In all the following H. pylori may be present as a cause EXCEPT
Ans. d). Gastric type metaplasia in Barrett's esophagus. (Ref. Robbin's, Pathology, 7th/ pg. 815; Harrison 18th/Ch. 151)Essentially all persons colonized with H. pylori develop a host response, which is generally termed chronic gastritis. The nature of the interaction of the host with the particular bacterial population determines the clinical outcome. H. pylori colonization increases the lifetime risk of peptic ulcer disease, noncardia gastric cancer, and B cell non-Hodgkin's gastric lymphoma. In contrast, a growing evidence indicates that H, pylori colonization (especially with cagA+- strains) protects against adenocarcinoma of the esophagus (and the sometimes related gastric cardia) and premalignant lesions such as Barrett's esophagusH. PYLORI# Most infected persons also have the associated gastritis but are asymptomatic.Morphology# H. pylori is a nonsporing, curvilinear gram-negative rod measuring approximately 3.5 x 0.5 mm.# H. pylori is part of a genus of bacteria that have adapted to the ecologic niche provided by gastric mucus.# The specialized traits that allow it to flourish include:- Motility (via flagella), allowing it to swim through viscous mucus- Elaboration of a urease, which produces ammonia and carbon dioxide from endogenous urea, thereby buffering gastric acid in the immediate vicinity of the organism- Expression of bacterial adhesins, such as Bab A, which binds to the fucosylated Lewis B blood-group antigens, enhances binding to blood group O antigen bearing cells.- Expression of bacterial toxins, such as cytotoxin association gene A (CagA) and vacuolating cytotoxin gene A (VacA).# After initial exposure to H. pylori, gastritis occurs in two patterns:- A predominantly antral-type gastritis with high acid production and elevated risk for duodenal ulcer, and- A pangastritis that is followed by multifocal atrophy (multifocal atrophic gastritis) with lower gastric acid secretion and higher risk for adenocarcinoma.# IL-1b is a potent pro-inflammatory cytokine and a powerful gastric acid inhibitor. Patients who have higher IL-1b production in response to H. pylori infection tend to develop pangastritis, while patients who have lower IL-1b production exhibit antral-type gastritis.TRANSMISSION# Oral-oral transmission,# Fecal-oral transmission, and# Environmental spread.Diseases associated with helicobacter pylori in fectionDisease AssociationChronic gastritisStrong causal associationPeptic ulcer diseaseStrong causal associationGastric carcinomaStrong causal associationGastric MALT lymphomaDefinitive etiologic roleDiagnostic Test# Noninvasive tests include a serologic test for antibodies, fecal bacterial detection, and a urea breath test.# Invasive tests are based on the identification of H. pylori in gastric biopsy tissue.# Detection methods in gastric tissue include visualization of the bacteria in histologic sections, bacterial culture, a rapid urease test, and bacterial DNA detection by the polymerase chain reaction.Current Treatment# Patients with chronic gastritis and H. pylori usually improve when treated with antibiotics.# Treatment includes antibiotics and hydrogen pump inhibitors.Tissue Morphology# Gastritis in the setting of environmental etiologies (including infection by H. pylori) tends to affect antral mucosa or both antral and body-fundic mucosa (pangastritis).# Several histologic features are characteristic:- Regenerative Change. In the neck region of the gastric glands mitotic figures are increased.- Metaplasia. The antral, body, and fundic mucosa may become partially replaced by metaplastic columnar absorptive cells and goblet cells of intestinal morphology (intestinal metaplasia)- Atrophy. Atrophy is quite frequently associated with autoimmune gastritis and pangastritis caused by H. pylori. Parietal cells, in particular, may be clearly absent in the autoimmune form.- Dysplasia. Dysplasia is thought to be a precursor lesion of gastric cancer in atrophic forms of gastritis, particularly with pernicious anemia (autoimmune gastritis) and H. pylori-chronic gastritis.
Pyloric metaplasia of duodenum
Atrophic gastritis
Intestinal metaplasia of stomach
Gastric type metaplasia in Barrett's esophagus
G.I.T.