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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 ...
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 ...
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 role of H. pylori in functional dyspepsia is controversial, and treatment for H. pylori may not lead to complete improvement of a patient's dyspepsia. [6] However, a recent systemic review and meta-analysis of 29 studies published in 2022 suggests that successful treatment of H. pylori modestly improves indigestion symptoms. [18]
It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin. Those with autoimmune atrophic gastritis ( Type A gastritis ) are statistically more likely to develop gastric carcinoma (a form of stomach cancer ), Hashimoto's thyroiditis , and achlorhydria .
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Functional heartburn is heartburn of unknown cause. [24] It is commonly associated with psychiatric conditions like depression and anxiety. It is also seen with other functional gastrointestinal disorders like irritable bowel syndrome and is the primary cause of lack of improvement post treatment with proton pump inhibitors (PPIs). [ 24 ]
A new study has suggested that damage to the upper gastrointestinal tract from conditions such as reflux, peptic ulcers, and prolonged use of NSAIDS may increase Parkinson’s risk by 76%.