Severe Gastritis Research Articles

Endoscopic and Histological Gastritis in University Students with Helicobacter pylori Infection.

Objective Although the characteristics of Helicobacter pylori infection have been extensively reported, there is a lack of consensus regarding its characteristics in young adults. The present study examined the endoscopic and histological characteristics of young adults who underwent eradication therapy for H. pylori infection. Methods We examined the H. pylori infection status of first-year students at Okayama University School of Medicine and Dentistry between 2014 and 2020. A total of 152 (6.8%) students who were positive for H. pylori antibody or pepsinogen tests were enrolled in the study. Among them, 107 students underwent endoscopy, and their biopsy samples were investigated. Seventy-five students were diagnosed with H. pylori infections. Results Of 75 H. pylori-positive patients, 57 (76.0%) had endoscopic atrophic gastritis, and 42 (56.0%) had histological atrophy. A few patients had severe atrophic gastritis. All 65 patients who underwent an eradication assessment were successfully treated. After successful eradication, 26 patients underwent endoscopic follow-up. The mean follow-up period was 32.9 months. A histological evaluation revealed that gastric antrum atrophy had subsided in 11 of 14 patients, and atrophy in the lesser curvature of the gastric body had subsided in 7 of 8 patients. Conclusion More than half of young adults with H. pylori infection had atrophic gastritis. We found mild atrophy in young adults, which subsided shortly after eradication treatment. This study provides a foundation for future studies to evaluate the validity of eradication therapy in preventing gastric cancer in patients.

Risk of map-like redness development after eradication therapy for Helicobacter pylori infection.

Map-like redness is a newly identified endoscopic risk factor for gastric cancer in patients who received Helicobacter pylori eradication therapy. However, the incidence rate of map-like redness in patients who received eradication, and the risk factors for the development of map-like redness remain unclear. We hence aimed to investigate the incidence rate of map-like redness at 1-year post H. pylori eradication, and evaluated its associations with map-like redness and gastric cancer in relation with gastric condition. Endoscopic severity of gastritis and map-like redness were retrospectively evaluated according to the Kyoto Classification of Gastritis in patients who had undergone endoscopy before and after H. pylori eradication therapy. The incidence rate of map-like redness for all 328 patients at a mean of 1.2 ± 0.6 years after eradication was 25.3% (95% confidence interval [CI]: 20.7%-30.4%). Patients who developed map-like redness were older, had more severe atrophy and intestinal metaplasia, a higher total score of the Kyoto Classification of Gastritis both before and after eradication, and a higher rate of gastric cancer history than patients who did not have map-like redness. On multivariate analysis, risk of map-like redness was increased in patients with intestinal metaplasia (odds ratio [OR]: 2.794, 95% CI: 1.155-6.757) and taking acid inhibitors (OR: 1.948, 95% CI: 1.070-3.547). Characteristics of H. pylori-positive patients with gastric cancer history were patients who were older (OR: 1.033, 95% CI: 1.001-1.066), taking acid inhibitors (OR: 4.456, 95% CI: 2.340-8.484), and with occurrence of map-like redness after eradication therapy (OR: 2.432, 95% CI: 1.264-4.679). Map-like redness is observed in one fourth of patients at 1-year post eradication. Patients who developed map-like redness were found to have severe intestinal metaplasia and taking acid inhibitors, and hence such patients require increased attention at surveillance endoscopy.

A case of severe immune checkpoint inhibitor-related gastritis requiring differential diagnosis from scirrhous carcinoma

A case of severe immune checkpoint inhibitor-related gastritis requiring differential diagnosis from scirrhous carcinoma

Residual Level Of Deltamethrin Induced Gastritis And Preventive Role Of Curcumin On Stomach Mucosa.

Benefits of Curcumin for health have been explained by different experimental models and clinical trials. It is a very potent antioxidant. Curcumin was found to play a preventive and curative role in both acute and chronic gastritis. Deltamethrin is a useful pesticide when applied with caution to crops. However, it also has noxious effects on gastric mucosa once ingested with sprayed crops. Its maximum permissible limit, MRL (Maximum Residual Level) as pesticide food residues is 5 mg/kg body weight as defined by WHO. However, there is still a potential to cause harm at these levels and maybe a serious potential health hazard. The present study aimed to: (a) determine the prevalence and severity of gastritis induced by deltamethrin when administered at MRL doses and (b) To observe the preventive effect on gastric mucosa against the action of Deltamethrin present as a residual pesticide in different vegetables and fruits. In this two-phase subacute toxicity study of seven weeks, forty Sprague Dawley rats were divided into eight subgroups. Control groups were kept on a normal diet and sesame oil. Out of the two treatment groups, one group was given deltamethrin (5 mg/kg body weight) orally along with curcumin 100 mg/kg body weight. The second group was first given deltamethrin (5mg/kg body weight) and curcumin (200mg/kg). All were culled at its end. The stomach samples were collected and processed to obtain histology slides for analysis via microscopy and micrometry. Grading was done to look for changes according to the "Visual Analogue Scale and Operative Link on Gastritis Assessment (OLGA)". The experimental deltamethrin group when compared to control groups, revealed mild changes in stomach histomorphology while curcumin-treated both groups; Group D (100 mg/kg) and Group E (200 mg/kg) showed no changes. Administration of Deltamethrin even in maximum residual dose (permissible) is proven to be toxic. Curcumin is hence proven to protect the gastric mucosa against the toxic effects of deltamethrin ingested in residual form.

Surviving Multiple Cardiac Arrests Secondary to Catastrophic Sero-Negative Antiphospholipid Syndrome: A Case Report

Antiphospholipid syndrome (APS) is an autoimmune disorder which predisposes to venous and arterial thrombosis due to the autoantibodies targeting phospholipids in cell membranes contributing to a pro-thrombotic state. The appropriately named catastrophic anti-phospholipid syndrome (CAPS) is distinguished from classical APS by the rapid involvement of 3+ organs, evidence of areas of small vessel occlusions, and significantly elevated anti-phospholipid titers (Cervera, 2018). To further complicate the matter, there is a growing body of evidence of the existence of sero-negative APS (SNAPS) that are negative for the classical lupus anticoagulant, anticardiolipin antibody (aCL), and anti-beta2 glycoprotein-I but may be positive for non-criteria APS antibodies. Presented below is a patient with SNAPS who responded to the therapy for CAPS despite negative classical autoantibodies. A 34 year old man with a past medical history of chronic alcohol use presented to the ED with a two day history of worsening shortness of breath. The patient was found to have an spO2 of 45-50% on room air and was quickly transitioned to a non-rebreather and subsequently BIPAP. Initial CBC was significant for WBC 22.1, Hg 19.3, Hct 58.5, MCV 100.8, and platelets of 166 consistent with neutrophilic leukocytosis and macrocytic polycythemia. D-dimer >20 was suggestive recent/on-going coagulation and/or fibrinolysis. Due to worsening respiratory failure, he was intubated and admitted to the ICU. While on 3 vasopressors he became bradycardic and a code blue was called for pulseless electrical activity (PEA). After 3 rounds of CPR he achieved return of spontaneous circulation (ROSC) and was taken for urgent CT imaging. After arriving in the radiology department he went into cardiac arrest for two rounds of CPR before achieving ROSC and being scanned and returning to the ICU. Polycythemia tests were drawn which revealed elevated erythropoietin of 52.1 (2.6-18.5) and ultimately negative JAK2. Chest CTA was significant for a PE with a heavy clot burden involving the entire right lung and the left upper and lower lobes. CT C/A/P showed findings of bilateral lower lobe pneumonia, severe gastritis, pancolitis, proctitis, pancreatitis with a 4.6cm pseudocyst, and fatty liver with congestive enhancement. Tissue-type plasminogen activator (tPA) bolus and infusion was initiated based on the imaging findings with the third cardiac arrest occurring 7 minutes later early in the morning. Repeat CBC revealed an Hgb/Hct of 22.2 g/dL and 71.5%, respectively, with a significant drop in platelets down to 103 with occasional large platelets consistent with peripheral destruction of platelets was noted on peripheral blood smear (PBS). Therapeutic phlebotomy of 300mL was subsequently performed with two additional cardiac arrests within 2 hours of each other before vascular surgery was able to perform thrombectomies of the involved pulmonary arteries and initiate catheter-directed thrombolysis. Platelet count dropped while on heparin to 25,000 so a HIT panel was ordered and he was transitioned to argatroban. At this point hematology was consulted who was concerned for CAPS and ordered aPL (anti-phospholipid) tests along with an appropriate panel of labs to rule out alternative causes. Peripheral blood smear did not reveal fragmentation of RBC to suspect TTP. Tests for ACL IgG/IgM and anti-beta2GPI IgG/IgM antibodies, COVID, HIV, ADAMTS deficiency, hereditary thrombophilia, and ANA were negative. High-dose steroids and daily plasma exchanges via vascath was initiated and within 12 hours there was significant improvement. He was extubated and off pressors in 24 hours with improved platelets. Lupus anticoagulant test results were reported after discharge with dVVT mix and PTT LA mix both being prolonged, however, repeat lupus anticoagulant 3 months later was negative. Given the potentially catastrophic effects of a missed CAPS diagnosis, a high level of clinical suspicion is needed as plasma exchange can quickly alleviate an otherwise disastrous condition. Further research into non-criteria APS autoantibodies (IgA)may be able to help guide future SNAPS diagnoses.

Investigating associations between HLA DQA1 ~ DQB1 haplotypes, H. pylori infection, metaplasia, and anti-CagA IgA seropositivity in a Turkish gastritis cohort.

Helicobacter pylori was reported as an important cause of gastritis, and gastric ulcers and CagA oncoprotein-producing H. pylori subgroups were blamed to increase the severity of gastritis. Disparities were reported in that the presence of serum anti-CagA IgA was not parallel with CagA-positive H. pylori cohabitation. We hypothesized that the HLA-DQA1 ~ DQB1 haplotypes in human populations include protective haplotypes that more effectively present immunogenic CagA peptides and susceptible haplotypes with an impaired capacity to present CagA peptides. We recruited patients (n = 201) admitted for gastroendoscopy procedures and performed high-resolution HLA-DQA1 and DQB1 typing. Serum anti-CagA IgA levels were analyzed by ELISA (23.0% positive), and H. pylori was classified as positive or negative in gastric mucosal tissue slides (72.6% positive). The HLA DQA1*05:05 allele (29.1%) and HLA DQB1*03:01 allele (32.8%) were found at the highest frequency among gastritis patients of Turkish descent. In HLA DQA1*05:05 ~ DQB1*03:01 double homozygous (7.3%) and heterozygous (40.7%) haplotype carriers, the presence of anti-CagA IgA decreased dramatically, the presence of H. pylori increased, and the presence of metaplasia followed a decreasing trend. The DQ protein encoded by HLA DQA1*05:05-DQ*03:01 showed a low binding affinity to the CagA peptide when binding capacity was analyzed by the NetMHCIIPan 4.0 prediction method. In conclusion, HLA DQA1 ~ DQB1 polymorphisms are crucial as host defense mechanisms against CagA H. pylori since antigen binding capacity plays a crucial role in anti-CagA IgA production.

Factors influencing occurrence of metachronous gastric cancer after endoscopic resection: a systematic review and meta-analysis

Background/Aims: Metachronous gastric cancer (MGC) can occur after endoscopic resection for gastric cancer. Further studies on factors other than <i>Helicobacter pylori</i> infection are needed. This systematic review and meta-analysis aimed to evaluate risk factors for metachronous recurrence of endoscopically resected gastric cancer.Methods: We searched medical literature published by February 2023 and identified patients with MGC after endoscopic resection for gastric cancer. The occurrence of MGC and the presence of intestinal metaplasia (IM), severe atrophic gastritis (AG), and <i>H. pylori</i> infection were quantitatively analyzed.Results: We identified 2,755 patients from nine cohort studies who underwent endoscopic resection for gastric cancer by 2018. Those with severe AG or presence of IM had a significantly higher incidence of MGC than those without (RR 2.00, 95% CI 1.35–2.98, I<sup>2</sup> = 52% for severe atrophy on antrum; RR 7.08, 95% CI 3.63–13.80, I<sup>2</sup> = 0% for antral IM). Absolute risk difference of MGC occurrence was 7.1% in those with severe AG and 9.2% in those with IM. The difference in incidence rate per 1,000 person-years was 17.5 person-years for those with severe AG and 24.7 person-years for those with IM. However, <i>H. pylori</i> eradication did not significantly affect the occurrence of MGC (RR 1.18, 95% CI 0.88–1.59, I<sup>2</sup> = 10%).Conclusions: Gastric cancer patients with severe AG or presence of IM had a 2.0-fold or 7.0-fold higher risk of MGC occurrence after endoscopic resection than those without, respectively. They need more stringent follow-up to monitor MGC occurrences (CRD42023410940).

An Overlooked Cause of Severe Gastritis

An Overlooked Cause of Severe Gastritis

<i>Helicobacter pylori</i> Persistence in Patients with Peptic Ulcer Disease and Chronic Gastritis in the Treatment with Antibiotics and Acid-Suppressive Agents

Background. Chronic gastritides still have no division into forms according to the data of the genotyping of Helicobacter pylori isolates. Monitoring the results of anti-Helicobacter pylori therapy cannot be limited to eradication, by taking into account the data on Helicobacter pylori detection in healthy individuals. Is increased acid production associated with the presence of virulent or nonvirulent strains?Objective. To search for the predominance of cagA or any allelic combination of vacA in the isolates from patients with mild and severe chronic gastritis and from those with peptic ulcer disease. To track the time course of changes in the disappearance and repeated gastric colonization with different Helicobacter pylori strains in patients with peptic ulcer disease immediately after anti-Helicobacter pylori therapy and 1.5–2 months later. To confirm or refute the fact that the increased acid production is associated with the presence of virulent Helicobacter pylori strains rather than with the persistence of nonvirulent strains.Methods. The Helicobacter pylori isolates from the gastric biopsy specimens taken from patients with chronic gastritis and peptic ulcer disease were genotyped for cagA and allelic combinations of vacA. The strains from patients who had received anti-Helicobacter pylori therapy were genotyped using the variable number tandem repeat (VNTR) method. Patients with an exacerbation of peptic ulcer disease and those wth an exacerbation of chronic pancreatitis with concomitant gastritis were compared from the level of acid production and from the belonging of Helicobacter pylori to virulent strains.Results. Patients with mild chronic gastritis were observed to have an abundance of nonvirulent allelic combination of vacAs2m2, which differed significantly from its frequency in both the patients with severe chronic gastritis and those with peptic ulcer disease. In the latter patients, the differences between the background bacteriological pattern and the pattern observed after 1.5–2 months had a high degree of significance; in these follow-up periods, in contrast to the control immediately after therapy, the number of eradications increased and the number of cagA-containing strains decreased due to the change of strains. Acid production was significantly higher in the patients with peptic ulcer disease than in those with chronic pancreatits and concomitant gastritis; the former patients show a statistically significant predominance of virulent strains; the latter patients had nonvirulent strains (at the same rate of Helicobacter pylori detection).Conclusion. Filling the blank spots in the study of helicobacteriosis remains relevant due to the progress of genetic methods in bacteriology and to the introduction of novel approaches to assessing the results of anti-Helicobacter pylori therapy.

Cost-effectiveness analysis of the artificial intelligence diagnosis support system for early gastric cancers.

The introduction of artificial intelligence into the medical field has improved the diagnostic capabilities of physicians. However, few studies have analyzed the economic impact of employing artificial intelligence technologies in the clinical environment. This study evaluated the cost-effectiveness of a computer-assisted diagnosis (CADx) system designed to support clinicians in differentiating early gastric cancers from non-cancerous lesions in Japan, where the universal health insurance system was introduced. The target population to be used for the CADx was estimated as those with moderate to severe gastritis caused by Helicobacter pylori infection. Decision trees with Markov models were built to analyze the cumulative cost-effectiveness of using CADx relative to the pre-artificial intelligence status quo, a condition reconstructed from data in published reports. After conducting a base-case analysis, we performed sensitivity analyses by modifying several parameters. The primary outcome was the incremental cost-effectiveness ratio. Compared with the status quo as represented in the base-case analysis, the incremental cost-effectiveness ratio of CADx in the Japanese market was forecasted to be 11,093 USD per quality-adjusted life year. The sensitivity analyses demonstrated that the expected incremental cost-effectiveness ratios were within the willingness-to-pay threshold of 50,000 USD per quality-adjusted life year when the cost of the CAD was less than 104 USD. Using CADx for EGCs may decrease their misdiagnosis, contributing to improved cost-effectiveness in Japan.

Morphological Spectrum of Gastritis in Endoscopic Biopsies and Its Association With Helicobacter pylori Infection.

Introduction Helicobacter pylori(H. pylori)infection is the most common cause of gastritis. The consequences of the persistent infection range from acute ulceration to the development of gastric neoplasia. The purpose of the study is to determine the histopathological pattern of gastritis in gastric biopsies and its association with H. pylori. Materials and methods This is a retrospective study of all the gastric biopsies received in the Department of Histopathology, Chughtai Institute of Pathology, Lahore, Pakistan from January 12, 2021 to April 10, 2021. Sections were cut from formalin-fixed, paraffin-embedded (FFPE) tissue blocks. Slides were stained with routine, special and immunohistochemical stains. The cases were then blindly reviewed by two pathologists with a special interest in Gastrointestinal Pathology. Microscopic features based on updated Sydney classification were recorded. The collected data were then analyzed by using SPSS version 20(IBM Corp., Armonk, NY). Results A total of 429 gastric biopsies were examined. Out of which, 202 (47.1%) were male and 227 (52.9%) were female with a female-to-male ratio of 1.2:1. Their ages ranged from 12 to 100 years and a peak in the fourth decade of life with a mean age of 43 years (median age 49 years). Among gastritis, activity was seen in 194 (45%) and chronicity in 237 (55%) cases. H. pylori was seen in 174 (40.5%) cases and there was a strong statistically significant association between H. pylori infection and severity of gastritis (p<0.001). Other parameters of Sydney classification, such as atrophic changes, were seen in 144 (33%) cases, and intestinal metaplasia in 10 (2.3%) cases. Conclusion H. pylori organism was the most common cause of gastritis in our environment. The severity of gastritis is directly related to the H. pylori infection. If neutrophils are identified on surface epithelium, then H. pylori should be searched with increased attention on morphology and/or on immunohistochemical stain of H. pylori. Chronic inflammation and H. pylori density can also guide treatment which is necessary to avoid complications.

Changes in Gastric Pathology after H. pylori Treatment in Community-Driven Research Aimed at Gastric Cancer Prevention.

Community-driven projects have characterized Helicobacter pylori (Hp) infection in Indigenous communities in the Northwest Territories (NT) and Yukon (YT), Canada. These projects address concerns about the frequent diagnosis of Hp infection among community members and its relation to gastric cancer deaths, perceived to occur with alarming frequency in this region. Projects included breath-test screening for Hp infection, gastroscopy with gastric biopsies, and treatment to eliminate Hp infection. Previous project results showed a high prevalence of stomach pathologies associated with increased cancer risk among Hp-positive participants at baseline. This analysis describes changes in precancerous gastric pathologies in project participants who had gastroscopy before baseline treatment during 2008-2013 and again in 2017. Throughout the study period, the same pathologist graded Hp density, active gastritis, chronic gastritis, atrophic gastritis, and intestinal metaplasia using the updated Sydney System. Of 310 participants from three communities with baseline pathology data, 69 had follow-up pathology data. Relative to baseline, the prevalence of Hp infection and precancerous gastric pathology was substantially lower at follow-up; most participants who were Hp-positive at baseline and Hp-negative at follow-up had reduced severity of active, chronic, and/or atrophic gastritis at follow-up. Though follow-up numbers are small, these results yield evidence that successful Hp treatment has the potential to reduce the risk of gastric cancer in Arctic Indigenous communities.

Prediction of &lt;i&gt;Helicobacter pylori&lt;/i&gt; Infection by Endoscopic Severity of Erythematous Gastritis in Asymptomatic Adults

Background/Aims: &lt;i&gt;Helicobacter pylori&lt;/i&gt; (&lt;i&gt;H. pylori&lt;/i&gt;) infection is correlated with erythematous gastritis, which is one of the endoscopic findings of the Sydney classification system. The present study evaluated the association between the endoscopic severity of erythematous gastritis and &lt;i&gt;H. pylori&lt;/i&gt; infection.Methods: We prospectively enrolled asymptomatic adults who were diagnosed with erythematous gastritis during screening esophagogastroduodenoscopy. A rapid urease test was performed in all participants to diagnose &lt;i&gt;H. pylori&lt;/i&gt; infection. The severity of erythematous gastritis was determined based on the Sydney classification system. The primary endpoint was the &lt;i&gt;H. pylori&lt;/i&gt; infection rate according to the severity of erythematous gastritis (mild to moderate vs. severe).Results: In total, 131 patients with erythematous gastritis were included. The rate of &lt;i&gt;H. pylori&lt;/i&gt; infection was 45.8% across all patients. Of the 131 included patients, 45 had mild gastritis, 43 had moderate gastritis, and 43 had severe gastritis. The &lt;i&gt;H. pylori&lt;/i&gt; infection rate was significantly different between patients with mild to moderate erythematous gastritis and those with severe erythematous gastritis (20.5% vs. 97.7%, respectively; &lt;i&gt;p&lt;/i&gt; = 0.000). After adjustment for potential confounding variables, the severity of erythematous gastritis was associated with the &lt;i&gt;H. pylori&lt;/i&gt; infection rate. The kappa value was 0.563, and interobserver variation was 14.43%.Conclusions: &lt;i&gt;H. pylori&lt;/i&gt; infection is observed to a moderate degree in patients with erythematous gastritis. The severity of erythematous gastritis is associated with the &lt;i&gt;H. pylori&lt;/i&gt; infection rate.

Improving the detection of Helicobacter pylori in biopsies of chronic gastritis: a comparative analysis of H&E, methylene blue, Warthin-Starry, immunohistochemistry, and quantum dots immunohistochemistry.

The objective of the study was to compare the consistency of various staining methods, including H&E, Methylene Blue, Warthin-Starry (W-S), Immunohistochemistry (IHC) and Quantum dots immunohistochemistry (QDs-IHC), in detecting Helicobacter pylori (HP) in cases of mild, moderate and severe chronic gastritis. Biopsy samples were obtained from 225 patients with chronic gastritis at the Department of Pathology, Yichang Central People's Hospital between January 2019 and October 2019. The presence of HP was detected using H&E, Methylene Blue, W-S, IHC, and QDs-IHC. The positive rates for HP detection using H&E, Methylene Blue, W-S, IHC, and QDs-IHC were 42.22%, 51.11%, 53.78%, 59.11%, and 58.67%, respectively. In cases of mild chronic gastritis, the consistency of test results between H&E, Methylene Blue, W-S, and QDs-IHC with IHC were Kappa=0.196, P=0.033, Kappa=0.706, P<0.001, Kappa=0.717, P<0.001, and Kappa=0.968, P<0.001, respectively. Similarly, in cases of moderate chronic gastritis, Kappa values between H&E, Methylene Blue, W-S, and QDs-IHC with IHC were 0.356, P<0.001, 0.655, P<0.001, 0.741, P<0.001, and 0.946, P<0.001, respectively. For cases of severe chronic gastritis, the Kappa values between the staining methods and IHC were 0.271, P=0.037, 0.421, P=0.002, 0.621, P<0.001, and 1, P< 0.001, respectively. The study showed that the positivity rate of IHC was significantly higher than that of H&E, Methylene Blue, and W-S in detecting HP infection in chronic gastritis cases. In terms of consistency with IHC, QDs-IHC was the most reliable staining method across all severity grades, while the agreement between H&E and IHC was poor, and that between Methylene Blue and W-S with IHC was average. Pathology departments may choose the most appropriate staining method based on their specific needs, considering the staining time, contrast, and cost of each method.

Two cases of severe gastritis associated with immune check point inhibitor therapy

In recent years Immune Check Point Inhibitors (ICIs) have played an integral role in the treatment of a wide variety of malignancies. Despite improvements in survival outcomes with immunotherapy, immune related Adverse Events (irAEs) are increasing in incidence

Gornje gastrointestinalno krvarenje, neuobičajena prezentacija Zlatokosinog sindroma

Gastrointestinal bezoars in the pediatric age group have an unusual presentation, and their clinical manifestation is mainly associ- ated with obstructive conditions of the gastrointestinal tract, and are generally made up of hair and food debris. In a smaller num- ber, it has been seen that from its usual location, which is the stomach, bezoar structures could extend into the duodenum, jejunum, ileum, and even colon, giving the appearance of a “Rapunzel tail”. We present the case of a 7-year-old girl with an atypical initial presentation of Rapunzel syndrome, secondary to a trichobezoar. The patient did not have previous psychiatric history, nor reports of any disturbance at school. She was admitted to the emergency room due to upper gastrointestinal bleeding and required a subsequent transfusion of blood products. During her hospitalization, an up- per digestive endoscopy was performed, with the diagnosis of Rapunzel syndrome, in addition to the presence of two Forrest II-C, III gastric ulcers and severe erythematous gastritis in the region of the antrum and body. Medical treatment was started without suc- cess, for which the bezoar had to be surgically removed. Therefore, we want to point out the importance of deepening certain aspects such as the medical history and background in this type of patient, since it is a disorder linked to behavioral and mood alterations; likewise, remember the less frequent clinical symp- toms such as upper gastrointestinal bleeding, but which in turn can be lethal if we don’t act promptly. In the same way, the compre- hensive approach with the support of the family and the intervention of psychology and/or psychiatry is vital to prevent recurrences.

Tubulointerstitial nephritis antigen-like 1 is a novel matricellular protein that promotes gastric bacterial colonization and gastritis in the setting of Helicobacter pylori infection.

The interaction between the gastric epithelium and immune cells plays key roles in H. pylori-associated pathology. Here, we demonstrate a procolonization and proinflammatory role of tubulointerstitial nephritis antigen-like 1 (TINAGL1), a newly discovered matricellular protein, in H. pylori infection. Increased TINAGL1 production by gastric epithelial cells (GECs) in the infected gastric mucosa was synergistically induced by H. pylori and IL-1β via the ERK-SP1 pathway in a cagA-dependent manner. Elevated human gastric TINAGL1 correlated with H. pylori colonization and the severity of gastritis, and mouse TINAGL1 derived from non-bone marrow-derived cells promoted bacterial colonization and inflammation. Importantly, H. pylori colonization and inflammation were attenuated in Tinagl1-/- and Tinagl1ΔGEC mice and were increased in mice injected with mouse TINAGL1. Mechanistically, TINAGL1 suppressed CCL21 expression and promoted CCL2 production in GECs by directly binding to integrin α5β1 to inhibit ERK and activate the NF-κB pathway, respectively, which not only led to decreased gastric influx of moDCs via CCL21-CCR7-dependent migration and, as a direct consequence, reduced the bacterial clearance capacity of the H. pylori-specific Th1 response, thereby promoting H. pylori colonization, but also resulted in increased gastric influx of Ly6Chigh monocytes via CCL2-CCR2-dependent migration. In turn, TINAGL1 induced the production of the proinflammatory protein S100A11 by Ly6Chigh monocytes, promoting H. pylori-associated gastritis. In summary, we identified a model in which TINAGL1 collectively ensures H. pylori persistence and promotes gastritis.

Atrophic gastritis rather than Helicobacter pylori infection can be an independent risk factor of colorectal polyps: a retrospective study in China

BackgroundColonoscopy is considered the most effective screening method for colorectal polyps. However, the longevity and complexity of the procedure makes it less desirable to screen for colorectal polyps in the general population. Therefore, it is essential to identify other independent risk factors. In this study, we explored the link between Hp infection, atrophic gastritis, and colorectal polyps to identify a new potential risk factors of colorectal polyps.MethodsIn this study, atrophic gastritis and intestinal polyps were diagnosed by endoscopy and pathology. All the 792 patients in this retrospective study were divided into sub-groups based on the presence of colorectal polyps. The correlation between polyps and atrophic gastritis was analyzed using the chi-square test and Kruskal-Wallis test. The receiver operating characteristic (ROC) curve was used to compare the predictive value for colorectal polyps between Hp infection and atrophic gastritis. Binary logistic regression was utilized to identify independent risk factors for colorectal polyps.ResultsPatients with colorectal polyps were primarily male with advanced age, and the number of patients with colorectal polyps had a higher association with smoking, alcohol drinking, and Hp infection than the control group. A positive correlation between the number of colorectal polyps and the severity of atrophic gastritis was observed. ROC analysis showed that atrophic gastritis was a better risk factors for colorectal polyps. Multivariate analysis identified atrophic gastritis as an independent risk factor for colorectal polyps (OR 2.294; 95% CI 1.597–3.296).ConclusionsAtrophic gastritis confirmed could be an independent risk factors for colorectal polyps.

Type A, Type B, and Non-atrophic Gastritis

The gastric cancer risk varies based on the etiology and severity of gastritis, which depends on a history of Helicobacter pylori infection and the secretory capacity of the stomach. Type A gastritis is associated with reverse atrophy of the corpus and type B with progressive atrophy extending from the antrum to the corpus. Diffuse or spotty redness in the corpus together with high serum pepsinogen (PG) II levels and a low PG I/II ratio are observed in patients with H. pylori infection when secretory capacity of the stomach is intact. Diffuse-type gastric cancer may develop near the gastric folds, which is a rare site of atrophy. Low serum PG I levels are associated with progressive gastric corpus atrophy and intestinal metaplasia in patients with chronic and previous H. pylori infections. This clinical scenario predisposes patients to intestinal-type gastric cancer, which originates in the atrophic and metaplastic gastric mucosa. Conversely, a high PG I/II ratio is observed in patients without H. pylori infection. Serum PG I levels and the PG I/II ratio are high in patients with acute H. pylori-negative gastritis, including drug-induced gastritis but are significantly low in autoimmune gastritis. Gastric neuroendocrine tumors may develop in patients with autoimmune gastritis or in those with long-term acid suppressant use. Fasting serum gastrin levels and the risk of neuroendocrine tumors are high in both cases. In this review, types of gastritis are summarized along with evaluation performed to determine the secretory capacity of the background gastric mucosa.

Autoimmune Gastritis Accompanied by a Schwannoma Presenting as a Subepithelial Tumor

Autoimmune gastritis (AIG), a chronic inflammatory disease occurs as a result of a complex interaction between host-related and environmental factors. AIG may progress to severe atrophic gastritis secondary autoimmune-mediated parietal cell destruction in the stomach. AIG can be diagnosed based on anti-parietal cell antibody tests and endoscopy, which reveals widespread gastric corpus atrophy in patients with low serum pepsinogen I levels, a low pepsinogen I/II ratio, and elevated serum gastrin levels on serological testing. Tissue biopsy findings, which include mucosal atrophy and lymphocytic infiltration of the lamina propria may be useful for diagnostic confirmation. Decreased gastric acid secretion causes hypergastrinemia and enterochromaffin-like (ECL) cell proliferation, which can lead to neuroendocrine tumor development. Additionally, an autoimmune response results in parietal and chief cell injury, and proliferating ECL cells are detected in the deep mucosal layers in patients with AIG. Therefore, this condition may easily be misdiagnosed as a subepithelial tumor, and establishing a differential diagnosis for other types of subepithelial tumor accompanied by AIG is challenging. We present the case of a 54-year-old woman who was diagnosed with AIG with a concomitant subepithelial tumor based on serologic tests and biopsy findings and underwent wedge resection, which confirmed diagnosis of a schwannoma.