Peptic ulcer disease Helicobacter pylori infection and

Helicobacter pylori infection and peptic ulcer disease... 

Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease a meta-analysis. Lancet 2002 359(9300) 14-22. 

Until recently, it was believed that excess stomach acid caused stomach ulcers. It has now been proved that the cause is instead a bacterial infection and that ulcers can be successfully treated with antibiotics. The 2005 Nobel Prize in Physiology or Medicine was awarded to Barry J. Marshall and J. Robin Warren for their discovery of the role of Helicobacter pylori in gastritis and peptic ulcer disease. 

Proton pump inhibitors (PPIs), such as omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole, are commonly prescribed to treat symptoms of heartburn, acid reflux, chest pain, dyspepsia, and chronic cough. PPIs inhibit the transfer of protons into the stomach lumen. Pharmacological acid suppression is thus used to treat gastroesophageal reflux disease (GERD) and esophagitis, peptic ulcers, and Helicobacter pylori infection as well as to prevent ulcer development with concurrent nonsteroidal anti-inflammatory drug use. 

Helicobacter pylori infections are now also accepted as the primary cause of peptic ulcer disease (PUD). In the US, approximately four to five million people suffer from PUD, and the economic consequences of the disease are responsible for as much as 3 to 4 billion in annual health care costs. The situation is even more serious in many developing countries, where HP infections, PUD and gastric cancer are major causes of morbidity. 

Answer Peptic ulcer disease is most frequently secondary to either Helicobacter pylori infection or use of NSAIDs. The patient does admit to NSAID use (naproxen), but should also be checked for concomitant H. pylori infection at time of endoscopy or by a serology test. If the patient was found to have H. pylori, an appropriate eradication regimen should be prescribed. The patient should also be counseled to avoid NSAIDs. The patient should be prescribed a proton pump inhibitor for 8 weeks to heal the ulcer. A repeat endoscopy should be done at that time to document ulcer healing and rule out gastric cancer. In addition, the patient should be counseled to stop smoking, which is a risk factor for more severe peptic ulcer disease. 

Finally, it is universally accepted at present that Helicobacter pylori infection has a definitive ethiological role in peptic ulcer disease, and that erradication therapy is warranted in these clinical scenarios. The majority of therapeutic trials have included the application of triple therapy with proton pump inhibitors or ranitidine bismuth citrate, clarithromycin and either amoxycillin or metronidazol and is to date the treatment of choice. However, recent studies have reported antibiotic resistance which can be one reason for failure of treatment of Helicobacter pylori infection [101-103], and new treatment strategies are therefore Wellcome. Flavonoids, in addition to their gastroprotective activity previously commented, have been also shown to inhibit Helicobacter pylori growth in vitro. In this way, Beil et al. [50]... 

Peptic ulcer disease is associated with Helicobacter pylori infection in 90% of patients with gastric and duodenal ulceration. Elimination of H. pylori infection with antibiotics heals the peptic ulcer and the associated symptoms. Combination therapy with antibiotics, anti-secretory agents, namely H2-receptor antagonists or proton pump inhibitors, and bismuth salts has significantly improved the clinical outcome of peptic ulcer disease. Not all strains of H. pylori cause peptic ulcer disease, and other factors are necessary for H. pylori colonization and disease to occur. Flagellated motile bacteria resist peristalsis and adhere to gastric epithelium in a highly specific manner. 

Abstract Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the development of peptic ulcer disease and gastric cancer. Adhesion of microbes to the target tissue is an important determinant for successful initiation, establishment and maintenance of infection, and a variety of different candidate carbohydrate receptors for H. pylori have been identified. Here the different the binding specifities, and their potential role in adhesion to human gastric epithelium are described. Finally, recent findings on the roles of sialic acid binding SabA adhesin in interactions with human neutrophils and erythrocytes are discussed. 

Peptic ulcer disease is one common illness that affects more than 6 million persons in the United States each year (Sandler et al. 2001) and is strongly linked wifii increased rate of cigarette smoking, alcohol intake, psychological stress, regular use of aspirin, and prolonged use of steroids. Infection with Helicobacter pylori also substantially increases the risk for peptic ulcer and its complications (Papatheodo-ridis et al. 2006). Essential oil of Cinnamomum zeylanicum also... 

Goodwin CS, Carrick J. Peptic ulcer disease and Helicobacter pylori infection. Curr Opin Gastroenterol 1991 7 108-1115. 

Most recently, the description of Helicobacter pylori in the gastric mucosa and its correlation with ulcer disease has suddenly and unexpectedly led to dramatic advances in the curing of peptic ulcer disease. It has also become clear that an infection predisposes to a form of gastric neoplasia. We still await a simple therapeutic regimen for eradication of this organism, but this will undoubtedly happen. 

Peptic ulcer disease is claimed to affect about 10% of the population over a lifetime and 3 % annually [2]. Peptic ulcer prevalence seems to be a cohort phenomenon closely connected to Helicobacter pylori Hp) infection [3], which is decreasing in the industrialized world due to the lower infection rate among younger people [2, 4]. Diagnosis of peptic ulcer is based on endoscopy or X-ray. In patients with earlier confirmed ulcer and repeated symptoms, diagnosis can be made on this ground. 

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