Giant Gastric Folds in Juvenile Polyposis

To advance the diagnostic accuracy of juvenile polyposis syndrome, an important yet often difficult diagnosis, we describe in detail a new and medically significant presentation. This hereditary and high-risk GI cancer syndrome is often associated with hereditary hemorrhagic telangiectasia, as in this 47-year-old female patient with a <i>SMAD4</i> germline pathogenic mutation. Total gastrectomy revealed giant gastric folds with inflamed foveolar hyperplasia consuming most of the gastric cardia and body but sparing the antrum. Together, this gross and histologic pathology mimics Ménétrier’s disease, an exceedingly rare and acquired protein-losing hypertrophic gastropathy. Classical gastric juvenile polyposis almost always and principally involves the antrum with multiple distinctive inflammatory <i>polyps</i> rather than the newly illustrated <i>giant gastric folds</i> of this case. No reports of giant gastric folds in juvenile polyposis have appeared in the literature. The distinction between juvenile polyposis and Ménétrier’s disease is essential due to their disparate clinical outcomes and management. The differential considerations for giant gastric folds and inflamed gastric foveolar hyperplasia are fully reviewed. On the basis of this report, the differential for giant gastric folds must now expand to include juvenile polyposis syndrome. Genetic testing for pathogenic germline mutations of the 2 known causative genes of this syndrome, namely <i>SMAD4</i> and <i>BMPR1A</i>, are readily available and should become part of the evaluation of giant gastric folds, particularly in view of the neoplastic and hereditary aspects of juvenile polyposis syndrome.

Helicobacteriosis: changes of the mucosa in disorder of motor functions (motorics) in the gastroesophagal and duodenogastral zones of the stomach

The morphological changes in the gastric mucosa in the presence of duodenogastric reflux and refluxesophagitis and their connection with the presence of Helicobacter pylori (HP) infection are studied. The endoscopic and histological examination of the stomach antral part was performed in 1251 patients with different gastroduodenal pathologies. HP was diagnosed by histological and real-time PCR methods. Among patients with different gastroduodenal pathologies the frequency of H. pylori infection was 77.9 %. Duodenogastric reflux was detected in 23.9 % of patients. In the presence of duodenogastric reflux, we have found a decrease in the risk of duodenal ulcer by a factor of 2.5, thus duodenogastric reflux may protect against the development of duodenal ulcer. In patients with duodenogastric reflux in the presence of H. pylori infection, significant differences from the group uninfected of Helicobacter pylori were found in the metaplasia frequency. A significant increase in the frequency of foveolar hyperplasia among patients with duodenogastric reflux was revealed. The prevalence of reflux-esophagitis in the study group was 8.3 %. No increased risk in reflux-esophagitis was observed either in the HP-positive or HP-negative cases. According to our finding, duodenogastric reflux was characterized by foveolar hyperplasia and metaplasia. We suggest that the presence or absence of H. pylori does not affect reflux-esophagitis.

Evaluation of Lineage Changes in the Gastric Mucosa Following Infection With Helicobacter pylori and Specified Intestinal Flora in INS-GAS Mice

Gastric adenocarcinoma develops in metaplastic mucosa associated with Helicobacter pylori infection in the stomach. We have sought to evaluate the precise lineage changes in the stomachs of insulin-gastrin (INS-GAS) mice infected with H. pylori and/or intestinal flora (Altered Schaedler’s Flora; ASF). Stomachs from groups infected with H. pylori contained progressive spasmolytic polypeptide-expressing metaplasia (SPEM) compared with germ-free and mice infected with ASF alone. The overall phenotype of the H. pylori-infected mice was dominated by Ulex europaeus lectin (UEAI)-positive foveolar hyperplasia that was distinct from GSII/CD44v9-positive SPEM. However, in the mice with H. pylori co-infected with ASF, we identified a subpopulation of UEAI-positive foveolar cells that co-expressed intestinal mucin 4 (MUC4). These regions of foveolar cells were variably positive for CD44v9 as well as TFF3. Interestingly, an intravascular lesion identified in a dual H. pylori/ASF-infected mouse expressed both UEAI and Muc4. Finally, we identified an increase in the number of tuft cells within the mucosa of H. pylori-infected groups. Our findings suggest that H. pylori infection promotes foveolar hyperplasia as well as metaplasia, while co-infection may promote progressive foveolar and metaplastic lesions as well as dysplasia. Grading of gastric lesions in mice as preneoplastic requires multiple immunostaining markers to assign lineage derivation and behavior.