy (OR 29.0, 95% CI 7.2–116.4). GC patients with AIG were more likely to present without distant metastases (OR 6.2, 95% CI 1.3–28.8) and to be treated with curative intention (OR 3.0, 95% CI 1.0–9.0). The five-year survival rates with 95% CI in GC patients with and with no AIG were 84.7% (83.8–85.6) and 53.5% (50.9–56.1), respectively (OR 0.25, 95% CI 0.08–0.75, p = 0.001).ConclusionsPernicious anemia leads to earlier diagnosis of GC in AIG patients and contributes significantly to a better clinical outcome.

Thiol/disulfide homeostasis and ischemia modified albumin levels in autoimmune gastritis and their relations with gastric emptying

Background/aim Autoimmune gastritis is an autoimmune and inflammatory disorder. The aim of this study is to examine dynamic thiol/disulfide homeostasis and ischemia modified albumin levels, and to analyze the association between thiol/disulfide homeostasis and gastric emptying time in autoimmune gastritis. Materials and methods Thiol/disulfide homeostasis tests and ischemia modified albumin levels were determined in 50 autoimmune gastritis patients and 53 healthy subjects. Patients with delayed and normal gastric emptying were compared by thiol/disulfide homeostasis tests. Results The results showed that native thiol (μmol/L), total thiol (μmol/L), and native thiol/total thiol ratio (%) of the patients with autoimmune gastritis decreased compared to the control group (177.7 ± 34.18 vs. 245.25 ± 33.83, P = 0.001, 227.25 ± 36.78 vs. 284.20 ± 27.19, P = 0.03, and 8.84 ± 1.1 vs. 7.74% ± 1.3%, P = 0.001). In addition, native thiol (μmol/L), total thiol (μmol/L), and native thiol/total thiol ratio (%) were found to be lower in patients with delayed gastric emptying (198.65 ± 24.27 vs. 167.12 ± 20.51, 241.81 ± 27.14 vs. 213.92 ± 26.35, 8.34 ± 1.29 vs. 7.20 ± 1.83, P = 0.001). Disulfide level, disulfide/native thiol, disulfide/total thiol (P = 0.001) ratios, and ischemia modified albumin levels (ABSU, 0.71 ± 0.08 vs. 0.83 ± 0.07) were found to be higher in autoimmune gastritis patients with delayed gastric emptying (P = 0.001). Conclusion The results showed that thiol/disulfide homeostasis in patients with autoimmune gastritis caused an increase in ischemia modified albumin and disulfide whereas a decrease in thiols. An altered thiol/disulfide balance was also observed in patients with delayed gastric emptying. These results suggest that the oxidative process is involved in patients with autoimmune gastritis.

Differential Helicobacter pylori Plasticity in the Gastric Niche of Subjects at Increased Gastric Cancer Risk.

Helicobacter pylori (H. pylori) represents an independent risk factor for Gastric Cancer (GC). First Degree Relatives (FDR) of GC subjects and Autoimmune Gastritis (AG) patients are both at increased risk for GC. H. pylori genetic heterogeneity within the gastric niche of FDR and AG individuals has been little explored. To understand whether they exploit an increased H. pylori stability and virulence, 14 AG, 25 FDR, 39 GC and 13 dyspeptic patients (D) were investigated by a cultural PCR-based approach characterizing single colonies-forming-units. We chose three loci within the Cytotoxin-associated gene-A Pathogenicity Island (CagPAI) (cagA,cagE,virB11), vacA, homA and homB as markers of virulence with reported association to GC. Inflammatory/precancerous lesions were staged according to Sydney System. When compared to D, FDR, similarly to GC patients, were associated to higher atrophy (OR = 6.29; 95% CI:1.23–31.96 in FDR; OR = 7.50; 95% CI:1.67–33.72 in GC) and a lower frequency of mixed infections (OR = 0.16; 95% CI:0.03–0.81 in FDR; OR = 0.10; 95% CI:0.02–0.48 in GC). FDR presented also an increased neutrophil infiltration (OR = 7.19; 95% CI:1.16–44.65). Both FDR and GC carried a higher proportion of CagPAI+vacAs1i1mx+homB+ profiles (OR = 2.71; 95% CI: 1.66–4.41 and OR = 3.43; 95% CI: 2.16–5.44, respectively). Conversely, AG patients presented a lower frequency of subtypes carrying a stable CagPAI and vacAs1i1mx. These results underline different H. pylori plasticity in FDR and AG individuals, and thus, a different host-bacterium interaction capacity that should be considered in the context of eradication therapies.

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

P-088 - Genetic polymorphisms and PG1/PG2 and G17 levels can predict gastric carcinoids in autoimmune atrophic chronic gastritis patients

P-088 - Genetic polymorphisms and PG1/PG2 and G17 levels can predict gastric carcinoids in autoimmune atrophic chronic gastritis patients

Utility of a laboratory score in the prediction of gastric emptying in autoimmune gastritis patients

Objectives: Patients with autoimmune gastritis may have symptoms suggestive of delayed gastric emptying. The aim of this study was to explore the predictive value of two scoring systems in the differentiation of delayed gastric emptying in patients with autoimmune gastritis.Methods: About 154 patients (106 women) with autoimmune gastritis whose gastric emptying test were available, were analyzed using two laboratory-based scoring systems: ‘global score’ (hemoglobin, mean corpuscular volume, gastrin, vitamin B12, and chromogranin A) and ‘simple score’ (hemoglobin, mean corpuscular volume, and gastrin) in order to discriminate delayed and normal gastric emptying.Results: The mean ‘simple score’ was 4.82 ± 0.94 for autoimmune gastritis patients with delayed gastric emptying and 0.72 ± 0.60 for patients with normal gastric emptying (p < 0.001). The mean ‘global score’ was 7.42 ± 0.81 for autoimmune gastritis patients with delayed gastric emptying and 1.176 ± 0.98 (p < 0.001) for patients with normal gastric emptying. There was also a positive correlation between severity of symptoms of patients with autoimmune gastritis and global (r = 0.83, p < 0.001) and simple scores (r = 0.81, p < 0.001).Conclusion: This model may help physicians, while evaluating autoimmune gastritis patients and deciding which patients need gastric emptying test. Gastric emptying study should be ordered in patients who are fulfilling the criteria proposed by these scoring systems.

Distinct metaplastic and inflammatory phenotypes in autoimmune and adenocarcinoma-associated chronic atrophic gastritis.

Autoimmune gastritis (AIG) and adenocarcinoma-associated chronic atrophic gastritis (CAG) are both associated with oxyntic atrophy, but AIG patients demonstrate an increased risk of carcinoid tumors rather than the elevated risk of adenocarcinoma observed with CAG. We therefore sought to compare the characteristics of the metaplastic mucosa in AIG and CAG patients. We examined markers for metaplasia (spasmolytic polypeptide expressing metaplasia (SPEM) and intestinal metaplasia) as well as proliferation (Ki67) and immune cell populations (neutrophils, macrophages, and eosinophils) in gastric sections from 16 female patients with autoimmune thyroiditis and AIG and 17 patients with CAG associated with gastric adenocarcinoma. Both AIG and CAG patients demonstrated prominent SPEM and intestinal metaplasia. However, AIG patients displayed significantly lower numbers of infiltrating macrophages and significantly reduced mucosal cell proliferation as compared to CAG patients. These findings indicate that, while both AIG and CAG patients display prominent oxyntic atrophy and metaplasia, the AIG patients do not show proliferative metaplastic lineages that would predispose to adenocarcinoma.