Gastric foveolar metaplasia and gastric heterotopia in the duodenum: no evidence of an etiologic role for Helicobacter pylori.
Summary of "Gastric foveolar metaplasia and gastric heterotopia in the duodenum: no evidence of an etiologic role for Helicobacter pylori."
Gastric-type epithelium and islands of oxyntic mucosa in duodenal biopsies are considered by some to be part of a spectrum of metaplastic change related to peptic disorders. This study was designed to assess prevalence and associations of metaplastic-heterotopic gastric mucosa in the duodenum. Demographic, clinical, and histopathologic data from patients who had duodenal biopsy specimens for a 12-month period were collected from a national database. The duodenal findings of patients with duodenitis, gastric metaplasia, and gastric heterotopia were correlated with gastric pathology, Helicobacter pylori status, and clinical information. Of 28 210 patients with duodenal biopsy specimens, 80.9% were healthy, 2.1% had active duodenitis, 2.2% gastric foveolar metaplasia without active inflammation ("peptic duodenopathy"), 4.8% gastric foveolar metaplasia with active inflammation ("peptic duodenitis"), and 1.9% gastric heterotopia. Helicobacter pylori was documented in 9.8% of patients with normal duodenum, 6.9% of those with gastric metaplasia without active inflammation, 15.8% of those with active duodenitis, and 29.1% of those with gastric foveolar metaplasia with active inflammation; 2.2% of 543 patients with gastric heterotopia had H pylori gastritis. Helicobacter pylori was detected in the metaplastic epithelium of 67.6% of patients with active inflammation and in 16.4% of those with metaplasia without inflammation. Gastric heterotopia was strongly associated with concurrent fundic gland polyps. In conclusion, active duodenitis was more common in patients with H pylori infection, but gastric metaplasia was not. We suggest that there is insufficient evidence to ascribe duodenitis with foveolar metaplasia to a "peptic" disorder, as "peptic duodenopathy" and "peptic duodenitis" seem to imply. Gastric heterotopia is likely a congenital lesion; its association with fundic gland polyps suggests that use of proton pump inhibitors may enhance its endoscopic detection.
Caris Diagnostics, Gastrointestinal Pathology, Irving, TX 75039, USA; Dallas VAMC and University of Texas Southwestern medical Center, Dallas, TX 75016, USA.
This article was published in the following journal.
Name: Human pathology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20656325
- DOI: http://dx.doi.org/10.1016/j.humpath.2010.04.010
Extra-ampullary duodenal adenocarcinomas are rare, and when studied, frequently have been grouped with jejunoileal adenocarcinomas. Nevertheless, anecdotal experiences suggest that these neoplasms may...
Patients with juvenile polyposis syndrome (JPS), a hereditary autosomal dominant hamartomatous polyposis syndrome, are at increased risk for colorectal adenocarcinoma. The upper gastrointestinal tract...
There are currently no accepted clinical guidelines for the surveillance of first-degree relatives (FDRs) of gastric cancer patients. The existence of intestinal metaplasia, as well as altered mucin e...
Gastric intestinal metaplasia (IM) occurs in response to different injuries, some of which involve increased risk for gastric cancer, whereas others may not. The background in which IM arises has not ...
The purpose of this study is to assess whether confocal laser endomicroscopy can reduce the biopsy number needed per patient for the detection of gastric intestinal metaplasia without the ...
Helicobacter pylori (H. pylori) is associated with gastric cancer in epidemiological studies.Gastric atrophy and intestinal metaplasia caused by H. pylori are considered as precancerous le...
No accurate, inexpensive and non-invasive test for gastric cancer screening is currently available. The investigators' recent study identified a1-antitrypsin and other proteins as potentia...
In case of gastric cancer, the incidence of HER-2 positivity (2+, 3+ on IHC and/or FISH (+)) is reported as similar as that of breast cancer, that is 22% of all cases. A recent ToGA Trial,...
This prospective, multi-center, non-interventional study will evaluate the effic acy and safety of Herceptin (trastuzumab) in routine clinical practice in Chines e patients with gastric or...
Medical and Biotech [MESH] Definitions
A synthetic methylprostaglandin E1 analog that reduces gastric acid secretion and enhances the gastric mucus-bicarbonate barrier. It is effective in the therapy of gastric ulcers and gives significant protection against NSAID-induced gastric mucosal damage. The drug also prevents cyclosporin A-induced damage to endocrine and exocrine pancreatic secretions. It shows a low order of acute toxicity and there is no evidence of embryotoxicity, fetotoxicity, teratogenicity, or mutagenicity in animal studies.
Abnormal distention of the STOMACH due to accumulation of gastric contents that may reach 10 to 15 liters. Gastric dilatation may be the result of GASTRIC OUTLET OBSTRUCTION; ILEUS; GASTROPARESIS; or denervation.
Vagal denervation of that part of the STOMACH lined with acid-secreting mucosa (GASTRIC MUCOSA) containing the GASTRIC PARIETAL CELLS. Since the procedure leaves the vagal branches to the antrum and PYLORUS intact, it circumvents gastric drainage required with truncal vagotomy techniques.
Endocrine cells which secrete GASTRIN, a peptide that induces GASTRIC ACID secretion. They are found predominantly in the GASTRIC GLANDS of PYLORIC ANTRUM in the STOMACH, but can also be found in the DUODENUM, nervous and other tissues.
Rounded or pyramidal cells of the GASTRIC GLANDS. They secrete HYDROCHLORIC ACID and produce gastric intrinsic factor, a glycoprotein that binds VITAMIN B12.