13c ubt test kit for h.pylori infection
The relationship between Helicobacter pylori and chronic gastritis and peptic ulcer is already familiar to people. With the deepening of research, some new research results initially revealed that HP is also inextricably linked with other diseases. Hepatic encephalopathy (hepatic coma) in patients with liver cirrhosis is often associated with elevated blood ammonia, and HP may be one of the "culprits" of ammonia production. Practice has proved that eradication of HP can improve the clopathy and is beneficial to the recoverurative effect of hepatic encephay of encephalopathy. Experts also found that there is a kind of bacteria in liver cancer tissue that is very similar to HP.
The pathogenesis of HP:
1. HP's flagella motility: HP relies on flagella motility to penetrate the mucous layer and reach the gastrointestinal mucosa surface.
2. Urease: HP can produce a large amount of urease, which has high enzyme activity and damages the gastric mucosal epithelium through immune pathways.
3. The virulence of HP: The infection rate of HP in the population is relatively high, but it is not completely proportional to the incidence of chronic gastritis and peptic ulcer. Some carriers do not get sick. There may be two reasons for this, namely the strength of HP's virulence and the body's defensive ability.
It has been confirmed that gastric infection caused by Helicobacter pylori is the main cause of gastritis. The detection rate of HP in active and severe gastritis is 90%-100%. The detection rate of HP in children with duodenal ulcer is about 52.6%-62.9%. Where HP turns negative, the recurrence rate of ulcers is low (less than 4%).
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