Special Issue "Peptic Ulcer Disease: From Pathophysiology to Novel Therapeutic Approaches"
A special issue of Gastrointestinal Disorders (ISSN 2624-5647).
Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 1235
Interests: brain–gut axis; experimental colitis; intestinal permeability; inflammatory bowel diseases; proinflammatory cytokines; adipokines; myokines; lipopolysaccharide; microbiota; obesity
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Peptic ulcer is a serious clinical entity that appears in the stomach or duodenum and can lead to the development of peptic ulcer disease (PUD). Despite many studies on the pathogenesis of peptic ulcers in the past, the mechanism of these gastrointestinal and duodenal disorders is still not fully understood. From a clinical point of view, the most common symptom of both gastric and duodenal ulcers is epigastric pain, characterized by a burning sensation, usually observed shortly after a meal with a gastric ulcer and 2–3 hours later with a duodenal ulcer. There are also other PUD “alert features”, including bleeding, anemia, early satiety, unexplained weight loss, progressive dysphagia or odynophagia, recurrent vomiting, and a family history of gastrointestinal cancer. Management of bleeding from a peptic ulcer is a common and serious challenge. While the incidence of PUD is currently declining due to pharmacotherapy based on proton pump inhibitors (PPIs), the incidence of inflammatory bowel disease (IBD) including Crohn’s disease and ulcerative colitis has increased in western lifestyle-adapted societies. Since the breakthrough discovery by Warren and Marshall in 1983 on the causative link between gastritis and the gram-negative spirochete Helicobacter pylori (H. pylori), we are now convinced that in addition to acid and pepsin, commonly considered as pathogenic factors, H. pylori is the major gastric pathogen in humans. This microorganism causes mucosal inflammation, leading to the development of primary PUD, but also worsens the course of this disorder. This bug produces urease which allows it to survive for years in the hostile acidic environment of the stomach due to alkalization of its microenvironment. Interestingly, there is an inverse relation between the prevalence of IBD and H. pylori infection. The H. pylori paradigm has now switched to nonsteroidal anti-inflammatory drugs (NSAIDs) and their main representative aspirin. The interaction between aspirin intake and H. pylori, which may increase the ulcer potential and risk of mucosal bleeding, has not been fully elucidated. The simultaneous presence of H. pylori infection in patients treated with drugs harmful to the gastric and duodenal mucosa increases their ulcer potential and the risk of peptic ulcer bleeding. The combination of NSAID and aspirin with anticoagulants, especially in the elderly, may exacerbate mucosal damage and ulcer complications.
The idea of the current Special Issue of Gastrointestinal Disorders is to offer the possibility of collecting high-quality publications and to provide an interdisciplinary approach by submitting original papers and updated reviews on various aspects of the pathogenesis of acute erosions, mucosal bleedings, and chronic peptic ulcers, including the effect of H. pylori, NSAID with or without novel anticoagulant therapies, clinical and experimental studies on protective action of classic antiulcer drugs, and novel therapeutics such as prodrugs releasing gaseous molecules or nutraceutical agents. Furthermore, the identification of physiological molecules, therapeutic targets, and new methods of treatment PUD in humans and different peptic ulcer animal models is awaited.
Prof. Dr. Tomasz Brzozowski
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