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Pathogenesis:
Acid resistant: Due to urease enzyme which converts urea into NH3. NH3 buffers the acidic
pH of stomach.
Adhesins: Mostly, H. pylori remains in the mucosa. Some of them express adhesins and gets
attached to the mucous lining. The adhesins are: - Adherence associated lipoprotein, - Blood
group antigen binding protein
2. Pathological changes:
Exotoxins: 1. Vacuolating cytotoxin, 2. Cytotoxin associated gene A (cagA)
The vacuolating cytotoxin forms vacuoles in the cytoplasm of lining epithelial cells. (actual
pathway, Presence of vacuolating cytoplasm expression of anionic channel osmotically
influx of water formation of vacuoles) and they also cause decreased proliferation of T-
cell and inhibits antigen presentation of B-cell. They also inhibit NO release from
macrophages and hence survives
Endotoxin: The LPS of bacteria mimics the antigen expressed on parietal cell of gastric
antrum. (that antigen is H/K ATPase pump)
- Smoking, eating salty food and canned food. Vitamin C and anti-oxidants have protective effect.
- Inverse relation with : GERD, Barret’s esophagus, adenocarcinoma of esophagus, inflammatory
condition like asthma.
Lab diagnosis:
Urea breath test and stool examination are done for monitoring treatment
Antibody detection: ELISA could be done to detect IgG in serum.