الفهرس 
H. Pylori and Related DisordersOnly 14 pages are availabe for public view
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Abstract
Helicobacter pylori first described by Robin Warren and Barry Marshall in 1982, the bacterium was classified as Campylobacter pylori; in 1989 it was included in a new genus, Helicobacter, and renamed Helicobacter pylori (Marshall et al., 1984).
H. pylori is a helical shaped Gram-negative bacterium, approximately 3 µm long, with a diameter of approximately 0.5 µm with two to six flagella. Helicobacter spp. are the only known microorganisms that can thrive in the highly acidic environment of the stomach, and their helical shape is thought to have evolved to penetrate and favor their motility in the mucus layer (Nathalie and Francis 2007).
H. pylori developed original characteristics testifying to a perfect adaptation to its ecological niche. With its flagella, the bacterium moves through the stomach lumen and drills into the mucus gel layer of the stomach. It produces adhesions that bind to membrane-associated lipids and carbohydrates and help its adhesion to epithelial cells. It produces large amounts of urease enzymes that metabolize urea to carbon dioxide and ammonia, which neutralize gastric acid. The survival of H. pylori in the acidic stomach is dependent on urease and it eventually dies without it. The ammonia that is produced is toxic to the epithelial cells and, with other products of H. pylori, including protease, catalase and phospholipases, causes damage to those cells (Sachs et al., 2003).
Although H. pylori infection is primarily acquired in childhood and its incidence remains low in adulthood, numerous studies have shown an increased prevalence of infection with age worldwide. Epidemiologic studies on elderly people, with a mean age of approximately 70 years, reported a prevalence of nearly 60% in asymptomatic subjects (Regev et al., 1999; Pilotto et al., 1996) and more than 70% among the most elderly patients with gastrointestinal diseases (Pilotto, 2001; Pilotto and Salles, 2002)).