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Gastric biopsies are often submitted with as clinical question Helicobacter pylori (HP) infection. Regularly, the morphology suggests a HP infection but the organism is not detected in special stains. This review presents a practical approach to deal with such biopsies. The first step is to exclude a false negative result of the search for HP, by ensuring that both antral and oxyntic mucosa are present, by the use of sensitive stains, identification of marked reactive changes, such as intestinal, pseudo-pyloric, pancreatic metaplasia that may suggest a diagnosis of (HP associated or autoimmune) atrophic gastritis, and finally identification of signs of the use of proton pump inhibitors (PPI) as in such biopsies, HP may sometimes be found only within parietal cells. The differential diagnosis should include lymphocytic gastritis, other diseases affecting the stomach, such as inflammatory bowel disease (IBD), vasculitis, granulomatous disease, viral infection, such as cytomegalovirus (CMV) or more rarely Epstein-Barr virus (EBV) infection, or other bacterial infections, such as Enterococcus and Treponema pallidum. Clinical input may be required to ensure the patient is not taking medication that may cause gastritis, such as antibiotics used for HP eradication or common medications that cause a form of gastropathy. When these have been excluded, a known cause has not been found and in such a case, the term idiopathic focal/diffuse gastritis can be used.

The main histologic feature of celiac disease is increased intraepithelial lymphocytes (IELs) with or without villous atrophy of the duodenal mucosa. The aim of this study was to document a broad range of additional morphologic changes in intestinal mucosa biopsy specimens from patients with celiac disease. Our cohort comprised 150 patients with positive tissue transglutaminase serologic findings; 7 were at Corazza stage A1, 58 at stage B1, and 85 at stage B2. IEL counts per 100 epithelial cells ranged from 34 to 156 (mean, 88.6); a significant neutrophilic infiltrate was present in 85 cases (56.7%); eosinophil count ranged from 3 to 50 per high-power field (mean, 14.6). Additional findings included morphologic changes in enterocytes in 68.7%, subepithelial collagen thickening in 45.3%, and associated lymphocytic gastritis in 30.4% of patients. We demonstrated that these underrecognized features, which can be misleading, are not uncommon in celiac disease and were positively associated with more advanced stages of the disease (P < .0001).

Organic basis of gastrointestinal symptoms is in the scope of many specialists. In this article lymphocytic gastritis, relatively newly described and not widely-known entity is presented. The lesion is characterized by presence of numerous mature lymphocytes in the surface and foveolar epithelium, as well as lymphocytic infiltration of the lamina propria. According to the definition at least 25 lymphocytes per 100 gastric epithelial cells is now required for the diagnosis. Literature found in wide range of databases was searched for morphological features of lymphocytic gastritis and its relationship with others coexisting or predisposing conditions or lesions. A strong positive correlation between celiac disease and Helicobacter pylori infection, and occurrence and severity of lymphocytic gastritis was revealed. A relationship was also found between lymphocytic gastritis and gastric lymphomas and other conditions.

Introduction Immune checkpoint inhibitors such as programmed cell death/−ligand 1 inhibitor and cytotoxic T‐lymphocyte‐associated antigen‐4 inhibitors have been widely used for various advanced malignancies. The mechanism of action for these inhibitors is the improvement of antitumor immunity via T‐cell modulation. On the contrary, immune‐related adverse events such as autoimmune colitis might arise in association with T‐cell activation. Upper gastrointestinal adverse events related to pembrolizumab have rarely been reported. Case presentation A 72‐year‐old man underwent laparoscopic radical cystectomy for muscle‐invasive bladder cancer (pT2N0M0). Multiple lymph node metastases appeared in the paraaortic region. First‐line chemotherapy comprising gemcitabine and carboplatin failed to stop disease progression. After the administration of pembrolizumab as second‐line treatment, the patient showed symptomatic gastroesophageal reflux disease. Esophagogastroduodenoscopic biopsy of the gastric body showed severe lymphoplasmacytic and neutrophilic infiltration. Conclusion We present acute gastritis related to pembrolizumab. Early eradication therapy may be able to control immune checkpoint inhibitor‐related gastritis.

Gastric carcinoma (GC) represents the most common cause of death in patients with common variable immunodeficiency (CVID). However, a limited number of cases have been characterised so far. In this study, we analysed the clinical features, bacterial/viral infections, detailed morphology and immune microenvironment of nine CVID patients with GC. The study of the immune microenvironment included automated digital counts of CD20+, CD4+, CD8+, FOXP3+, GATA3+ and CD138+ immune cells, as well as the evaluation of PD-L1 expression. Twenty-one GCs from non-CVID patients were used as a control group. GC in CVID patients was diagnosed mostly at early-stage (n = 6/9; 66.7%) and at younger age (median-age: 43y), when compared to non-CVID patients (p < 0.001). GC pathogenesis was closely related to Helicobacter pylori infection (n = 8/9; 88.9%), but not to Epstein-Barr virus (0.0%) or cytomegalovirus infection (0.0%). Non-neoplastic mucosa (non-NM) in CVID-patients displayed prominent lymphocytic gastritis (100%) and a dysfunctional immune microenvironment, characterised by higher rates of CD4+/CD8+/Foxp3+/GATA3+/PD-L1+ immune cells and the expected paucity of CD20+ B-lymphocytes and CD138+ plasma cells, when compared to non-CVID patients (p < 0.05). Changes in the immune microenvironment between non-NM and GC were not equivalent in CVID and non-CVID patients, reflecting the relevance of immune dysfunction for gastric carcinogenesis and GC progression in the CVID population.

Lymphocytic gastritis (LG) is uncommon and presents histologically with a nonspecific inflammatory pattern. It is most often associated with celiac disease and Helicobacter pylori gastritis and is rarely associated with other conditions including lymphoma. LG is of clinical importance since its recognition should prompt further clinical evaluation for other disorders. Lymphocytic gastritis (LG) is uncommon and presents histologically with a nonspecific inflammatory pattern. It is most often associated with celiac disease and Helicobacter pylori gastritis and is rarely associated with other conditions including lymphoma. LG is of clinical importance since its recognition should prompt further clinical evaluation for other disorders.

Background: Refractory coeliac sprue (RCS) with an immunophenotypically aberrant clonal intraepithelial lymphocyte (IEL) population is considered a cryptic form of intestinal T cell lymphoma. Aims: To investigate the distribution of the abnormal and monoclonal IEL population in the digestive tract of RCS patients. Patients and methods: We compared the frequency of lymphocytic gastritis (LG) and lymphocytic colitis (LC), together with IEL phenotype and T cell clonality, in gastric and colonic samples from 15 adults with RCS (all with aberrant CD3 intracytoplasmic+ surface− CD8− clonal IELs on duodenojejunal biopsies), 18 patients with active coeliac disease (ACD), and 10 patients with coeliac disease (CD) on a gluten free diet (GFD-CD) by means of immunohistochemistry and multiplex polymerase chain reaction amplification of the T cell receptor γ gene (TCR-γ) rearrangement. Blood samples of nine RCS patients were also tested for clonality. Results: LG was found in 9/14 (64%), 11/18 (61%), and 3/10 (30%) patients with RCS, ACD, and GFD-CD, respectively, while LC was found in 6/11 (55%), 3/4 (75%), and 2/3 (66%) patients. Contrary to CD, all samples from patients with LG and LC showed an aberrant IEL phenotype. Monoclonal TCR-γ rearrangements were detected in 8/13 (62%), 8/10 (80%), and 4/9 (44%) of gastric, colonic, and blood samples, respectively, from RCS patients, while in CD patients such rearrangements were only found in 2/25 (8%) gastric samples. Conclusion: The immunophenotypically aberrant monoclonal IEL population present in the small intestine of patients with RCS frequently disseminates to the blood and the entire gastrointestinal epithelium, suggesting that this is a diffuse gastrointestinal disease.

Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. “Gastritis” is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62–73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa–associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori–induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn’s disease are distinct morphologic entities. Lymphocytic gastritis and eosinophilic gastritis have a variety of clinical associations. Carditis is a controversial topic: currently opinions are divided as to whether it is the result of gastroesophageal reflux or a proximal extension of H. pylori infection from the remainder of the stomach.

An increase in gastric intraepithelial lymphocytes has been observed in some patients with the typical small intestinal changes of celiac disease. To date, no clinical parameters have been described that identify the subset of patients more likely to have gastric involvement. In this study we compared the clinical features of celiac disease patients with and without lymphocytic gastritis to determine if the presence of gastric involvement at diagnosis portends a more severe form of celiac disease. We reviewed the pathology reports and hematoxylin and eosin-stained slides of 304 patients with biopsy-proven celiac disease diagnosed over an 11-year period. Thirty-nine of these patients had lymphocytic gastritis. Compared to patients without gastric involvement, those with lymphocytic gastritis were statistically more likely to be diagnosed at an earlier age and present with more profound laboratory findings and duodenal mucosal damage compared to patients with celiac disease without gastric involvement. These findings indicate that in the pediatric population, the presence of lymphocytic gastritis in celiac disease defines a unique group of patients with more severe disease (by clinical and laboratory measures) at the time of diagnosis.