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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. [17]
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 ...
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.
Rotavirus is the most common cause of gastroenteritis in children, [25] and produces similar rates in both the developed and developing world. [20] Viruses cause about 70% of episodes of infectious diarrhea in the pediatric age group. [13] Rotavirus is a less common cause in adults due to acquired immunity. [27]
There are many causes of infectious diarrhea, which include viruses, bacteria and parasites. [29] Infectious diarrhea is frequently referred to as gastroenteritis. [30] Norovirus is the most common cause of viral diarrhea in adults, [31] but rotavirus is the most common cause in children under five years old. [32]
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The eradication of H. pylori can lead to an increase in acid secretion, [40] leading to the question of whether H. pylori-infected GERD patients are any different from non-infected GERD patients. A double-blind study, reported in 2004, found no clinically significant difference between these two types of patients with regard to the subjective ...