H. pylori infection is also associated with a 1–2% lifetime risk of stomach cancer and a less than 1% risk of gastric MALT lymphoma.In the absence of treatment, H. pylori infection – once established in its gastric niche – is widely believed to persist for life. In the elderly, however, infection likely can disappear as the stomachs mucosa becomes increasingly atrophic and inhospitable to colonization. The proportion of acute infections that persist is not known, but several studies that followed the natural history in populations have reported apparent spontaneous elimination.It is possible for H. pylori to re-establish in a person after eradication. This recurrence can be caused by the original strain (recrudescence), or be caused by a different strain (reinfection). According to a 2017 meta-analysis by Hu et al., the global per-person annual rates of recurrence, reinfection, and recrudescence is 4.3%, 3.1%, and 2.2% resepctively. It is unclear what the main risk factors are.Mounting evidence suggests H. pylori has an important role in protection from some diseases. The incidence of acid reflux disease, Barretts esophagus, and esophageal cancer have been rising dramatically at the same time as H. pyloris presence decreases. In 1996, Martin J. Blaser advanced the hypothesis that H. pylori has a beneficial effect by regulating the acidity of the stomach contents. The hypothesis is not universally accepted as several randomized controlled trials failed to demonstrate worsening of acid reflux disease symptoms following eradication of H. pylori.
The forces responsible for the movement of the lateral body wall folds are poorly understood, and a better understanding of these forces would help to explain why gastroschisis occurs mostly to the right of the umbilicus, while other ventral body wall defects occur in the midline.At least six hypotheses have been proposed for the pathophysiology:

Failure of mesoderm to form in the body wall
Rupture of the amnion around the umbilical ring with subsequent herniation of bowel
Abnormal involution of the right umbilical vein leading to weakening of the body wall and gut herniation
Disruption of the right vitelline (yolk sac) artery with subsequent body wall damage and gut herniation
Abnormal folding of the body wall results in a ventral body wall defect through which the gut herniates
Failure to incorporate the yolk sac and related vitelline structures into the umbilical stalkThe first hypothesis does not explain why the mesoderm defect would occur in such a specific small area. The second hypothesis does not explain the low percentage of associated abnormality compared with omphalocele. The third hypothesis was criticized due to no vascular supplement of anterior abdominal wall by umbilical vein. The fourth hypothesis was commonly accepted, but it was later shown that the right vitelline artery (right omphalomesenteric artery) did not supply the anterior abdominal wall in this area. More evidence is needed to support the fifth hypothesis.