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Rapid urease test, also known as the CLO test (Campylobacter-like organism test), is a rapid diagnostic test for diagnosis of Helicobacter pylori. [1] The basis of the test is the ability of H. pylori to secrete the urease enzyme, which catalyzes the conversion of urea to ammonia and carbon dioxide.
Several anti-ulcer dosing regimens that combine antibiotics and proton pump inhibitors (PPI) to treat helicobacter pylori (H. pylori) induced peptic ulcer disease (PUD). The role of antibiotic in the therapies is to eradicate H. pylori, while the action of PPI is to reduce gastric acid secretion. The anti-ulcer dosing regimens generally repair ...
H. pylori is able to adhere to the surface of the phagocytes and impede their action. This is responded to by the phagocyte in the generation and release of oxygen metabolites into the surrounding space. H. pylori can survive this response by the activity of catalase at its attachment to the phagocytic cell surface. Catalase decomposes hydrogen ...
Gastritis caused by H. pylori infection is termed Helicobacter pylori induced gastritis, and listed as a disease in ICD11. [ 6 ] [ 7 ] More than 80% of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology.
English: One mechanism H. pylori has to combat the acidic environment of the stomach is the urease enzyme. This enzyme can be found on the surface of and inside the cell. It takes urea and water from the bloodstream and stomach and converts them to ammonia and carbon dioxid
The success of H. pylori cure depends on the type and duration of therapy, patient compliance and bacterial factors such as antibiotic resistance. Patients most often fail to respond to initial H. pylori eradication therapy because of noncompliance or antibiotic resistance. Patients should be queried about any side effects, missed doses, and ...
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Atrophic gastritis under low power. H&E stain. Autoimmune metaplastic atrophic gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor. [6] Achlorhydria induces G cell (gastrin-producing) hyperplasia, which leads to hypergastrinemia.
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