Helicobacter pylori and Nonmalignant Diseases (original) (raw)
Related papers
Helicobacter, 2000
Background. It has been suggested that the incidence of gastroesophageal reflux disease (GERD) increases after successful eradication of Helicobacter pylori infection. We present data on development of GERD from a controlled study of H. pylori eradication in 165 duodenal ulcer patients. Methods. Patients (mean age, 55 years; 102 men; current smokers; n ϭ 74) were randomly assigned 2 : 1 to receive omeprazole, 40 mg twice daily, in combination with either amoxicillin, 750 mg twice daily, or placebo. Endoscopy and dyspeptic symptoms, including heartburn, were assessed at inclusion and at 6, 12, and 24 months after treatment. In addition, symptoms were assessed at 18 months. Patients with erosive esophagitis
Helicobacter pylori infection and peptic ulcer disease
Current Opinion in Gastroenterology, 1993
Nearly all peptic ulcers are caused by either Helicobacter pylori infection or the use of non-steroidal anti-inflammatory drugs (NSAIDs), which include aspirin. As H. pylori infection is becoming less prevalent in developed countries, NSAIDs are an increasingly important cause of ulceration, including ulcers complicated by gastrointestinal (GI) bleeding. Only about 15% of H. pylori-infected people develop an ulcer in their lifetime, with the risk determined by virulence of the H. pylori strain, host genetics and environment (particularly smoking). NSAID-induced ulcers are largely the result of suppression of gastroprotective cyclooxygenase (COX)-1. The presence and type of ulcers cannot be accurately predicted from symptoms, and the differential diagnosis is broad. Older dyspeptic patients and those with 'alarm' symptoms or signs require upper GI endoscopy to exclude upper GI cancer and make a diagnosis. Younger patients with simple dyspepsia are treated empirically with a course of proton pump inhibitors (PPIs) or an H. pylori 'test-and-treat' strategy. For H. pylori-associated ulcers, H. pylori eradication treatment induces healing and prevents relapse. NSAID ulcers are treated by NSAID withdrawal and a course of PPI; NSAID-naive users requiring continuing treatment who are positive for H. pylori need bacterial eradication, whereas others should be prescribed a concomitant PPI or selective COX-2 inhibitor. Treatment of functional dyspepsia is difficult and requires a multifactorial approach.
European journal of gastroenterology & hepatology, 2004
Discussions concerning the increased incidence of gastro-oesophageal reflux disease (GORD) after Helicobacter pylori eradication continue. In this study we aimed to evaluate the presence of co-existing GORD in (1) duodenal ulcer patients after successful H. pylori eradication, (2) patients with persistent H. pylori infection after attempts at eradication, and (3) controls in whom H. pylori eradication had not been attempted. A prospective study of 255 patients with duodenal ulcer who were assigned to H. pylori eradication or to control treatment (omeprazole for 4 weeks) and followed up for 1 year or until peptic ulcer relapse. GORD was determined in the patients who had reflux oesophagitis on endoscopy at the beginning of the study and/or in patients without reflux oesophagitis if they experienced heartburn and/or regurgitation at least twice a week associated with impairment of daily activities. The study revealed a significant decrease (from 44.6% to 21.7%; P < 0.001) of patien...
Peptic ulcer disease by Helicobacter pylori infection and gastro esophageal reflux disease
2018
Maria Ana Redal1, Waldo Horacio Belloso2, Paula Scibona2, Leonardo Garfi2 and Santiago Isolabella2,3 1Molecular Medicine and Genomics Unit, Institute for Basic Sciences and Experimental Medicine, and Department of Cellular and Molecular Biology, Hospital Italiano de Buenos Aires School of Medicine, Buenos Aires, 2Clinical Pharmacology Section, Internal Medicine Service, and Department of Pharmacology and Toxicology, Hospital Italiano de Buenos Aires School of Medicine 3Central Pharmacy Service, Hospital Italiano de Buenos Aires Argentina
Alimentary Pharmacology and Therapeutics, 2000
Helicobacter pylori and non-steroidal anti-in¯ammatory drugs (NSAIDs) are considered the two most important aetiological factors in the genesis of peptic ulcers and their complications. 1, 2 It is reasonable to consider a potential interaction between both factors since H. pylori causes mucosal in¯ammation, which could predispose the patient to further injury when the mucosa is exposed to gastrotoxic agents such as NSAIDs. Furthermore, the frequency of H. pylori infection increases with age, and it is recognized that in elderly patients NSAID use is associated with a greater incidence of complications. 3 Unfortunately, how H. pylori interacts with NSAID-associated gastroduodenal disease is unclear and previous studies on the role of H. pylori in NSAID induced ulcer disease have yielded con¯icting results. 4±15 Furthermore, these studies have analysed different type of lesions with different clinical perspectives (e.g. endoscopic lesions with/without symptoms). In addition, several studies have shown that patients infected with H. pylori strains carrying the CagA and VacA cytotoxin have a higher risk of developing clinically signi®cant diseases, including gastric or duodenal ulcers. Whether H. pylori infection with these virulence factors increases the risk of ulcer development or bleeding in patients taking NSAIDs is not known.
Caspian Journal of Internal Medicine, 2010
Background: Helicobacter Pylori (H.P) and Non Steroidal Anti inflammatory Drugs (NSAID) are the most common cause of peptic ulcer Disease (PUD). This study was designed to identify endoscopic, clinical and demographic features of patients with H.P positive in comparison with NSAID related PUD. Methods: From December 2004 to March 2008, 5885 patients underwent upper GI Tract endoscopy in a large referral Teaching Hospital of Babol Medical University. All patients with endoscopic diagnosis of PUD were enrolled in the study. H.P positive patients were assigned as group A and NSAID user as group B. Then their clinical, demographic, endoscopic characteristics were compared. Results: A total of 749 (12.3%) patients diagnosed as Duodenal Ulcer (DU), among them 600 subjects were eligible for analysis. Three hundred thirty one (55.2%) were H.P positive, 80 (13.3%) were NSAID user and 189 (31.5%) had non H.P non NSAID related ulcer. Two hundred ninety seven patients diagnosed having Gastric Ulcer (G.U), 143 (48.2%) were H.P positive, 46 (15.5%) were NSAID user and 108 (36.3%) had non H.Pylori, non NSAID related ulcer. Mean age of patients with G.U was 54.2±17 and D.U was 46.9±17.5 years (p<0.04). Anterior wall of bulb and antrum were the most common site of patients with D.U and G.U respectively. Conclusion: This study shows non H.Pylori non NSAID related ulcers comprise a significant portion of peptic ulcer disease in north of Iran.