Enterochromaffin-like (ECL) cells Hyperplasia in Fundic Gland Polyp and Its Association with the Usage of Proton Pump Inhibitors

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Solitary Peutz-Jeghers Type Polyp of Jejunum with Gastric Fundic and Antral Gland Lining Mucosa: A Case Report and Review of Literature

Solitary Peutz-Jeghers type polyps are characterized by a hamartomatous polyp of the gastrointestinal (GI) tract in a patient without mucocutaneous pigmentation, family history of Peutz-Jeghers syndrome, or STK11/LKB1 mutations. Histologically identical to the polyps in Peutz-Jeghers syndrome, these sporadic polyps can arise anywhere along the GI tract, with typical arborizing smooth muscles extending from the muscularis mucosa. While the lining mucosa is generally the same as the organ in which it arises, gastric pyloric and osseous metaplasia have been reported in intestinal polyps in Peutz-Jeghers syndrome. Herein, the authors report the first case of a small intestinal solitary Peutz-Jeghers type polyp with gastric antral and fundic gland lining mucosa. A 43-year-old male was admitted for small bowel obstruction. Diagnostic laparoscopy revealed jejuno-jejunal intussusception with an associated polyp measuring 7.2 cm. Histological examination showed a hamartomatous polyp with arborizing smooth muscle bundles extending from the muscularis mucosae. The polyp was lined by non-dysplastic gastric antral and fundic gland mucosa, and was sharply demarcated from the adjacent non-polypoid intestinal mucosa. Colonoscopy, esophagogastroduodenoscopy and small bowel enteroscopy revealed no additional polyps or masses. Thorough investigation of the patient's family history was negative for Peutz-Jeghers syndrome or mucocutaneous pigmentation. Molecular analysis of the lesion was negative for STK11/LKB1 mutations. A diagnosis of solitary Peutz-Jeghers type polyp of the small bowel with gastric antral and fundic gland mucosal lining was rendered.

The Apelinergic System Immuno-Detection in the Abomasum and Duodenum of Sheep Grazing on Semi-Natural Pasture

Apelin (APLN) is an adipokine mainly produced by adipose tissue and related to an individual’s nutritional status as well as digestive apparatus functions. In this work, APLN and its receptor (APLNR) were investigated, by immunohistochemistry, in the abomasum and duodenum of 15 Comisana × Appenninica adult sheep reared in a semi-natural pasture. Organ samples were collected after maximum pasture flowering (M × F group) and after maximum pasture dryness (M × D group); the experimental group (E × p group) received a feed supplementation of 600 grams/day/head of barley and corn in addition to M × D group feeding. APLN and APLNR were identified in the lining epithelium and the fundic gland chief cells of the abomasum. APLNR was observed in the lining epithelium, in the crypts and the serotonin secreting cells of the duodenum. Similar reactivity was observed between the M × F and E × p groups, while the M × D group showed a lower intensity of immunostaining for both APLN and APLNR in all positive structures but the duodenal serotonin neuroendocrine cells. Hence, our findings show that the E × p group presents a picture quite overlapped with M × F and suggest that food supplementation has a maintaining effect on the apelinergic system expression in the investigated digestive tracts of the sheep.

Pathological Diversity of Gastric Cancer from the Viewpoint of Background Condition

<b><i>Background:</i></b> The prevalence of <i>Helicobacter pylori</i> infection and chronic atrophic gastritis is decreasing in Japan, which has led to a decline in the incidence of gastric cancer. However, there are various subtypes of gastric cancer that arise from the background mucosa without <i>H. pylori</i> infection, and their histological characteristics are distinct from those of gastric cancer with chronic atrophic gastritis. <b><i>Summary:</i></b> In this review, after a brief overview of conventional gastric carcinoma with <i>H. pylori</i> infection, including its molecular classification, histological characteristics of gastric cancer after eradicating <i>H. pylori</i> are described. The clinicopathological characteristics of gastric cancer independent of <i>H. pylori</i> infection are then explained. Autoimmune gastritis (type A gastritis) increases the risk of gastric adenocarcinoma and neuroendocrine tumors. Gastric carcinoma without <i>H. pylori</i> infection has various histological subtypes, including fundic gland-type adenocarcinoma (oxyntic gland adenoma), foveolar-type adenocarcinoma/adenoma, signet ring cell carcinoma, and adenocarcinoma of the esophagogastric junction. In addition, some familial gastric cancer syndromes, including hereditary diffuse gastric cancer, familial adenomatous polyposis, and gastric adenocarcinoma and proximal polyposis of the stomach, are also discussed. <b><i>Key Messages:</i></b> Although the incidence of gastric cancer will decrease in the near future, the diversity of gastric cancer pathology will be enhanced because <i>H. pylori</i>-negative gastric cancer will have a significant impact on the clinical practice guidelines for gastric cancer. Gastroenterologists and pathologists should be aware of the morphological diversity of <i>H. pylori</i>-negative gastric cancer, and attention should be paid to the status of the background gastric mucosa while examining gastric cancer.