PubMed · 9590067
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S Miyabayashi. 1998. [Fumarase deficiency].. https://pubmed.ncbi.nlm.nih.gov/9590067/
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Helicobacter pylori is the major cause of chronic gastritis worldwide. With an estimated rate of infection of over one half of the world's population, it is responsible for extensive morbidity and mortality. Infection with this organism does not appear to spontaneously resolve. Instead it reaches a chronic stage from which a number of outcomes are possible. This article reviews those outcomes that have been linked to H. pylori and explores the pathogenesis while attempting to resolve the discrepant paths infection can take. The associations include duodenal and gastric ulcers and the majority of gastric lymphomas of B-cell type derived from the mucosa-associated lymphoid tissue (MALT). Chronic gastritis has also been shown to evolve into atrophy with intestinal metaplasia in certain populations. This change in the gastric epithelium has been linked with an increased risk of gastric adenocarcinoma. Microsc. Res. Tech. 48:313-320, 2000. Published 2000 Wiley-Liss, Inc.
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BACKGROUND: The accumulation of periodic acid Schiff (PAS)-positive material in the epithelium in microvillous atrophy (MVA) is diagnostic but unexplained. It occurs earlier in the epithelial life cycle than the formation of microvillous inclusions and warrants further investigation. METHODS: Scanning photometry was used to assess the distribution of the PAS-positive material within epithelial cells and to assess how this changed with position on the crypt-villus axis. Thiery staining was applied to test the PAS positivity of the secretory granules, and quantitative ultrastructural morphometry was used to study secretory granule distribution in the epithelium. RESULTS: The PAS abnormality arose in upper crypt epithelium in congenital and late-onset MVA and continued up the villus. Thiery staining demonstrated that the secretory granules were PAS positive. Quantitative morphometry showed that secretory granules in congenital MVA were predominantly present in upper crypt and declined in the low villus. In late-onset MVA, secretory granules arose in the upper crypt but predominated in the low villus region. No evidence of secretory granule coalescence with the apical membrane was seen, although evidence of crinophagy was observed. Secretory granule profiles were seen, indicating that they formed part of a membrane-bound vesicular network within the cell, rather than existing simply as discrete bodies. The Golgi complex appeared normal. CONCLUSIONS: The secretory granules are responsible for the PAS-positive staining in upper crypt and low villus regions in MVA. They appear to form an intracytoplasmic vesicular network, undergo crinophagy, and decline in prominence in the low to midvillous region. The absence of evidence of coalescence with the apical membrane indicates that the secretory granules arise from a post-Golgi block in exocytosis rather than from endocytosis of gut luminal contents. Periodic acid-Schiff positivity in upper villous regions arises from microvillous inclusions and lysosomal bodies.