Treatment of H. pylori is required in all of the following expect?

H. pylori is Gram-negative and spiral, and has multiple flagella at one end, which make it motile, allowing it to burrow and live beneath the mucus layer adherent to the epithelial surface. It uses an adhesin molecule (BabA) to bind to the Lewis b antigen on epithelial cells. Here the surface pH is close to neutral and any acidity is buffered by the organism's production of the enzyme urease. This produces ammonia from urea and raises the pH around the bacterium and between its two cell membrane layers. H. pylori exclusively colonises gastric-type epithelium and is found in the duodenum only in association with patches of gastric metaplasia. It causes chronic gastritis by provoking a local inflammatory response in the underlying epithelium . This depends on numerous factors, notably expression of bacterial cagA and vacA genes. The CagA gene product is injected into epithelial cells, interacting with numerous cell-signalling pathways involved in cell replication and apoptosis. H. pylori strains expressing CagA (CagA+) are more often associated with disease than CagA- strains. Most strains also secrete a large pore-forming protein called VacA, which causes increased cell permeability, efflux of micronutrients from the epithelium, induction of apoptosis and suppression of local immune cell activity. Several forms of VacA exist and pathology is most strongly associated with the s1/ml form of the toxin. The distribution and severity of H. pylori-induced gastritis determine the clinical outcome. In most people, H. pylori causes a mild pangastritis with little effect on acid secretion and the majority develop no significant clinical outcomes. In a minority is is responsible for causation of gastric lypomas,gastric carcinoma, gastric ulcers, duodenal ulcers Ref Davidson edition23rd pg798