Ashley Johnson 2007
Bryan Kratz 2007
Lorraine Scanlon 2008
Alina Spivak 2007
stomach ulcers, nonsteroidal anti-inflammatory drugs (NSAIDS), granulation tissue fibroblasts, macrophages, proliferating endothelial cells, microvessels, acetylcholine, gastrin, mast cells, histamine, gastric acid secretion, parietal cells, gastric cancer, salt, cigarette smoking, hypergastrinemia, proton pump inhibitor (PPI), CagA Gene, Interleukin-1 β, apical junctions, antibiotics, treatment
Due to the 1983 discovery of H. pylori bacteria as the leading cause of peptic ulcers, the understanding of the disease dramatically changed. We now know that stress and spicy foods are not the leading causes of peptic ulcers. Symptoms including acute abdominal pain, vomiting of blood, and weight loss are characteristic of peptic ulcers. Ulcers form because of the inflammation caused by H. pylori leading to sensitivity of gastric cells to the acid secreted by the infected patient’s stomach. Although more than half of the world’s population is infected with H. pylori, most people remain asymptomatic. Current research suggests that several bacterial virulence genes such as CagA and VacA, as well as the individual host’s genetic predisposition, are factors that influence progression of disease. The mechanism of H. pylori infection has been recently examined in detail clarifying the morphological changes of the host cell and how this promotes the formation of a peptic ulcer. Present studies to explain the persistence of H. pylori and propose how this bacterium evolved key mechanisms to evade the host’s immune response. Due to the advances in the understanding of peptic ulcers, effective treatments have been proposed to treat and eliminate this disease.
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