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Chronic gastritis (Including helicobacter infection)

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Chronic gasstritis is defined as the presence of chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia usually in the absence of erosions. The epithelial changes may become dysplastic and constitute a background for the development of carcinoma. Chronic gastritis is notable for distinct causal subgroups and for patterns of histologic alterations that vary in different parts of the world. In the western world the prevalence of histologic changes indicative of chronic gastritis exceeds 50% in the later decades of life.

The major etiologic associations of chronic gastritis are as folows:

Chronic infection by H.pylori
Immunologic (autoimmune) in association with pernicious anemia
Toxic, as with alcohol ingestion and cigarette smoking Postsurgical, especially after antrectomy with gastroenterostomy with reflux of bilious duodenal secretions
Motor and mechanical, including obstruction, bezoars (luminal concretions) and gastric atony.
Radiation
Granulomatous conditions
Miscellaneous-amyloidosis, graft-versus-host disease

Helicobacter pylori

By far the most important etiologic association is chronic infection by the bacillus H.pylori. As evident in this and later discussions, this organism plays a critical role in several major gastric disease . H.pylori is present in 90% of patients with chronic gastritis affecting the antrum. Colonization rates increase with age reaching 50% in asymptomatic American elders over 50 years of age. Prevalence of infection among elders in Puerto Rico exceeds 80%. In this and other areas where infection in endemic the organism seems to be acquired in childhood and persists for decades. Most infected persons also have the associated gastritis but are asymptomatic. Nevertheless, infected persons are at increased risk for the development of peptic ulcer disease and possibly gastric cancer.

H.pylori is a nonsporing , curvilinear gram-negative rod measuring approximately 3.5* 0.5ìm. 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 H.pylori to flourish include the following:

Motility (via flagella) allowing it to swim through viscous mucus
Elaboration of urease, which produces ammonia from endogenous urea thereby buffering gastric acid in the immediate vicinity of the organism
Binging of H.pylori organisms to gastric epithelial cells via a bacterial adhesin; binding is enhanced with epithelial cells that bear the blood group O antigen

H.pylori strains that express the cagA gene are strongly associated with duodenal ulcer; the function of the 120-140kD protein product is unknown. Such strains frequently express the vacA gene also, which codes for an 87-kD vacuolating cytotoxin. These two proteins, along with bacterial lipopolysaccharide endotoxin and other protein products appear to act as proinflammatory substances. H.pylori appears to be capable of initiating and perpetuating a chronic state of gastric mucosal injury. Patients with chronic gastritis and H.pylori usually improve when treatd with antimicrobial agents, and replapses are associated with reappearance of this organism.

Autoimmune gastritis

This form of gastritis accounts for less than 10% of cases of chronic gastritis. It results from the presence of autoantibodies to the gstric gland parietal cells and intrinsic factor including one against the acid-producing enzyme, H+,K+,ATPase. Gland destruction and mucosal atrophy lead to loss of acid production. In the most severe cases, production of intrinsic factor is lost, leading to pernicious anemia. This uncommon form of gastritis is seen in association with other autoimmune disorders, such as Hashimoto thyroiditis and Addison disease.

Clinical features

Chronic gastritis usually causes few symptoms. Nausea, vomiting and upper abdominal discomfort may occur. Individuals with advanced gastritis from H.pylori or other environmental causes are often hypochlorhydric, owing to parietal cell damage and atrophy of body-fundic mucosa. Because parietal cells are never completely destroyed however , these patients do not develop achlohydria or pernicious anemia. Serum gastrin levels are usualy within the normal range or only modestly elevated. Most important is the relationship of chronic gastritis to the development of peptic ulcer and gastric carcinoma. Most patients with a peptic ulcer, whether duodenal or gastric, have H.pylori infection. The long-term risk of gastric cancer in persons with autoimmune gastritis is 2 to 4 % which is considerably greater than the normal population.

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