Background Although many studies have found an association between Helicobacter pylori infection and the development of gastric cancer, many aspects of this relation remain uncertain. Methods We prospectively studied 1526 Japanese patients who had duodenal ulcers, gastric ulcers, gastric hyperplasia, or nonulcer dyspepsia at the time of enrollment; 1246 had H. pylori infection and 280 did not. The mean follow-up was 7.8 years (range, 1.0 to 10.6). Patients underwent endoscopy with biopsy at enrollment and then between one and three years after enrollment. H. pylori infection was assessed by histologic examination, serologic testing, and rapid urease tests and was defined by a positive result on any of these tests. Results Gastric cancers developed in 36 (2.9 percent) of the infected and none of the uninfected patients. There were 23 intestinal-type and 13 diffuse-type cancers. Among the patients with H. pylori infection, those with severe gastric atrophy, corpus-predominant gastritis, and intestinal metap...

Helicobacter pylori infection and the development of gastric cancer

Retrospective study: The diagnostic accuracy of conventional forceps biopsy of gastric epithelial compared to endoscopic submucosal dissection (STROBE compliant).

An international group of endoscopists, surgeons, and pathologists gathered in Paris for an intensive workshop designed to explore the utility and clinical relevance of the Japanese endoscopic classification of superficial neoplastic lesions of the GI tract. This report summarizes the conclusions of the workshop and proposes a general framework for the endoscopic classification of superficial lesions of the esophagus, stomach, and colon. The clinical relevance of this classification is demonstrated in tables that show the relative proportion of each subtype in the esophagus, stomach, and colon, assessing the risk of submucosal invasion and the risk of lymph node metastases. In the esophagus, stomach, and colon, neoplastic lesions of the digestive tract are called ‘‘superficial’’ at endoscopy when the endoscopic appearance suggests either a small cancer or a noninvasive neoplastic lesion (dysplasia/adenoma). If invasive, ‘‘superficial’’ tumors correspond to the T1 stage of the TNM classification, in which invasion is limited to the mucosa and submucosa. ‘‘Superficial’’ tumors are nonobstructive, usually are asymptomatic, and often are detected as an incidental finding or by screening. In Japan, neoplastic lesions of the stomach with a ‘‘superficial’’ endoscopic appearance are classified as subtypes of ‘‘type 0.’’ The term ‘‘type 0’’ was chosen to distinguish the classification of ‘‘superficial’’ lesions from the Borrmann classification, proposed in 1926 for ‘‘advanced’’ gastric tumors, which included types 1 to 4. Within type 0, there are polypoid and non-polypoid subtypes. The nonpolypoid subtypes include lesions with a small variation of the surface (slightly elevated, flat, and slightly depressed) and excavated lesions. The Japanese Gastric Cancer Association (JGCA) also added a type 5 for unclassifiable advanced tumors. The complete modification for gastric tumors becomes:

The Paris endoscopic classification of superficial neoplastic lesions : esophagus, stomach and colon.

https://www.gastrojournal.org/article/S0016-5085(01)00796-X/pdf

Chronic pancreatitis: Diagnosis, classification, and new genetic developments

These guidelines provide a practical and evidence-based resource for the management of patients with Barrett's oesophagus and related early neoplasia. The Appraisal of Guidelines for Research and Evaluation (AGREE II) instrument was followed to provide a methodological strategy for the guideline development. A systematic review of the literature was performed for English language articles published up until December 2012 in order to address controversial issues in Barrett's oesophagus including definition, screening and diagnosis, surveillance, pathological grading for dysplasia, management of dysplasia, and early cancer including training requirements. The rigour and quality of the studies was evaluated using the SIGN checklist system. Recommendations on each topic were scored by each author using a five-tier system (A+, strong agreement, to D+, strongly disagree). Statements that failed to reach substantial agreement among authors, defined as >80% agreement (A or A+), were revisited and modified until substantial agreement (>80%) was reached. In formulating these guidelines, we took into consideration benefits and risks for the population and national health system, as well as patient perspectives. For the first time, we have suggested stratification of patients according to their estimated cancer risk based on clinical and histopathological criteria. In order to improve communication between clinicians, we recommend the use of minimum datasets for reporting endoscopic and pathological findings. We advocate endoscopic therapy for high-grade dysplasia and early cancer, which should be performed in high-volume centres. We hope that these guidelines will standardise and improve management for patients with Barrett's oesophagus and related neoplasia.

https://gut.bmj.com/content/gutjnl/63/1/7.full.pdf

British Society of Gastroenterology guidelines on the diagnosis and management of Barrett's oesophagus

Background—Use of the conventional Western and Japanese classification systems of gastrointestinal epithelial neoplasia results in large diVerences among pathologists in the diagnosis of oesophageal, gastric, and colorectal neoplastic lesions. Aim—To develop common worldwide terminology for gastrointestinal epithelial neoplasia. Methods—Thirty one pathologists from 12 countries reviewed 35 gastric, 20 colorectal, and 21 oesophageal biopsy and resection specimens. The extent of diagnostic agreement between those with Western and Japanese viewpoints was assessed by kappa statistics. The pathologists met in Vienna to discuss the results and to develop a new consensus terminology. Results—The large diVerences between the conventional Western and Japanese diagnoses were confirmed (percentage of specimens for which there was agreement and kappa values: 37% and 0.16 for gastric; 45% and 0.27 for colorectal; and 14% and 0.01 for oesophageal lesions). There was much better agreement among pathologists (71% and 0.55 for gastric; 65% and 0.47 for colorectal; and 62% and 0.31 for oesophageal lesions) when the original assessments of the specimens were regrouped into the categories of the proposed Vienna classification of gastrointestinal epithelial neoplasia: (1) negative for neoplasia/dysplasia, (2) indefinite for neoplasia/dysplasia, (3) non-invasive low grade neoplasia (low grade adenoma/ dysplasia), (4) non-invasive high grade neoplasia (high grade adenoma/ dysplasia, non-invasive carcinoma and suspicion of invasive carcinoma), and (5) invasive neoplasia (intramucosal carcinoma, submucosal carcinoma or beyond). Conclusion—The diVerences between Western and Japanese pathologists in the diagnostic classification of gastrointestinal epithelial neoplastic lesions can be resolved largely by adopting the proposed terminology, which is based on cytological and architectural severity and invasion status. (Gut 2000;47:251‐255)

https://gut.bmj.com/content/gutjnl/47/2/251.full.pdf

The Vienna classification of gastrointestinal epithelial neoplasia

Background —The pathology of non-alcoholic chronic pancreatitis has not yet been sufficiently studied. Aims —To identify the major changes of pancreatic tissue in patients surgically treated for non-alcoholic chronic pancreatitis. Patients —Pancreatectomy specimens from 12 patients with non-alcoholic chronic pancreatitis, including four patients with autoimmune or related diseases (Sjogren’s syndrome, primary sclerosing cholangitis, ulcerative colitis, and Crohn’s disease), were reviewed. Methods —Morphological changes were studied histologically and immunohistochemically (to type inflammatory cells) and compared with the pancreatic alterations found in 12 patients with alcoholic chronic pancreatitis. Results —In patients with non-alcoholic chronic pancreatitis, with or without associated autoimmune or related diseases, pancreatic inflammation particularly involved the ducts, commonly resulting in duct obstruction and occasionally duct destruction. None of these features was seen in alcoholic chronic pancreatitis which, however, showed pseudocysts and calcifications. Conclusion —The pancreatic changes in patients with non-alcoholic chronic pancreatitis clearly differ from those with alcoholic chronic pancreatitis. The term chronic duct destructive pancreatitis is suggested for this type of pancreatic disease.

https://gut.bmj.com/content/gutjnl/41/2/263.full.pdf

F Borchard

Papers

The Vienna classification of gastrointestinal epithelial neoplasia

Non-alcoholic duct destructive chronic pancreatitis

Primary duct-destructive chronic pancreatitis, possibly of autoimmune origin

Pathology of chronic idiopathic duct-destructive pancreatitis