Sulfomucins in Helicobacter pylori–Associated Chronic Gastritis in Children: Is This Incipient Intestinal Metaplasia?

Abstract

This finding may represent a "minimal" form of incomplete intestinal metaplasia (type III). Because the nine patients had been untreated, the change is probably reversible. Two follow-up biopsies in patients in whom H. pylori had been treated and eradicated showed absence of sulfated mucins. Although these findings cannot be regarded as fully developed type III intestinal metaplasia, it is possible that left untreated, the alteration may persist and evolve into some other complication. This conclusion justifies follow-up of these patients.

Histopathology and expression of Ki-67 and cyclooxygenase-2 in childhood Helicobacter pylori gastritis

“…Because the Ki-67 protein is present during all active phases of the cell cycle, but is absent from resting cells, it makes an excellent marker for cell proliferation. 25 Increased epithelial cell proliferation has also been observed in H. pylori-associated gastritis, 7 atrophic gastritis, 26 and gastric cancer. 27,28 Our study also showed increased gastric glandular and foveolar epithelial cell proliferation in H. pylori-infected children, and this was correlated with acute and chronic inflammation, H. pylori density, glandular atrophy, intestinal metaplasia, and COX-2 expression.…”

“…Intestinal metaplasia is also known to be rare in children; nevertheless, we found that low-grade intestinal metaplasia occurred in 13.5% of infected children, but that intestinal metaplasia was absent in all H. pylori-uninfected children. Cohen et al 25 showed that alcian blue-periodic acid Schiff (PAS) staining, suggestive of a "minimal" form of incomplete intestinal metaplasia, was positive in 8 of 15 infected children, although this was not apparent on H&E-stained tissue samples. This result supports our result with respect to the occurrence of minimal changes of intestinal metaplasia at an early stage of infection.…”

Evaluation of gastric histology in children and adolescents with Helicobacter pylori gastritis using the Update Sydney System

“…However, a previous study with similar goals studied 15 patients -some of them more than once -, whereas another study compared the histological assessment of 19 infected patients to that of 45 healthy controls (5,11) . The second limitation is the method of staining used in the study, because some authors reported that staining with alcian blue-periodic acid Schiff (PAS) enhances the detection of incomplete intestinal metaplasia due to the detection of sulphated mucossubstances (6) . This is an important limitation as it could prevent the detection of incomplete intestinal metaplasia.…”

“…Helicobacter pylori gastritis has unique features in children, such as the nodular aspect of the gastric antrum, antral predominance of gastritis in most patients, and uncommon diagnosis of gastric atrophy and intestinal metaplasia. Nevertheless, sulphomucincontaining cells have been described in the gastric mucosa of H. pylori infected children, suggesting that incomplete intestinal metaplasia (type III) can develop even during childhood and evolve into complete intestinal metaplasia in adults (6) . The Updated Sydney System has provided guidelines for classifying, grading and reporting on endoscopic and histological assessment of gastric mucosa (7) .…”

Selected Reaction Monitoring to Differentiate and Relatively Quantitate Isomers of Sulfated and Unsulfated Core 1 O-Glycans from Salivary MUC7 Protein in Rheumatoid Arthritis

“…Ulcerative colitis pathogenesis has been associated with an increase in sulfated O-glycans (13), and sulfated mucins have also been identified in patients with Helicobacter pylori infection (14) and in severe ventilatorassociated pneumonia (15).…”