WHAT IS HELICOBACTER PYLORI?
Helicobacter pylori is a gram-negative bacterium which colonises gastric epithelium. It has evolved the ability to overcome the highly acidic environment of the stomach by metabolising urea to ammonia, thus generating a neutral environment. Helicobacter pylori infection is associated with low socioeconomic status and crowded living conditions, especially in childhood. Helicobacter pylori is a helical, or spiral-shaped, bacterium that lives in the stomach. No one knows how long it has been working its mischief,but the best guess is that it has been around for several millennia. Infection with H. pylori is associated with a number of diseases including stomach and duodenal ulcers, as well as certain cancers. However, only a small fraction of infected people experience noticeable symptoms,and for that reason diagnosis of the infection is quite low when compared to the number of people who are actually infected. Even in those who eventually develop ulcers, these symptoms—which include burping, nausea, and burning or aching in the stomach—are usually subtle and can be confused with other diseases. As a result, the infection often goes undetected for many years.It is precisely because H. pylori infection is not associated with a hallmark set of outward symptoms that it took centuries to establish the relationship between H. pylori infection and ulcers.
H. Pylori Infection
Helicobacter pylori infects about 50% of the world’s population and is a major cause of chronic gastritis, is strongly associated with the development of gastric and duodenal ulcers and has been linked with gastric adenocarcinoma and B-cell mucosa-associated lymphoid tissue lymphoma . H. pylori Infection results in a sequence of events, ultimately resulting in the development of some gastrointestinal disorders. The sequence was first suggested by Correa et al. in 1975 and has since been supported by many other studies. Colonization of the gastric mucosa by H. pylori first lead to the induction of an inflammatory response, predominantly by Th1 (T helper cells type 1). The initial acute gastritis is followed by active chronic gastritis, which lasts for life if the infection is not treated. Nevertheless, H. pylori-positive subjects are mostly unaware of this inflammation due to the lack of clinical symptoms. The Th1 response results in epithelial cell damage rather than in the removal of H. pylori because H. pylori is not an intracellular pathogen.
The ongoing presence of H. pylori thus causes a lifelong proinflammatory response coupled to cellular damage and initiates the histological cascade. The continuous production of reactive oxygen species that results from the ongoing inflammation can result in DNA damage, thus inducing the multiple mutations thought to be required for initiation of the cancer c. Among the new methods of magnifying endoscopy, a prototype of endocytoscopy developed by Olympus was used for ex vivo visualization of Helicobacter pylori on experimentally infected gastric biopsies. Moving bacteria were observed at 1100× magnification, giving hope for a possible direct detection during endoscopy. Kim et al. also used magnifying endoscopy on 103 patients to classify the gastric surface according to four patterns: flat, irregular, papillary or nonstructured, which were then compared to the updated Sydney System for histologic gastritis. Histologic gastritis was found in 91% of the biopsy sections with a nonflat type, and among them, 96% were confirmed to harbor H. pylori infection. In another study, the magnified endoscopic findings in the gastric body were classified into four patterns and then correlated with histology results. Type 1 pattern corresponded to normal gastric mucosa, types 2 and 3 to H. pylori -infected mucosa and type 4 to atrophy. The sensitivity and specificity for these endoscopic findings were 92.7% and 100% for type 1, and 100% and 92.7% for types 2 and 3 together, respectively.