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Endoscopy in Pregnancy. IN: Pregnancy in Gastrointestinal Disorders. 2nd ed. Bethesda, MD: American College of Gastroenterology. 2007. pp 10-17.
This chapter about endoscopy in pregnancy is from a monograph that presents updated information about pregnancy in women with gastrointestinal disorders. The authors stress that the spectrum of gastrointestinal diseases in the pregnant patient is virtually identical to that in nonpregnant women. However, options for evaluating pregnant patients are somewhat limited because barium studies and other radiographic techniques subject the fetus to the risks of radiation. However, endoscopy can play a crucial role in the diagnosis and treatment of various disorders in the pregnant patient. The chapter focuses on bringing readers up to date on the research in the area covered, the recommended treatments, and patient management concerns, notably issues of maternal and fetal safety. Topics include the use of upper endoscopy for diagnosing nausea, vomiting, esophagitis, ulcers, and gastritis; the use of lower endoscopy to evaluate rectal bleeding and inflammatory bowel disease (IBD); sigmoidoscopy and colonoscopy; endoscopic retrograde cholangiopancreatography (ERCP) used to evaluate gallstones; percutaneous endoscopic gastrostomy (PEG) placement to assist patients who cannot sustain adequate nutritional intake; and the use of sedation for endoscopic tests in women who are pregnant. The authors conclude that endoscopy appears to be safe in pregnancy. They recommend that procedures be performed after the first trimester if possible, following guidelines to minimize radiation and excessive sedation. Endoscopists are encouraged to consult with an obstetrician in challenging, complicated cases. 1 table. 17 references.
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Gastric Preneoplastic Lesions and Epithelial Dysplasia. Gastroenterology Clinics of North America. 36(4): 813-830. December 2007.
This article on gastric preneoplastic lesions and epithelial dysplasia is from a special issue of Gastroenterology Clinics of North America that focuses on the pathology and clinical relevance of neoplastic precursor lesions of the gastrointestinal tract, liver, and pancreaticobiliary system. The authors note that the incidence of gastric cancer is declining. However, gastric cancer remains the second most common cause of cancer-related deaths worldwide. Topics include the mucosal changes that precede gastric dysplasia, gastric epithelial dysplasia, the grading of gastric dysplasia, and molecular biology factors, including the role of tumor suppressor genes, oncogenes, microsatellite instability, and hypermethylation. The authors emphasize the possible role of Helicobacter pylori (H. pylori) infection in gastric cancer development. They conclude that the optimal surveillance strategy for patients who have H. pylori gastritis is still uncertain. In current routine practice, only dysplasia is a definitive indication for aggressive surveillance or endoscopic therapy or both. 7 figures. 1 table. 135 references.
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Rifaximin: Recent Advances in Gastroenterology and Hepatology. Gastroenterology and Hepatology. 3(6): 474-483. June 2007.
This article reviews data that have been presented at medical meetings or published in medical journals since the publication of a 2006 review of rifaximin in this journal. Rifaximin is an antibiotic that was initially developed to treat bacteria-related diarrhea, but its uses have increased as the understanding of the role of enteric bacteria has advanced. The author presents data that suggest rifaximin may be useful in several enteric conditions, including Clostridium difficile-associated diarrhea, cryptosporidial diarrhea, Helicobacter pylori-associated gastritis, inflammatory bowel disease (IBD), pouchitis, traveler’s diarrhea, diverticular disease, hepatic encephalopathy, small intestinal bacterial overgrowth, and irritable bowel syndrome. For each condition, the author reviews the related research, focusing on administration and dosage, as well as patient selection. The author concludes that rifaximin may be beneficial as monotherapy or in combination with other agents for the treatment of multiple enteric conditions. 2 figures. 5 tables. 72 references.
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Association and Clinical Implications of Gastroesophageal Reflux Disease and H. pylori. Practical Gastroenterology. 30(1): 40-48. January 2006.
This article considers the interrelationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori (H. pylori) infection. The incidence of GERD and its complications, including Barrett's esophagus and adenocarcinoma of the esophagus and gastric cardia have increased, but the incidence of H. pylori related gastroduodenal peptic ulcer disease and distal gastric adenocarcinoma has decreased in Western Europe and the United States. H. pylori infection eradication does not cause GERD, but there is possibly a protective and negative effect of H. pylori in patients with GERD. This protective effect is related to the virulence of the infecting strain and the distribution and severity of gastritis. The negative effect is the increase in peptic ulcer disease and gastric adenocarcinoma. In patients who require long term therapy with proton pump inhibitors (PPIs), a test-and-treat strategy may be appropriate, since PPI therapy might increase the risk of atrophic gastritis and its potential for B12 malabsorption and gastric cancer in H. pylori infected individuals. The author concludes that this is an evolving area with important implications for both individual patients as well as for the nations of the world. 36 references.
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Eosinophilic Esophagitis: Climbing to New Understandings. Today's Dietitian. 8(5): 28-32. May 2006.
This article describes eosinophilic esophagitis (EE), a rapidly emerging chronic illness in both pediatric and adult gastroenterology. Most commonly caused by a food allergy, EE is a serious condition that can cause chronic feeding problems. The author reviews the etiology, symptoms, diagnosis and treatment of EE, including the use of elimination diets, elemental diets, food reintroduction, and medications. EE is characterized by an abnormal accumulation of eosinophils (a type of white blood cell) in the lining of the esophagus. The most common cause of EE is an allergy to milk, eggs, soy, corn, wheat, beef, chicken, shellfish, peanuts, or potatoes. Symptoms include dysphagia, food impaction, nausea and vomiting, failure to thrive, abdominal or chest pain, poor appetite, malnutrition, and difficulty sleeping. Diagnosis is based on upper endoscopy with biopsy. One section reviews the arguments that support nutritional versus medical therapy for children with EE. A final section helps dietitians guide families in making the best treatment choice for children with EE. If nutritional management is chosen, the patient care team must including dietitians, the family, and other health care providers. Drug therapy is an option required for some patients and chosen by others. Readers are referred to five online resource organizations for more information. 5 references.
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Helicobacter Pylori: What Do We Still Need to Know?. Journal of Clinical Gastroenterology. 40(1): 15-19. January 2006.
Helicobacter pylori is a common gastric infection that causes serious complications in a minority of individuals. Although a great deal is known about this disease, there remain many unanswered questions. This article addresses these gaps in knowledge and the author hypothesizes that a number of the unanswered questions are related to a putative increase in gastric acid secretion that may have taken place during the past 200 years. The uncertainties addresses include why the prevalence of the disease is falling within the developed population, the interrelationship between H. pylori infection and gastroesophageal reflux disease, the differences in the international incidence of gastric cancer, and the changing complications of H. pylori over time. With the improving socioeconomic conditions at the end of the 19th century following the Industrial Revolution and the beginning of the 20th century with better nutrition and stature, acid secretion may have increased and H. pylori gastritis may have become more antral predominant. This is the phenotype of duodenal ulceration that also protects against gastric cancer. By the middle of the 20th century, therefore, gastric cancer was declining, but duodenal ulcer peaked. At this time, the prevalence of H. pylori began fall, either as a result of better hygiene and nutrition or possibly because of increasing acid secretion. The author notes that these speculations are not based on objective scientific evidence but rather are an interpretation of circumstantial evidence that fits with the changing patterns of disease seen over time. 26 references.
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Nutrition in the Elderly. IN: Buchman, A., ed. Clinical Nutrition in Gastrointestinal Disease. Thorofare, NJ: Slack Incorporated. 2006. pp 165-182.
This chapter about nutrition in the elderly is from a comprehensive textbook that compiles available data, clinical experience, and research on the role of nutrition in the management of patients with disorders that affect the gastrointestinal (GI) tract. The authors note that many factors influence nutritional status, including nutrient intake, biosynthesis of nutrients such as vitamin D, nutrient absorption by the GI tract, and the subsequent metabolism of nutrients. Aging affects these factors in a variety of ways, possibly altering nutrient requirements and placing older individuals at risk of malnutrition. The chapter discusses the consequences of malnutrition in the elderly, GI function and nutrient absorption, atrophic gastritis, calcium absorption in aging, changes in body composition with aging, sarcopenia, obesity in the elderly, changes in energy metabolism with aging, protein requirements in elderly individuals, micronutrient requirements, nutritional assessment, nutrition support in this population, treatment of specific micronutrient deficiencies, oral nutrition supplements, and the use of enteral nutrition (EN) and parenteral nutrition (PN). A final section considers the ethics of nutrition support. The authors conclude that although there is still much to be learned about the interaction between nutrition and aging, it is clear that malnutrition is associated with an increased risk of morbidity and mortality, and nutrition support can improve clinical outcome in selected elderly populations. 5 figures. 1 table. 166 references.
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Helicobacter Pylori and Gastro-Oesophageal Reflux Disease. Alimentary Pharmacology and Therapeutics. 22 (Supl 1): 32-40. August 2005.
Epidemiological studies show a negative association between Helicobacter pylori infection and gastroesophageal reflux disease (GERD) and its complications. This article reviews the epidemiological association between H. pylori and GERD and the effect of eradicating H. pylori on GERD. The authors discuss the physiological mechanism by which the infection might influence GERD. The authors also look at interactions between H. pylori and the proton pump inhibitor (PPI) therapy used to treat GERD. H. pylori infection improves the control of gastric acidity by PPIs and this produces a small advantage in the clinical control of reflux disease. The infection prevents rebound acid hypersecretion occurring when PPI therapy is discontinued. However, concerns have been expressed that the body gastritis induced by PPI therapy in H. pylori-infected subjects might increase the risk of gastric cancer. The authors conclude that, at present, it is unclear whether H. pylori should be eradicated in GERD patients. 1 figure. 68 references.
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Host Epithelial Interactions with Helicobacter Pylori: A Role for Disrupted Gastric Barrier Function in the Clinical Outcome of Infection?. Canadian Journal of Gastroenterology. 19(9): 543-552. September 2005.
Infection of the human stomach with the bacterium Helicobacter pylori may develop into gastritis, ulceration, adenocarcinoma, and mucosal lymphomas. However, the pathogenic mechanisms that determine which clinical outcome occurs from this microbial-epithelial interaction remain poorly understood. Disruptions of the epithelial (stomach lining) barrier function may contribute to pathology and postinfectious complications in a variety of gastrointestinal infections. This review discusses the implications of H. pylori persistence on gastric disease. The authors emphasize the role of myosin light chain kinase, claudins, and matric metalloproteinases in gastric permeability defects, and their contribution to the development of cancer. These mechanisms and the associated signaling events may represent new therapeutic targets to control the disease processes induced by H. pylori, a microbial pathogen that colonizes the stomach of over 50 percent of the human population. 3 figures. 1 table. 158 references.
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Stomach and Duodenum. IN: Digestive Disorders 2005. Palm Coast, FL: Medletter Associated. pp 19-24. 2005.
This chapter on the stomach and duodenum is from a White Paper on digestive disorders, including conditions that affect the esophagus, stomach, gallbladder, bile ducts, small intestine, and large intestine. This chapter covers normal anatomy of the stomach and duodenum, and the causes, symptoms, diagnosis, and treatment of gastritis, and peptic ulcer disease (PUD). Gastritis is an inflammation of the gastric mucosa, the inner lining of the stomach. The author describes the most common infection of the stomach, that caused by Helicobacter pylori bacteria. Gastritis can also be caused by medications, autoimmune reactions, or hypersensitivities or allergies. The symptoms of gastritis are indigestion and a worsening of abdominal pain after meals. Gastritis is usually diagnosed with endoscopy; infection is treated with antibiotics and with medications to suppress gastric acid production. Peptic ulcers are deep, nonhealing mucosal defects in the stomach, often caused by Helicobacter pylori infection or drug effects. People with gastric ulcers experience pain soon after eating, are frequently afraid to eat, and often lose weight. Peptic ulcers are diagnosed with an upper GI series or endoscopy; treatment includes use of medications that suppress gastric acid secretion and antibiotics to eradicate H. pylori infection. One chart summarizes the common drug therapy used for peptic ulcers. 1 table.
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Effect of Helicobacter Pylori Eradication on Gastroesophageal Reflux Disease. Journal of Clinical Gastroenterology. 38(9): 750-755. October 2004.
Gastroesophageal reflux disease (GERD) is a common disorder characterized by the return (reflux) of acidic stomach contents (gastric acid) back into the esophagus. The effect of the eradication of Helicobacter pylori infection on GERD is controversial. For example, an increased incidence of reflux esophagitis has been reported after H. pylori eradication in patients with gastritis or peptic ulcer disease. This article reports on a study undertaken to investigate the effect of H. pylori eradication in patients with GERD (n = 34 enrolled patients; 18 patients completed the study). Three months after the treatment to eradicate H. pylori (with triple antibiotic therapy), there was no significant change in any of the 24-hour esophageal pH recording parameters or mean lower esophageal sphincter (LES) resting pressure. There was a significant decrease in the scores for heartburn and regurgitation. Esophagitis persisted in 16 patients and disappeared in 2 patients. The authors conclude that H. pylori eradication does not have any effect on gastroesophageal acid reflux in patients with reflux esophagitis 3 months after eradication, but significant improvement is achieved in some reflux-associated symptoms. 1 figure. 3 tables. 36 references.
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Gastritis. Riviera Beach, FL: AmeriPath, Inc. 2004. 2 p.
This fact sheet helps readers understand gastritis, inflammation of the lining of the stomach. The fact sheet considers the causes of gastritis, including Helicobacter pylori infection; treatment and follow up options for chronic gastritis; the implications of antibiotic therapy; and recommended questions to ask of one's physician. The fact sheet concludes with a list of sources of additional information, primarily the web site addresses of professional and voluntary organizations.
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Medical Treatment of Acute Pancreatitis. Gastroenterology Clinics of North America. 33(4): 855-869. December 2004.
Acute pancreatitis (AP) is one of the most common diseases in gastroenterology. This article reviews the medical treatment of acute pancreatitis. Topics covered include prognostic markers for the severity of acute pancreatitis; enteral nutrition versus total parenteral nutrition; nasogastric tube or orally feeding; prevention of ulcers and gastritis in pancreatitis patients; fluid resuscitation and rehydration; treatment of pain; the role of antibiotics in treatment of acute pancreatitis; endoscopic sphincterotomy; and obsolete treatment concepts. During the last decade, an increasing incidence of AP was observed, mostly because of a higher sensitivity of diagnostic tests. The authors stress that discrimination between mild edematous disease (75 percent to 85 percent of all cases) with mortality below 1 percent, and severe hemorrhagic-necrotizing pancreatitis (15 percent to 25 percent of all cases) with a fatal outcome in 10 percent to 24 percent is important. Both clinical courses can occur regardless of the underlying etiology of the disease. Eighty percent of all cases of AP are linked etiologically to gallstone disease or immoderate alcohol consumption, while pancreatitis caused by hypercalcemia (excessive amounts of calcium in the blood), hyperlipidemia (high levels of blood lipids, including cholesterol), or infectious agents is rare. The authors emphasis that the requirement for frequent clinical assessments, laboratory studies, and reevaluation of organ destruction employing CT or MRI strongly argues against treating these patients on an outpatient basis. 2 figures. 2 tables. 54 references.
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Esophagus and Stomach. Orlando, FL: Mosby, Inc. 2003. 200 p.
In this textbook, established experts cover all of the essential information on the esophagus and stomach. The book offers thirteen chapters: gastroesophageal reflux disease; other causes of esophagitis; Barrett's esophagus; esophageal motility disorders; transfer dysphagia; rings, webs, stenoses, and diverticula of the esophagus; esophageal cancer; Helicobacter pylori gastritis and other gastric infections; peptic ulcer disease; gastroparesis and other gastric motor abnormalities; non-ulcer dyspepsia; foreign bodies of the upper gastrointestinal tract; and gastric cancer, lymphoma, and carcinoids of the stomach. The authors focus on differential diagnosis, pitfalls, and evidence-based management approaches. Each chapter begins with a chapter outline, includes extensive tables and illustrations, and concludes with a list of recommended readings. A subject index concludes the volume.
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Gastritis and Gastropathy. In: Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 1394-1415.
Gastritis, simply defined as the inflammation of the gastric (stomach) mucosa, is a condition, not a disease. This chapter on gastritis and gastropathy is from a lengthy, two-volume textbook that integrates the various demands of science, technology, expanding information, good judgment, and common sense into the diagnosis and management of gastrointestinal patients. The author provides a discussion of useful strategies that gastroenterologists and pathologists can use to optimize the diagnosis of gastric diseases. Topics include a recommended clinicopathological approach to gastritis, tools used to diagnose and classify gastric conditions, Helicobacter pylori gastritis, infectious gastritis, autoimmune gastritis, lymphocytic gastritis, granulomatous gastritis, chemical (reactive) gastropathy, hemorrhagic gastropathy, vascular gastropathies, hypertrophic gastropathies, and gastric cardia. 13 figures. 2 tables. 200 references.
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Helicobacter Pylori Gastritis and Other Gastric Infections. In: Katzka, D.A. and Metz, D.C., eds. Esophagus and Stomach. Orlando, FL: Mosby, Inc. 2003. p. 115-127.
The role of Helicobacter pylori in the causation of peptic ulcers is now generally accepted. However, most people with H. pylori infection have normal secretion levels of gastric acid and therefore do not develop peptic ulcers. This chapter on H. pylori gastritis and other gastric infections is from a textbook on the esophagus and stomach in which the authors focus on differential diagnosis, pitfalls, and evidence-based management approaches. The chapter covers pathogenesis, clinical presentation, diagnosis, treatment, and the role of confirmatory testing after eradication therapy. A brief section discusses other gastric infections and gastritis. The chapter begins with a chapter outline, includes extensive tables and illustrations, and concludes with a list of recommended readings. 8 figures. 6 tables. 15 references.
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Helicobacter Pylori and Reflux Disease. Alimentary Pharmacology and Therapeutics. 17(3): 297-305. February 2003.
The falling prevalence of Helicobacter pylori infection and related diseases (peptic ulcer disease, gastric cancer) in developed countries has been paralleled by an increased recognition of gastroesophageal reflux and its complications. This article considers the role of H. pylori and reflux disease (gastroesophageal reflux disease or GERD). The epidemiological data do not support a role for H. pylori in the pathogenesis of reflux disease, but suggest a negative association with the increasing incidence of esophageal disease. This has led some investigators to propose a 'protective' role of H. pylori infection against the development of esophageal diseases. In these patients, pre-existing lower esophageal sphincter (LES) dysfunction, susceptibility to reflux, unmasking of latent reflux, and the patterns and severity of gastritis are probably important factors contributing to the development of esophageal diseases. The most likely mechanism by which H. pylori infection may protect against reflux is by decreasing the potency of the gastric refluxate in patients with corpus-predominant gastritis. The prevalence of H. pylori infection in patients with reflux disease is probably no greater than that in those without reflux, and there are conflicting data indicating that reflux symptoms or erosive esophagitis develop after H. pylori eradication. The authors note that it is also unclear whether H. pylori augments the antisecretory effects of proton pump inhibitors or accelerates the development of atrophic gastritis. 58 references.
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Surgery for Peptic Ulcer Disease and Postgastrectomy Syndromes. In: Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 1441-1454.
The surgical treatment of peptic ulcer is most frequently required when complications of previously unappreciated ulcers occur. This chapter on surgery for peptic ulcer disease (PUD) and postgastrectomy syndromes is from a lengthy, two-volume textbook that integrates the various demands of science, technology, expanding information, good judgment, and common sense into the diagnosis and management of gastrointestinal patients. The chapter covers elective surgery for PUD, surgery for duodenal ulcer, surgery for gastric ulcer, surgical treatment of peptic ulcer complications (hemorrhage, perforation, obstruction), and complications of the surgery for peptic ulcer, including recurrent ulcer, dumping syndrome, postvagotomy diarrhea, alkaline reflux gastritis, delayed gastric emptying, and gastric cancer. 13 figures. 3 tables. 132 references.
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Alteration of Histological Gastritis After Cure of Helicobacter Pylori Infection. Alimentary Pharmacology and Therapeutics. 16(11): 1923-1932. November 2002.
It is still disputed whether gastric (stomach) atrophy or intestinal metaplasia improves after the cure of Helicobacter pylori infection. If these condition improve, cure of the infection may reduce cancer risk. This article reports on a literature survey undertaken to clarify the histological changes after the cure of H. pylori infection. The authors reviewed 52 selected reports from 1,066 relevant articles. The extracted data were pooled according to histological parameters of gastritis based on the updated Sydney system. Activity improved more rapidly than inflammation. Eleven of 25 reports described significant improvement of atrophy. Atrophy was not improved in one of four studies with a large sample size (more than 100 samples) and in two of five studies with a long follow up period (longer than 12 months), suggesting that disagreement between the studies was not totally due to sample size or follow up period. Methodological flaws, such as patient selection, and statistical analysis based on the assumption that atrophy improves continuously and generally in all patients might be responsible for the inconsistent results. Five of 28 studies described significant improvement of intestinal metaplasia. The authors conclude that activity and inflammation were improved after the cure of H. pylori infection. Atrophy did not improve generally among all patients, but improved in certain patients. 5 tables. 65 references.
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Current Role of Surgery in Peptic Ulcer Disease. In: Feldman, M.; Friedman, L.S.; Sleisenger, M.H. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 2002. p. 797-809.
Effective medical treatment of peptic ulcer disease (PUD) and improved techniques of controlling upper gastrointestinal (GI) hemorrhage (bleeding) nonoperatively have greatly limited the role of surgery in PUD. This chapter on the current role of surgery in PUD is from a comprehensive and authoritative textbook that covers disorders of the gastrointestinal tract, biliary tree, pancreas, and liver, as well as the related topics of nutrition and peritoneal disorders. Topics include the historical basis for the surgical treatment of PUD, the physiological basis for peptic ulcer surgery, operations for duodenal ulcer, Roux-en-Y gastrojejunostomy, operations for benign gastric (stomach) ulcer, early and late postoperative, disorders associated with delayed gastric emptying and gastric stasis, bile (alkaline) reflux gastritis, gastric adenocarcinoma, syndromes associated with rapid gastric emptying, and current controversies on the role of surgery in peptic ulcer disease. The chapter includes a mini-outline with page citations, full-color illustrations, and extensive references. 12 figures. 2 tables. 77 references.
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Favourable Effect of an Acidified Milk (LC-1) on Helicobacter Pylori Gastritis in Man. European Journal of Gastroenterology and Hepatology. 13(1): 25-29. January 2001.
The supernatant of Lactobacillus johnsonii La1 culture was shown to be bactericidal and to have a partial, acid independent suppressive effect on Helicobacter pylori in humans. This study investigated the effect of L. johnsonii La1 acidified milk (LC-1) on H. pylori infection in 53 volunteers infected with H. pylori. Volunteers were randomized to received either LC-1 or placebo 180 milliliters twice a day for 3 weeks. All subjects also received clarithromycin 500 milligrams twice a day (bid) during the last two weeks of acidified milk therapy. Esophagogastroduodenoscopy and biopsies were performed at inclusion and repeated 4 to 8 weeks after the end of the treatment. H. pylori infection was confirmed by urease test and histology. Results showed that LC-1 ingestion induced a decrease in H. pylori density in the antrum (the passage from the esophagus to the stomach, i.e., the first part of the stomach) and the corpus (the body of the stomach). LC-1 also reduced inflammation and gastritis activity in the antrum and of activity in the corpus. Clarithromycin eradicated H. pylori in 26 percent of the subjects; LC-1 did not improve the antibiotic effect. These results suggest that H. pylori infection and gastritis can be down regulated by LC-1. 4 tables. 33 references.
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Dyspepsia. In: Edmundowicz, S.A., ed. 20 Common Problems in Gastroenterology. New York, NY: McGraw-Hill, Inc. 2002. p. 59-80.
The complaint of upper abdominal pain or dyspepsia encompasses a wide variety of clinical presentations and diagnoses, ranging from mild gastrointestinal infections to such life-threatening conditions as perforated duodenal ulcer and pancreatic cancer. This chapter on dyspepsia is from a book that focuses on the most common gastroenterological problems encountered in a primary practice setting. The chapter is organized to support rapid access to the information necessary to evaluate and treat most patients with this problems. Topics include the prevalence of dyspepsia; principal diagnosis, including nonulcer dyspepsia, gastroesophageal reflux disease (GERD), duodenal ulcer, gastric ulcer, and gastritis; the typical presentation; key elements of the patient history, including symptoms indicative of serious conditions, the use of nonsteroidal antiinflammatory drugs (NSAIDs), and dsypeptic symptoms; the physical examination; ancillary tests, including those to detect Helicobacter pylori, endoscopy, upper gastrointestinal radiography, and esophageal pH monitoring and manometry; treatment strategies for H. pylori infection, nonulcer dyspepsia, GERD, gastritis, duodenal ulcers, gastric ulcers, and NSAID gastropathy; patient education; common clinical errors; controversies in this area; and emerging concepts. The chapter includes a chapter outline for quick reference, the text itself, a diagnostic and treatment algorithm, and selected references. This chapter also contains the five color plates that serve the entire text. 6 figures. 6 tables. 32 references.
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Gastric Cancer and Helicobacter Pylori. Alimentary Pharmacology and Therapeutics. 16 (Supplement 4): 83-88. July 2002.
This review article discusses gastric (stomach) cancer, the second most common cause of death from malignancy in the world. The pathogenesis of stomach cancer is comparatively well understood and its etiology (cause) multifactorial. Non-cardia gastric cancer usually arises in a stomach that has been inflamed over a long period and where atrophy and intestinal metaplasia have supervened. The most common cause of gastric inflammation is infection with Helicobacter pylori. Colonization with this organism increases the relative risk of developing stomach cancer by about six. The likelihood of stomach cancer increases with the severity and extent of the gastritis. Severity is influenced by the virulence of the infecting organism, the genetics of the host, bile reflux, dietary factors, and the presence of hypochlorhydria which influences the extent, as well as the severity, of the inflammation. The only predisposing factor which can easily be manipulated is H. pylori infection, which can be successfully treated in 80 to 90 percent of cases using a 1 week therapeutic regimen. 1 table. 27 references.
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Gastritis and Other Gastropathies. In: Feldman, M.; Friedman, L.S.; Sleisenger, M.H. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 2002. p. 810-827.
Gastritis is defined as microscopic inflammation of the stomach, thus biopsy is required for definitive diagnosis. This chapter on gastritis and other gastropathies is from a comprehensive and authoritative textbook that covers disorders of the gastrointestinal tract, biliary tree, pancreas, and liver, as well as the related topics of nutrition and peritoneal disorders. Topics include classification; chronic, nonspecific gastritides, including diffuse antral-predominant gastritis, multifocal atrophic gastritis, and diffuse corporal atrophic gastritis; infectious gastritis, including that due to viruses, bacteria, fungi, or parasites; granulomatous gastritides, including sarcoidosis and xanthogranulomatous gastritis; distinctive forms of gastritis, including collagenous gastritis, lymphocytic gastritis, and eosinophilic gastritis; miscellaneous forms of gastritis, including gastritis cystica profound and gastric graft-versus-host disease (GVHD); reactive gastropathies (acute erosive gastritis), including medications, alcohol, cocaine, stress, radiation, bile reflux, ischemia, bezoar, prolapse gastropathy, linear gastric erosions in a hiatal hernia (Cameron's ulcer), and congestive gastropathy (portal hypertensive gastropathy); and hyperplastic gastropathies, notably Menetrier's disease and hyperplastic, hypersecretory gastropathy. The chapter includes a mini-outline with page citations, full-color illustrations, and extensive references. 11 figures. 1 table. 217 references.
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Diseases of the Gastroesophageal Mucosa: The Acid-Related Disorders. Totowa, NJ: The Humana Press, Inc. 2001. 199 p.
Gastric acid-related diseases are among the most commonly encountered disorders in clinical practice. The last decade has witnessed profound changes in the clinical approach to this family of conditions, which includes gastroesophageal reflux disease (GERD), peptic ulcers of all etiologies (causes), and dyspepsia (heartburn). This text emphasizes the diagnosis and treatment of these conditions, with subtext on epidemiology and pathophysiology (where their understanding is important for management conditions). Eleven chapters cover the management of peptic ulcer disease; the epidemiology, demographics and pathophysiology of Helicobacter pylori-related diseases, including gastritis, ulcers, and cancer; the diagnosis and treatment of Helicobacter-pylori related diseases; the management of nonsteroidal antiinflammatory drug (NSAID) related ulcers; nonvariceal upper gastrointestinal bleeding; Zollinger-Ellison syndrome and other acid-hypersecretory states; dyspepsia and nonulcer dyspepsia; the epidemiology and pathophysiology of gastroesophageal reflux disease (GERD); the diagnosis and treatment of GERD; Barrett's esophagus and adenocarcinoma; and extraesophageal manifestations of GERD. Each chapter includes a list of references and a subject index concludes the text.
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Effect of Helicobacter Pylori Eradication Therapy on Dyspepsia Symptoms in Industrial Workers in Japan. Alimentary Pharmacology and Therapeutics. 15(6): 805-811. June 2001.
The relationship between Helicobacter pylori infection and non ulcer dyspepsia (heartburn, impaired digestion) is still controversial. The potential benefits and risks of the treatment could depend on local conditions, such as the prevalence of the infection and the local rates of gastric (stomach) cancer. This article reports on a study undertaken to evaluate the effects of H. pylori eradication therapy on non ulcer dyspepsia symptoms in industrial workers in Japan. A total of 615 employees of an industrial corporation were examined for H. pylori infection and symptom scores: 215 H. pylori positive non ulcer dyspepsia cases underwent eradication therapy. Symptom scores were also analyzed 12 months after the eradication therapy. Serum pepsinogen A and pepsinogen C levels were analyzed and chronic atrophic gastritis was serologically diagnosed. The symptom score improved significantly in the cured cases, but not in the non cured cases. The authors conclude that in both groups (cases with atrophic gastritis and cases with chronic gastritis only) the cure of H. pylori infection was effective in improving non ulcer dyspepsia symptoms. 1 figure. 3 tables. 35 references.
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Helicobacter Pylori. In: Feldman, M.; Friedman, L.S.; Sleisenger, M.H. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 2002. p. 732-746.
Helicobacter pylori is a slow growing, microaerophilic, highly motile, gram negative spiral organism whose most striking biochemical characteristic is the abundant production of protease. H. pylori infection elicits robust inflammatory and immune responses that are lifelong unless the infection is cured. This chapter on H. pylori is from a comprehensive and authoritative textbook that covers disorders of the gastrointestinal tract, biliary tree, pancreas, and liver, as well as the related topics of nutrition and peritoneal disorders. Topics include epidemiology, including prevalence in healthy individuals and transmission in infection; virulence factors, such as colonization factors, and factors mediating tissue injury; acute infection; chronic infection, including chronic nonatrophic gastritis and chronic atrophic gastritis; diagnostic strategies; treatment options, including antibiotics used in regimens to eradicate H. pylori, adjunctive agents used in regimens to eradicate H. pylori, therapeutic regimens to treat H. pylori infections, therapeutic strategies, definition of cure, follow of patients after antimicrobial therapy, and treatment of patients whose initial course of therapy failed; and immunization. The chapter includes a mini-outline with page citations, full-color illustrations, and extensive references. 4 figures. 7 tables. 160 references.
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Long-Term Effects of Cure of Helicobacter Pylori Infection on Patients with Atrophic Body Gastritis. Alimentary Pharmacology and Therapeutics. 16(10): 1701-1708. October 2002.
Helicobacter pylori infection induces atrophic body gastritis (chronic inflammation of the stomach, associated with degeneration of the stomach mucosa), but the long-term effect of its cure on body atrophy is unclear. This article reports on a study undertaken to investigate the long term effects of H. pylori cure on gastric (stomach) morpho-functional parameters in patients with atrophic body gastritis. Forty patients with atrophic body gastritis were cured of H. pylori infection. At eradication assessment (6 to 12 months), in eight of the 40 patients, body atrophy was no longer observed, whereas in 32 of the 40 it remained substantially unchanged. In the 8 patients with reversed body atrophy, gastrinemia decreased significantly with respect to pretreatment values, and basal and stimulated acid secretion increased significantly after cure. In the 32 patients still presenting body atrophy, gastrinemia was similar to pretreatment values. At follow up, the eight patients with revered body atrophy continued with normal gastrinemia, but in the 19 patients with continued atrophy, both corporal atrophy and intestinal metaplasia remained substantially unchanged. The authors conclude that following successful treatment in patients with atrophic body gastritis and H. pylori infection, long-term histological investigations are crucial in order to detect reversed body damage or to confirm continued body atrophy. 4 figures. 2 tables. 35 references.
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Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. St. Louis, MO: Saunders. 2002. (CD-ROM).
This CD-ROM is an interactive version of a definitive compendium of current clinical knowledge in gastroenterology and hepatology. The authors offer a balanced, detailed account of the basic science of the digestive system, as well as complete coverage of current diagnosis and management. Readers will find up-to-date discussions of the cell biology and molecular biology that determine the digestive system's function, in addition to descriptions of organ physiology and the pathophysiology of the signs, symptoms and laboratory abnormalities of organ disease. The program contains an expanded section on the liver, integrates the latest endoscopic scanning and therapeutic techniques, discusses the latest perspective in possible roles of H.pylori in dyspepsia and gastric cancer, contains information on possible causes of non-ulcer dyspepsia, presents expanded coverage of GI bleeding, with description of the latest techniques for diagnosis and treatment, contains new information on genetic markers for cancer of the colon, post liver transplantation for hepatitis and diagnostic tests for celiac disease, offers a complete description of effective responses for inflammatory bowel disease and Crohn's disease, and discusses relevant histological criteria for the diagnosis of Barrett's esophagus, gastritis, IBD and celiac disease. The program features a separate section on problems involving multiple organs such as AIDS, systemic manifestation of GI disease and abdominal pain and bleeding. The program is illustrated with full-color photographs and drawings.
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Gastritis. Gastrointestinal Endoscopy Clinics of North America. 11(4): 717-740. October 2001.
Upper gastrointestinal (GI) endoscopy with biopsy has become an essential tool in the diagnosis of gastritis and gastropathy in both adults and children. In this article, the clinical, endoscopic, and histologic features of major forms of gastritis relevant to the pediatric population are reviewed. Topics include the anatomic landmarks of the stomach, the terminology and classification of gastritis, acute gastritis, Helicobacter pylori gastritis, non-Helicobacter pylori infectious gastritis, immune-mediated gastritis, lymphocytic gastritis, allergic gastritis, chemical gastropathy, and other forms of gastritis. The author concludes that a wide variety of disorders, both systemic and limited to the GI tract, may affect the stomach in children. Although the clinical symptoms and signs of gastric involvement are frequently nonspecific, attention to the relevant clinical history, and correlation of laboratory data, endoscopic findings, and biopsy pathology, permit a specific diagnosis in many cases. 6 figures. 143 references.
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Acid Suppression in the Management of Gastro-Oesophageal Reflux Disease: An Appraisal of Treatment Options in Primary Care. Alimentary Pharmacology and Therapeutics. 15(6): 765-772. June 2001.
Gastroesophageal reflux disease (GERD) is one of the most common conditions presenting to the primary care physician. Despite progress in understanding and treatment of the disease, strategies for capitalizing on these advances are less well developed. In many practices, H2 receptor antagonists still remain the most widely prescribed treatment for GERD, despite the availability of the more effective acid suppressant proton pump inhibitors (PPIs). This review article examines the relative effectiveness of acid suppressant drugs in minimizing esophageal acid exposure (the return of stomach acid to the esophagus) and outlines the evidence for the superiority of PPIs over standard dose H2 antagonists in symptom relief, erosion healing, and prevention of relapse in GERD. Current prescribing patterns and considerations for the general practitioner are also examined. The availability and impact of over the counter H2 antagonists on the treatment of GERD and their relative cost effectiveness versus PPIs are also addressed. The authors note that a hierarchy of drug efficacy applies in principle to all GERD patients, with or without esophagitis. This hierarchy ranges from full dose PPI to half dose PPI to high dose H2 antagonist to standard dose H2 antagonist or prokinetic therapies. The most effective initial therapy for GERD is also likely to be the most cost effective one, if treatment failure leads to higher utilization of medical resources. The authors also review the application of these recommendations to the management of non endoscoped GERD, endoscopy negative GERD, and low grade esophagitis as well as higher grade esophagitis. 3 figures. 1 table. 46 references.
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Cure of Helicobacter Pylori Infection in Elderly Patients: Comparison of Low Versus High Doses of Clarithromycin in Combination with Amoxicillin and Pantoprazole. Alimentary Pharmacology and Therapeutics. 15(7): 1031-1036. July 2001.
Advancing age may influence the pharmacokinetics of the antibiotic clarithromycin. No studies have yet compared the effects of different dosages of clarithromycin in combination with a proton pump inhibitor (PPI) and amoxicillin in elderly patients. This article reports on a study undertaken to compare the efficacy and tolerability of clarithromycin 250 milligrams versus clarithromycin 500 milligrams twice daily (b.d.) in combination with pantoprazole (a PPI) and amoxicillin in elderly patients. Subjects were 154 elderly patients with Helicobacter pylori associated ulcer disease or chronic gastritis (inflamed stomach). They were randomized to receive pantoprazole 40 milligrams daily plus amoxicillin 1 gram and either clarithromycin 250 milligrams b.d. (PAC 250) or clarithromycin 500 milligrams b.d. (PAC 500). Two months after therapy, endoscopy and gastric (stomach) biopsies were repeated. The cure rates of H. pylori infection in the PAC 250 and PAC 500 groups were, respectively 83 percent and 79 percent (using the intention to treat, or ITT, analysis) and 94 percent and 88 percent respectively (using the per protocol, or PP, analysis). Significant decreases in chronic gastritis activity both in the body and the antrum of the stomach were found in H. pylori cured patients, independently of clarithromycin dosage. Four patients in PAC 250 (5 percent) and seven in PAC 500 (9 percent) reported adverse events. Of these, one patient in PAC 250 (25 percent) and three in PAC 500 (43 percent) discontinued the study because of these drug related side effects. The authors conclude that in elderly patients, 1 week triple therapy with a PPI, amoxicillin, and clarithromycin is a highly effective and well tolerated anti H. pylori treatment. With this combination, clarithryomycin at the lower dose of 250 milligrams b.d. achieved excellent cure rates and minimized adverse events and costs. 2 tables. 22 references.
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Gastrointestinal and Liver Infections. In: Farthing, M.J.G.; Ballinger, A.B., eds. Drug Therapy for Gastrointestinal and Liver Diseases. Florence, KY: Martin Dunitz. 2001. p. 107-141.
Infections of the gastrointestinal tract and liver are the most common disorders of the alimentary tract in both the industrialized and in the resource-poor countries of the world. This chapter on gastrointestinal and liver infections is from a textbook that reviews the drug therapy for gastrointestinal and liver diseases. Diarrhea is the most common manifestation of gastrointestinal infection, but there are many other important clinical syndromes, including esophagitis, gastritis, intestinal obstruction, and proctitis and perianal disease. Bacterial and parasitic infections of the liver and biliary tract are also a major cause of morbidity and mortality worldwide, producing liver abscess, cholangitis, and biliary obstruction, and chronic liver disease with portal hypertension. This chapter provides a brief summary of the pathophysiology of the diseases, the rationale for drug intervention, and appropriate treatment regimens as indicated by current knowledge. The chapter concludes with a drug list that summarizes mode of action, and other aspects of clinical pharmacology where appropriate, drug doses, common adverse affects, and drug interactions. 1 figure. 11 tables. 128 references.
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GERD and H. Pylori: Does It Matter?. Practical Gastroenterology. 25(7): 26, 31-32, 34, 36-37. July 2001.
The incidence of gastroesophageal reflux disease (GERD) and esophageal adenocarcinoma (cancer of the esophagus) have increased in recent years while the incidence of peptic ulcer disease (PUD) and distal gastric (stomach) cancer have declined. Given the simultaneous decline in Helicobacter pylori infection, it is tempting to propose a relationship between H. pylori infection and these opposing time trends. This review article puts into perspective the current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD. While H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from developing GERD and its complications. The most likely mechanism whereby H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. 4 figures. 20 references.
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Does Helicobacter Pylori Affect Gastric Mucin Expression? Relationship Between Gastric Antral Mucin Expression and H. Pylori Colonization. European Journal of Gastroenterology and Hepatology. 13(1): 19-23. January 2001.
Helicobacter pylori colonizes the mucous gel layer, the surface epithelium, and the glands of the stomach. It has previously been shown that H. pylori infection causes aberrant expression of gastric mucins MUC 5 and MUC 6. This study aimed to determine the distribution of MUC 5 and MUC 6 in the gastric antrum (the passage from the esophagus to the stomach, i.e., the first part of the stomach) of patients with dyspepsia, and to investigate changes in this pattern in the presence of H. pylori and after successful eradication. Gastric antrum biopsy specimens were examined by immunohistochemistry for mucin gene (MUC 5 and MUC 6) expression. The study included 49 patients positive for H. pylori, in 36 of whom successful eradication was performed, and 11 H. pylori negative patients. There was a gradient of MUC 5 expression, higher to lower, from the surface to the glands, which was more pronounced before eradication. Increased MUC 5 synthesis in the mucous neck cells and in the glands was found after H. pylori eradication. MUC 6 was synthesized in the glands more than in the mucous neck cells or foveola. MUC 6 was also secreted into the lumen and probably comprised the superficial part of the unstirred mucous layer. The authors conclude that the change in MUC 5 synthesis may reflect H. pylori colonization. 6 figures. 18 references.
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H. Pylori Eradication for Individuals on Chronic NSAID Therapy: Should We Kill the Bug If You Need the Drug?. Practical Gastroenterology. 25(5): 12, 16, 19, 23-24. May 2001.
Although it is widely agreed that Helicobacter pylori (a bacterium) causes peptic ulcer disease, controversy persists regarding the impact of H. pylori infection on the incidence of NSAID associated complications. This article considers the role of H. pylori eradication for individuals on chronic NSAID therapy. H. pylori gastritis can increase protective prostaglandin levels in the upper GI tract mucosa, but there is little evidence that eradication of infection leads to an increased risk for clinically significant events in those taking NSAIDs. Since both H. pylori and NSAIDs increase ulcer risk, elimination of either risk factor does not provide protection against the other. Given the prevalence of NSAID associated toxicity, preventive strategies to reduce NSAID side effects remain important. In addition, a compelling argument can be made for H. pylori testing of chronic NSAID users at increased risk for ulcer disease, from the cost effectiveness standpoint. Testing for H. pylori does not appear to be indicated for all patients starting on NSAID therapy. Patients with a pre existing history of peptic ulcer disease should be tested for H. pylori and treated with antibiotics if the test is positive, in order to reduce recurrence of H. pylori associated ulcers. 1 figure. 14 references.
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Helicobacter Pylori-Related Diseases: Demographics, Epidemiology, and Pathophysiology of Gastritis, Ulcers, and Cancer. In: Freston, J.W. Diseases of the Gastroesophageal Mucosa: The Acid-Related. Totowa, NJ: The Humana Press, Inc. 2001. p.29-41.
Gastric acid-related diseases are among the most commonly encountered disorders in clinical practice. This chapter on the demographics, epidemiology, and pathophysiology of gastritis, ulcers and cancer is from a text that emphasizes the diagnosis and treatment of these conditions. Helicobacter pylori is a common bacterial infection of the gastric mucosa. The infection is generally asymptomatic, but it may cause a variety of gastrointestinal diseases that are associated with significant morbidity and mortality. In some cases, increased acid secretion can lead to the formation of duodenal ulcers. In other hosts, acid secretion may be reduced, leading to an association with gastric ulcers as well as gastric carcinoma and lymphoma. Topics include prevalence of H. pylori in developing countries, host factors, route of transmission, reinfection, bacteriology, virulence factors, acute versus chronic gastritis, the pathogenesis of ulcer formation, and the pathogenesis of H. pylori and gastric cancer. 1 table. 45 references.
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Hemorrhoids and More: Common Causes of Blood in the Stool. Digestive Health and Nutrition. 3(4): 24-26. July-August 2001.
Most rectal bleeding is caused by hemorrhoids, which usually can be simply and effectively treated. This article reviews the many other conditions, including some serious disorders, that can cause blood in the stool. The author reminds readers that bleeding from any part of the nearly 40 foot long digestive tract can cause blood in the stool. Accurate and timely diagnostic tests are important to determine the cause of any bleeding. Bleeding higher up in the gut, from the esophagus or stomach, can result in stools with a black, tarry appearance. Bleeding from the lower end, such as the colon, or in large amounts, can appear as pure blood, blood clots, or as blood mixed with or streaking the stool. Another kind of blood, occult or hidden blood, may not be visible at all. A number of prescription and over the counter (OTC) medications can cause bleeding in the stomach and small intestine. The blood thinning drug warfarin also can induce bleeding in the intestine, as can some antibiotics. Other causes of bleeding can include ulcers, gastritis (inflammation of the stomach lining), ulcerative colitis, Crohn's disease, polyps (small growths inside the intestine), diverticular disease, abnormalities in the blood vessels (vascular anomalies), anal fissures (tears) and fistulas (abnormal openings between the anal canal and other organs, such as the bladder), and abscesses (pockets of infection. The author reiterates the importance of timely diagnosis, including a thorough patient history and evaluation of symptoms. Diagnostic tests can include blood tests, digital rectal examination, endoscopy, colonoscopy, sigmoidoscopy, fecal occult blood test, barium x rays, angiography (x rays of blood vessels), and nuclear scanning. Treatment depends on the source and extent of the bleeding.
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Improvement in Atrophic Gastritis and Intestinal Metaplasia in Patients in Whom Helicobacter Pylori Was Eradicated. Annals of Internal Medicine. 134(5): 380-386. March 6, 2001.
Glandular atrophy and intestinal metaplasia (changes in the cells of the intestinal lining) are precancerous lesions; whether Helicobacter pylori infection or its eradication affects these lesions is controversial. This article reports on a study undertaken to determine whether eradication of H. pylori is associated with improvement in glandular atrophy and intestinal metaplasia after at least 1 year. The single blind prospective trial included 163 consecutive patients with dyspepsia and H. pylori infection, seen at an academic gastroenterology clinic in Japan. The intervention consisted of a 1 week course of a proton pump inhibitor and antibiotic therapy. In the 115 patients in whom H. pylori was eradicated, inflammation and mean neutrophil activity had decreased by 1 to 3 months, and both glandular atrophy in the corpus (the main body of the stomach) and intestinal metaplasia in the antrum had decreased by 12 to 15 months. Glandular atrophy in the corpus improved in 34 of 38 patients (89 percent) with atrophy before treatment, and intestinal metaplasia in the antrum improved in 28 of 46 patients (61 percent) who had metaplasia at baseline. In the 48 patients in whom eradication was unsuccessful, no significant histologic changes were observed. The authors conclude that in the year after successful H. pylori eradication, precancerous lesions improved in most patients. 1 figure. 1 table. 20 references.
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Overexpression of Co-Stimulatory Molecules in Peripheral Mononuclear Cells of Helicobacter Pylori-Positive Peptic Ulcer Patients: Possible Difference in Host Responsiveness Compared With Non-Ulcer Patients. European Journal of Gastroenterology and Hepatology. 13(1): 11-18. January 2001.
Helicobacter pylori is the principal cause of gastritis and peptic ulcer disease. However, H. pylori positive patients do not always have peptic ulcer. This study was carried out in order to determine the difference in host immune reaction to H. pylori between patients with peptic ulcer and those without. The study included 10 H. pylori positive patients with peptic ulcer, 10 H. pylori positive nonulcer patients, and 10 healthy volunteers who were examined for expression of surface molecules in peripheral blood mononuclear cells. The results showed more mononuclear cells expressed molecules ICAM-1, VLA-4, Leu-M3 in H. pylori positive ulcer patients than in nonulcer patients and healthy volunteers. There were also more cells expressing CD28, SLex, CD4, HLA-DR, and NU-B2 in H. pylori positive ulcer patients than in nonulcer patients and healthy volunteers. There were fewer cells expressing CD8 in H. pylori positive ulcer patients than in nonulcer patients and healthy volunteers. The authors conclude that H. pylori infection may cause immunological reactions which are reflected in peripheral mononuclear cells. However, the activity and characteristics of peripheral mononuclear cells, in terms of expression of adhesion molecules, may differ between ulcer and nonulcer patients who are infected with H. pylori. 8 figures. 31 references.
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Gastric Biopsy. Gastrointestinal Endoscopy Clinics of North America. 10(4): 723-738. October 2000.
This article focuses on the global settings where biopsy is done, on the practical issues of how to perform gastric biopsy, and what might be the benefit. The section on biopsy tips is condensed to provide practical information that offers some new information even for experienced endoscopists. The authors cover the three histological zones of the stomach (cardiac, oxyntic, and antral), when to biopsy to rule out neoplasia, and biopsy in benign gastric mucosal disease. The biopsy tips section covers a description of the biopsy location, special information needed for the pathologist, biopsy of histological zones, mapping the stomach, focal lesions, and acid suppression after multiple biopsies or large snare biopsy or polypectomy. At the time of biopsy of suspected or overt neoplasms, the endoscopist should try to determine whether tissue for special studies should be obtained; and whether the setting is such that biopsies from multiple sites might be indicated. The authors stress that there is a poor correlation between color changes and histologic abnormalities and emphasize that red mucosa is not reliably associated with gastritis, even though many clinicians insist on diagnosing gastritis on this inaccurate conclusion. 1 figure. 1 table. 57 references.
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Peptic Ulcer Disease: Dietary Factors, Its Repair and Relationship with Helicobacter Pylori Infection: Endoscopic Duodenitis, Gastric Metaplasia and Helicobacter Pylori. Journal of Gastroenterology and Hepatology. 16(5): 513-518. May 2001.
This article reports on a study undertaken to investigate the relationship between gastric metaplasia (changes in the cell structure in the stomach lining) and Helicobacter pylori in patients with endoscopic duodenitis (inflammation of the first section of the small intestine, as measured by endoscopy). The subjects were 57 patients with endoscopic duodenitis with or without H. pylori associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate, and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria. There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori positive and H. pylori negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori negative group, whereas the incomplete type was frequently observed in the H. pylori positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation. 3 figures. 6 tables. 16 references.
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Standard Acid Reflux Testing Revisited. Digestive Diseases and Sciences. 46(3): 603-605. March 2001.
Patients who present with uncontrolled esophageal acid reflux (return of the stomach's gastric acid to the esophagus) symptoms require endoscopy to determine the presence or absence of ulcers and stenoses (narrowed areas), acid reflux testing to determine if acid reflux is present, and manometry to evaluate esophageal peristalsis and spastic states. These studies are usually done in stages, at separate times. This article reviews the standard acid reflux testing in a cohort of 210 patients. Esophageal manometry catheters currently in use have an incorporated infusion channel. This allows the instillation of a dilute acid meal after esophageal manometry has been completed. Standard acid reflux testing can then be done using dynamic positioning and physiologic maneuvers. When combined with an esophagogastroduodenoscopy (EGD), these three studies provide all information necessary within 2 to 3 hours to determine further treatment of these patients. Of the 210 patients who underwent these studies, a hiatus hernia was present in 84 percent. An ineffective lower esophageal sphincter (the ring of muscle between the esophagus and the stomach) was found in 64 percent. Esophageal hypocontractility (not enough contraction in the esophagus) was present in 18 percent, hypercontractility (too much contraction) in 14 percent, and dysmotility (dysfunctional movement of contents through the esophagus) was found in 32 percent. Acid reflux disease was found in the hiatus hernia in 14 percent and acid reflux to the level of the lower esophagus in 16 percent, middle esophagus in 13 percent, and upper esophagus in 40 percent. Distal esophagitis (inflammation) was present in 47 percent, esophageal ulceration in 29 percent, gastric prolapse in 11 percent, gastritis in 52 percent, bile reflux disease in 10 percent, and Barrett's epithelium (changes in the cells lining the esophagus; a precancerous condition) in 5 percent. The author concludes that an extremely high number of patients with esophageal acid reflux disease show dysmotility patterns. Standard acid reflux testing using dynamic positioning will identify most patients with significant acid reflux disease. When combined with an EGD, complete testing for acid reflux disease can be performed at one setting. The author calls for additional studies comparing dynamic acid reflux testing to 24 hour pH testing. 1 table. 5 references.
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Gastritis: An Inflammation of the Stomach Lining. Yardley, PA: The StayWell Company: KRAMES Health and Safety Education. 2000. 2 p.
This brochure describes gastritis, a painful inflammation of the stomach lining. Gastritis and its symptoms can be relieved with treatment. The brochure lists common signs and symptoms, causes, the diagnostic approach used, specialized tests that may be used to confirm the diagnosis, treatment options, the importance of avoiding alcohol intake and smoking, reducing stress, and how the patient can participate in his or her own care. One sidebar includes an illustration of the stomach and a brief description of its physiology and the pathology of gastritis. The brochure is illustrated with full-color drawings. 8 figures.
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Risk of Ulcer Bleeding in Patients Infected with Helicobacter Pylori Taking Non-Steroidal Anti-Inflammatory Drugs (commentary). Gut. 46(3): 310-311. March 2000.
This article reports on a study to determine whether Helicobacter pylori is an independent risk factor for bleeding peptic ulcer in users of nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin. The prospective matched case control study included 132 patients with a bleeding peptic ulcer (n = 124) or hemorrhagic gastritis (n = 8) at endoscopy who had taken an NSAID in the previous week, and 136 controls who had taken NSAIDs without gastrointestinal complications. The controls were recruited from rheumatology and geriatric outpatient clinics. H. pylori was present in 57 percent of cases and 43 percent of controls. The adjusted odds ratio of bleeding from a peptic ulcer owing to H. pylori infection in NSAID users was 1.81 and was similar in aspirin and nonaspirin NSAID users. Peptic ulcer bleeding was also statistically significantly associated with a history of previous ulcer bleeding, dyspepsia within the previous 3 months, and drinking alcohol, but not with smoking. The authors contend that about 16 percent of bleeding peptic ulcers in NSAID users could be attributed to H. pylori infection. NSAID users infected with H. pylori have an almost doubled risk of bleeding peptic ulcer compared with uninfected NSAID users. 12 references.
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Usefulness of Helicobacter Pylori Stool Antigen Test to Monitor Response to Eradication Treatment in Children. Alimentary Pharmacology and Therapeutics. 15(2): 203-206. February 2001.
The monitoring of the results of eradication treatment is a crucial step for patients with Helicobacter pylori gastritis. A noninvasive test for H. pylori antigens in stools (HpSA) was recently validated for children. This article reports on a study undertaken to evaluate the accuracy of HpSA in monitoring eradication treatment in children. In 60 children, H. pylori gastritis was diagnosed by endoscopy and the 13C urea breath test. The children were treated and returned for a followup 13C urea breath test 6 weeks after the end of treatment. Children were considered cured when the 13C urea breath test was negative. Stool were collected at baseline and at 2 and 6 weeks. Stool antigens were measured by HpSA. According to 13C urea breath test, 6 weeks after the end of treatment, 49 children were cured and 11 were still H. pylori positive. The sensitivity and specificity of HpSA on stools collected 2 weeks after therapy were 100 percent. At 6 weeks, specificity was 93.9 percent and sensitivity 100 percent. Results by visual reading were concordant with the plate reader in all but two cases at baseline. The authors conclude that HpSA is accurate for monitoring treatment in children as early as 2 weeks after therapy, when information is most useful and unachievable with other tests. In addition, the HpSA is more cost effective than the 13C urea breath test and it is not available everywhere. Results of the HpSA by visual reading are accurate, and this can make the test cheaper and more practical. 1 figure. 1 table. 8 references.
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Community Acquired Acute Helicobacter Pylori Gastritis (editorial). Journal of Gastroenterology and Hepatology. 15(12): 1353-1355. December 2000.
This editorial comments on a study (printed in the same journal issue) that examined the efficacy of a short term Helicobacter pylori eradication therapy on acute gastritis. Among the 15 patients with hemorrhage acute gastritis who were randomly allocated to group A (eradication therapy) or group B (lansoprazole), 10 of the patients started to receive treatment within 1 day after the disease onset. The other five patients began the eradication therapy 4 to 6 days after disease onset (group C). All group A patients were cured after the 1 week treatment and therefore, they became H. pylori negative. Group B and C patients had erosions or ulcers after the 1 week treatment and so received an additional 3 week administration of LPZ. The authors of the research conclude that in patients with acute gastritis, caused by an initial H. pylori infection, eradication therapy was efficacious in achieving early healing. This therapy should therefore be started as soon as possible after disease onset. The editorial cautions that other factors need to be taken into consideration. The editorial notes that it is unclear whether the symptomatic response reported in the study was related to the therapy given, the natural history of the disease or both. The editorial also reminds readers that the spectrum of the initial presentation of H. pylori infection remains unknown. Most clinicians agree that the diagnosis of H. pylori infection should prompt therapy, but diagnosis is often not confirmed by endoscopy. For clinical purposes, this is unimportant, but the editorial stresses that the research presented in the accompanying article cannot support the conclusions the researchers made, without the confirmation of diagnosis through endoscopy. 29 references.
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Cure of Helicobacter Pylori Infection in Atrophic Body Gastritis Patients Does Not Improve Mucosal Atrophy But Reduces Hypergastrinemia and Its Related Effects on Body ECL-Cell Hyperplasia. Alimentary Pharmacology and Therapeutics. 14(5): 625-634. May 2000.
The effects of Helicobacter pylori eradication on atrophic body gastritis are controversial. This article reports on a study undertaken to investigate the effect of triple therapy on atrophic body gastritis in H. pylori positive patients and its effect on morphofunctional gastric parameters. Consecutive patients (n = 35) with atrophic body gastritis with histological or serological evidence of H. pylori infection were treated. Before and 6 and 12 months after H. pylori eradication the patients were evaluated for fasting gastrinemia and pepsinogen I, basal and peak acid output, and detailed histological assessment including the ECL cell proliferative patterns. Six months after treatment, 25 out of 32 patients were cured (78 percent). Cure of infection was associated with improvement in both basal and stimulated acid secretion, as well as with reduction in hypergastrinemia. In contrast, the eradication had no effect on body corporal atrophy and intestinal metaplasia, or pepsinogen I levels. These results were confirmed at 12 months after eradication. A statistical inverse correlation was obtained between the corporal chronic infiltrate score and peak acid output values. A total of 53 percent of atrophic body gastritis patients showed a regression in severity of body ECL cell hyperplastic change. The authors conclude that cure of H. pylori infection in patients with atrophic gastritis reverses some adverse effects on gastric function and ECL cell hyperplasia. 3 figures. 2 tables. 38 references.
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Gastroesophageal Reflux Disease: Under the Surface of Heartburn Lies a Potentially Serious Disease. AJN. American Journal of Nursing. 100(9): 24D, 24F, 24H. September 2000.
This article familiarizes nurses with gastroesophageal reflux disease (GERD), a potentially serious disease that can be the cause of many patient's symptoms of heartburn. Heartburn is the most common symptom of GERD, which is caused by a weakened or inappropriately relaxed lower esophageal sphincter (the ring of muscle between the stomach and the esophagus). GERD is the most prevalent of the acid related disorders, which also include dyspepsia, gastritis, and peptic ulcer disease. The primary symptom of GERD is heartburn, which typically occur two to three hours after ingestion of a large or fatty meal or when lying down. When the gastric acid is in contact with the esophagus repeatedly or for long periods of time, the esophagus can become damaged and irritated; this can also cause the development of precancerous cells. A careful history can help differentiate between cardiac chest pain, panic attacks, other sources of esophagitis, and GERD. Diagnostic tests can include barium swallow test, esophageal manometry or esophageal pH, esophagoscopy, and the Bernstein test. These diagnostic studies assess esophageal motility (movement of contents through the esophagus), clearance, and the causes of gastroesophageal reflux. Treatment goals for patients with GERD are to eliminate the symptoms, decrease the reflux, and make the refluxed material less irritating to the esophagus. Treatment includes dietary and lifestyle changes, drug therapy, and sometimes surgery. 1 figure. 15 references.
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Gastrointestinal Bleeding in Infancy and Childhood. Gastroenterology Clinics of North America. 29(1): 37-66. March 2000.
Gastrointestinal (GI) bleeding is an alarming problem in children. Although many causes of GI bleeding are common to children and adults, the frequency of specific causes differs greatly, and some lesions, such as necrotizing enterocolitis or allergic colitis, are unique to children. This article reviews the spectrum of GI bleeding in infants and children. The author discusses the causes (etiology), diagnostic evaluation, and management, and highlights the differences with adult medicine. The more common causes of upper GI bleeding in children are ulcer and gastritis, esophagitis, and varices (enlarged veins or arteries). A detailed history and careful physical examination accompanied by limited laboratory studies may identify the underlying cause and predict the severity of gastrointestinal hemorrhage. Endoscopy is the preferred diagnostic procedure because it is sensitive and specific and, for some lesions, provides the means for immediate treatment. Medical therapy (drugs) is similar for adults and children, differing mostly in the dosage of medications. One table lists pediatric doses for medications commonly used in upper gastrointestinal bleeding. Endoscopic therapy may be used in children with an actively bleeding focal lesion or with a lesion at high risk of rebleeding. Surgery is reserved for bleeding that is uncontrollable by less invasive interventions. The latter part of the article reviews lower GI bleeding, noting that age is an important factor in diagnosis of etiology (cause). Colonoscopy is the preferred diagnostic modality for rectal bleeding. The article concludes with a brief description of small bowel hemorrhage, usually due to Meckel's diverticulum (a congenital anomaly), duplications of the bowel, or idiopathic necrotizing enteritis. 4 figures. 3 tables. 212 references.
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Gastrointestinal Bleeding in Older People. Gastroenterology Clinics of North America. 29(1): 1-36. March 2000.
Aging is associated with an increased rate of comorbidity, greater medication use, and atypical presentations. The aging of the population makes the evaluation and management of gastrointestinal bleeding makes the evaluation and management of gastrointestinal bleeding in older people a special and increasingly common clinical challenge. In this article, the unique features and common causes of upper and lower gastrointestinal bleeding in older people are reviewed. The hospital course of elderly patients with upper gastrointestinal bleeding appears to be similar to that of younger patients with respect to the use of endoscopic therapy for bleeding and rebleeding, need for general anesthesia for endoscopy, rates of admission to an intensive care unit, blood transfusion requirements, frequency of surgery, and duration of hospital stay. The authors consider some important management issues including hemodynamic resuscitation, anticoagulation, and endoscopic and surgical therapy. The authors review specific upper gastrointestinal bleeding lesions, including esophagitis and gastritis, peptic ulcer disease (particularly that caused by nonsteroidal antiinflammatory drugs), and variceal bleeding; and specific lower gastrointestinal bleeding lesions, including colonic diverticula, angiodysplasia, colonic ischemia, and inflammatory bowel disease. The authors also conclude that planning for care beyond the acute bleeding episode in this population is critical and involves an understanding of the importance of rehabilitation and community based services and involvement of a caregiver. 11 tables. 153 references.
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Helicobacter Pylori Gastritis and Gastric Physiology. Gastroenterology Clinics of North America. 29(3): 687-703. September 2000.
This article reviews Helicobacter pylori gastritis and gastric physiology. Helicobacter pylori gastritis (stomach inflammation) can alter stomach physiology, leading to increased or decreased acid secretion, depending on the pattern of gastritis present. These changes in physiology are related to the disease outcome, with increased acid secretion leading to duodenal ulcer disease and reduced acid secretion being a risk factor for gastric (stomach) cancer. Gastric acid secretion also affects the pattern of gastritis induced by the infection, with low acid secretion leading a pangastritis and possibly atrophy. This two way interaction between H. pylori gastritis and gastric acid secretion is important in understanding the role of H. pylori infection in the response to proton pump inhibitor therapy. This interaction explains the more profound control of gastric acid secretion in H. pylori positive patients and why rebound acid hypersecretion is confined to H. pylori negative subjects. 6 figures. 60 references.
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Helicobacter Pylori Infection and Gastric Cancer in the Asia Pacific Region. Asian Pacific Gastroenterology News. Issue 4: 11. June 2000.
Helicobacter pylori infection causes histological gastritis; chronic gastritis from long term H. pylori infection results in gastric mucosal atrophy, which eventually progresses to intestinal metaplasia and sometimes to gastric (stomach) cancer. This brief article reviews the problem of H. pylori infection and gastric cancer in the Asia Pacific region. The author reports data that show just over 10 percent of H. pylori infected persons in Japan may develop gastric cancer. The prevalence of asymptomatic H. pylori infection differs greatly between countries, being low in developed countries and high in developing countries. Because H. pylori is transmitted via the fecal to oral route, and children are more readily infected than adults, the author notes that conducting a survey on H. pylori infection is the same as assessing the water supply and sewage systems of a country. The present prevalence of H. pylori infection in Japan is extremely low at an early age, as in other developed countries, and subsequently shows a rapid increase until it reaches a plateau of approximately 70 percent at 50 years of age. The author also explores the different incidence of gastric cancer as it varies between countries. It is suggested that H. pylori infection leads to histological chronic gastritis, regardless of the strain of the organism, and after that the course of the disease depends on environmental factors (diet, age), virulence of H. pylori strains, and host factors including genetics. The author concludes by calling for additional research collaboration between countries in the Asia Pacific region. 1 figure.
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Helicobacter Pylori Infection in Childhood: Results of Management with Ranitidine Bismuth Citrate Plus Amoxicillin and Tinidazole. Journal of Gastroenterology and Hepatology. 15(11): 1243-1250. November 2000.
This article reports on a study undertaken to verify whether a triple therapy bismuth citrate plus amoxicillin and tinadazole eradicates Helicobacter pylori infection in pediatric patients (children). Fifty children (30 females; mean age 12.4 years; range 10 to 15 years) who had upper abdominal complaints and H. pylori associated gastroduodenal disease were treated with a 4 week course of ranitidine bismuth citrate (400 mg, twice daily) plus oral tinidazole (20 mg per kg) and amoxicillin (50 mg per kg) for the first 2 weeks. The endoscopic diagnoses were: esophagitis (7 cases), gastritis (6 cases), gastroduodenitis (43 cases), duodenitis (1case), gastric ulcer (2 cases), and duodenal ulcer (13 cases). H. pylori was eradicated in 40 patients (80 percent) and clinical improvement was noticed in 39 (78 percent) of symptomatic subjects. Duodenal ulcers were healed in all the children, but lymphoid nodular hyperplasia was persistent in all patients, independent of the H. pylori status. The potentially drug related adverse events were registered in seven patients (14 percent) and dark stools were observed in 48 patients (96 percent). Drug related adverse events included blackening of the tongue (6 patients), diarrhea (1 patient), and disturbance of taste (2 patients). No children withdrew from the study because of either side effects or clinical laboratory changes. No patient had toxic levels of blood bismuth. The authors conclude that findings suggest that the present treatment regimen is effective enough in the resolution of H. pylori associated peptic ulcer disease (PUD) of childhood. 3 tables. 47 references.
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Helicobacter Pylori Infection, Gastritis and Gastric Cancer: A Short-Term Eradication Therapy for Helicobacter Pylori Acute Gastritis. Journal of Gastroenterology and Hepatology. 15(12): 1377-1381. December 2000.
Acute gastritis (stomach inflammation), caused by an initial infection of Helicobacter pylori, may resolve spontaneously, but the infection sometimes becomes chronic. The authors of this article examined the efficacy of a short term H. pylori eradication therapy on acute gastritis. Among the 15 patients with hemorrhage acute gastritis who were randomly allocated to group A (eradication therapy) or group B (lansoprazole), 10 of the patients started to receive treatment within 1 day after the disease onset. The other five patients began the eradication therapy 4 to 6 days after disease onset (group C). Eradication therapy consisted of a daily oral administration of each of 30 milligrams lansoprazole (LPZ) once a day; 400 milligrams clarithromycin, twice a day; 1000 milligrams amoxicillin, twice a day; and 300 milligrams rebamipide, three times a day, for one week. If the endoscopy was normal, medication was stopped for the following 4 weeks before gastric endoscopy was performed again in order to assess H. pylori eradication. All group A patients were cured after the 1 week treatment and, therefore, they became H. pylori negative. Group B and C patients had erosions or ulcers after the 1 week treatment and so received an additional 3 week administration of LPZ. Four weeks later, their gastritis was cured and except for one group B patient, they became H. pylori negative. The authors conclude that in patients with acute gastritis, caused by an initial H. pylori infection, eradication therapy was efficacious in achieving early healing. This therapy should therefore be started as soon as possible after disease onset. 1 table. 25 references.
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Review Article: Helicobacter Pylori Vaccines-the Current Status. Alimentary Pharmacology and Therapeutics. 14(9): 1107-1118. September 2000.
In this review article, the authors take a look at the current status in the development of a vaccine against the human pathogenic bacterium, Helicobacter pylori, a major etiologic factor (cause) of peptic ulcer disease and gastric adenocarcinoma. Various animal models are now in use from mice infected with H. pylori, through gnotobiotic pigs and primates, to ferrets naturally infected with their own Helicobacter, H. mustelae. A significant problem remains the requirement for a suitable mucosal adjuvant. Detoxification or the use of low doses of adjuvants already available may provide a solution, and new immune stimulating compounds have been tested with some success. New approaches include the delivery of Helicobacter antigens by DNA immunization, microparticles, or live vectors such as attenuated salmonella and the examination of alternative routes of vaccine administration. The phenomenon of post immunization gastritis and improvements in vaccine efficacy are also discussed. A major area of interest is the mechanism by which immunization actually influences Helicobacter colonization. This remains a mystery: antibodies appear to be unimportant whereas CD4 positive T cells are essential. Finally, the authors offer their viewpoint on whom should be immunized when a final vaccine becomes available. 63 references.
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Helicobacter Pylori Infection, Gastritis and Gastric Cancer: Helicobacter Pylori Infection Among Japanese Children. Journal of Gastroenterology and Hepatology. 15(12): 1382-1385. December 2000.
In Japan, there are few reports describing Helicobacter pylori infection among young children. This article reports on a study undertaken to identify risk factors associated with H. pylori in school aged children in Japan. Subjects were first grade students of three elementary schools (n = 310) and second grade students of a junior high school (n = 300). Personal information, such as students' medical history, parents' history, family size, siblings, and household pets, was collected using a questionnaire. Saliva samples and personal information were collected twice. Among the children, factors related to Helicobacter antibody in saliva included spending a longer period of time in a nursery school or kindergarten and a maternal history of stomach disease. Birth order, sleeping situation, and number of siblings were not factors that were significantly related to Helicobacter antibody in the saliva. Chewing food for the infant, family size, rooms in the household, sharing a bedroom during childhood, pets, a past history, and a paternal history were not related to positivity. The results indicate that transmission is person to person, mainly through close contact with other children and intrafamilial infection. H. pylori infection seems to occur frequently early in life, probably before 6 years of age. 2 tables. 29 references.
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Helicobacter Pylori: An Emerging Infectious Disease. Nurse Practitioner. 25(8): 40, 43-44, 47, 50, 53-55. August 2000.
Helicobacter pylori is the most common chronic bacterial infection in the world, colonizing the stomachs of more than 50 percent of the human population. The discovery of this bacterium has changed the concept of care and management for peptic ulcer disease (PUD), mucosa associated lymphomas, gastritis, and gastric carcinoma (stomach cancer). Although the mode of transmission is not definitively known, person to person contact is suspected. This article discusses H. pylori, the associated clinical syndromes and diseases, risk factors, and current pharmacologic management. In the United States, H. pylori prevalence increases by 10 percent with each decade of life. The infection is more prevalent in groups of lower socioeconomic status. Crowded living conditions, such as in institutions, increase the incidence and prevalence. Controversy exists regarding testing patients for H. pylori who present with complaints consistent with dyspepsia. Those who should be tested for H. pylori include patients who have a history of PUD and have not been treated for H. pylori in the past, and patients with a history of MALT lymphoma. A recent report suggests screening patients with a parental history of gastric cancer. For outpatient diagnosis, serology or a urea breath test can be used with high sensitivity and relatively low cost. A variety of treatment protocols may be used to eradicate H. pylori; however, only two are currently approved by the Food and Drug Administration. One regimen consists of amoxicillin, clarithromycin, and omeprazole for 14 days; the second regimen uses amoxicillin, clarithromycin, and lansoprazole for 10 days. Reinfection rarely occurs after successful treatment of H. pylori. A posttest with which readers can quality for continuing education credits is appended to the article. 3 figures. 2 tables. 44 references.
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Long-Term Omeprazole Treatment in Resistant Gastroesophageal Reflux Disease: Efficacy, Safety, and Influence on Gastric Mucosa. Gastroenterology. 118(4): 661-669. April 2000.
The efficacy and safety of long term acid suppression (to treat recurrent gastroesophageal reflux disease, or GERD) remains a subject for debate. This article reports on a study of patients refractory reflux esophagitis who were undergoing maintenance therapy with a regimen of greater than 20 mg omeprazole daily for a mean period of 6.5 years (range, 1.4 to 11.2 years). Patients with severe reflux esophagitis resistant to long term therapy with H2 receptor antagonists and who were not eligible for surgery were evaluated at least annually for endoscopic relapse and histological changes in the gastric corpus (the base of the stomach). In 230 patients (mean age, 63 years at entry; 36 percent were older than 70 years), there were 158 relapses of esophagitis during 1490 treatment years (1 per 9.4 years), with no significant difference in relapse rates between Helicobacter pylori positive and negative patients. All patients rehealed during continued therapy with omeprazole at the same or higher dose. The annual incidence of gastric corpus mucosal atrophy was 4.7 percent in H. pylori positive patients and 0.7 percent in H. Pylori negative patients, which was mainly observed in elderly patients who had moderate or severe gastritis at entry. In patients with baseline moderate or severe gastritis, the incidences were similar: 7.9 percent and 8.4 percent, respectively. Corpus intestinal metaplasia was rare, and non dysplasia or neoplasms were observed. The adverse event profile was as might be expected from this elderly group of patients. The authors conclude that long term omeprazole therapy (up to 11 years) is highly effective and safe for control of reflux esophagitis. 3 figures. 3 tables. 40 references.
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Pathophysiology of GERD: Role of the Stomach. Practical Gastroenterology. 24(1): 16, 18, 21-22, 24, 26. January 2000.
Although the esophagus is the site of injury for gastroesophageal reflux disease (GERD), the stomach is the origin of the refluxate and its pressure gradients and emptying rates augment the degree of physiological and pathological reflux. This article explores the role of the stomach in the pathophysiology of GERD. This disease happens more readily if a positive pressure gradient is established between the stomach and the esophagus. This condition is more likely to occur if the stomach contains large amounts of fluids and solids available for reflux. In addition, reflux will cause mucosal damage only if the refluxate has a composition that is harmful to the esophageal mucosa, whereas reflux of gastric contents at pH 7 is unlikely to cause esophagitis. The author reviews these important gastric factors influencing GERD, including gastric emptying, acid and pepsin secretion, and the influence of Helicobacter pylori infection. The author does not consider duodenogastric reflux and its associated bile and pancreatic enzymes in this article. Patients with reflux are rarely hypersecretors of acid, but H. pylori infection and its associated corpus gastritis decrease intragastric acidity and appear to prevent GERD complications. This seminal observation may help explain the increasing prevalence of heartburn, Barrett esophagus, and adenocarcinoma of the esophagus in the Western world that seems to be paralleling the fall in the infection rate with H. pylori. 2 figures. 2 tables. 31 references.
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Pediatric Gastrointestinal Mucosal Biopsy: Special Considerations in Children. Gastrointestinal Endoscopy Clinics of North America. 10(4): 669-712. October 2000.
In most disorders of the gastrointestinal (GI) mucosa that occur in both children and adults, the mucosal manifestations are the same. This article focuses on those disorders and the approaches to GI procedures and mucosal biopsy that are of a particularly or peculiarly pediatric nature (i.e., are different from those in adults). The authors discuss issues pertaining to endoscopy and other techniques of mucosal biopsy in children, because some approaches and techniques are considerably different from those in adults. In children as in adults, most mucosal biopsies are taken at upper GI endoscopy or colonoscopy, with rectal suction biopsy (RSB) being performed occasionally and blind esophageal suction biopsy very rarely. The authors caution that major problems can arise in pediatric endoscopy when children are approached and instrumented like adults. The authors describe the preparation of the child and family, sedation, bowel preparation, and fasting. The authors include a section discussing disorders in which there are special features in children that may be significantly different from adults, including gastroesophageal reflux disease (GERD), idiopathic eosinophilic esophagitis, Barrett's esophagus, Helicobacter pylori infections, Crohn's disease, allergic gastritis, celiac gastritis, chronic granulomatous disease, Menetrier's disease, neonatal gastropathies, Henoch Schonlein gastritis, cow's milk protein enteritis, microvillous inclusion disease, tufting enteropathy, autoimmune enteropathy, inflammatory bowel disease, pseudomembranous colitis, necrotizing enterocolitis, glycogen storage disease, Hirschsprung's disease, intestinal neuronal dysplasia, and colorectal cancer. 217 references.
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Review Article: Is Helicobacter Pylori Status Relevant in the Management of GORD?. Alimentary Pharmacology and Therapeutics. 14(Supplement 3): 31-42. October 2000.
This article explores the growing interest in the relationship between Helicobacter pylori infection and gastroesophageal reflux disease (GERD). The authors note that this relationship is complex, as yet not fully clear, and probably based on multiple factors. The prevalence of H. pylori infection in patients with GERD is similar, but more often lower than in matched controls. There is a negative correlation between H. pylori infection and the severity of GERD. There are many hypothetical mechanisms by which H. pylori infection may protect from the development of GERD. Conversely, there are many possible mechanisms by which H. pylori infection could theoretically foster the GERD. Patients after H. pylori eradication may develop GERD, and this seems to suggest a protective role of H. pylori infection, but other possible explanations include weight gain after H. pylori eradication, changes in dietary habits and smoking, and preexisting GERD. Long term therapy of GERD in patients infected with H. pylori may lead to rapid progression of atrophic gastritis (stomach inflammation), intestinal metaplasia and dysplasia, and increase the risk of developing gastric (stomach) cancer. More recently, it has been shown that H. pylori infection may interfere with the acid suppressive therapies used for treating GERD. The authors propose that the progression of gastritis depends on the threshold of acid output at which H. pylori can flourish. Any decrease of acid secretion changes the behavior of H. pylori. During proton pump inhibitor (PPI) treatment, H. pylori redistribution occurs within the stomach. The authors also discuss Barrett's esophagus, as growing evidence is compiled on the associated risk of adenocarcinoma. The literature seems to demonstrate that the prevalence of H. pylori infection of the stomach in Barrett's esophagus patients is not different from that exhibited by controls, roughly one third of the subjects. Intestinal metaplasia (overgrowth) of the gastric cardia (the proximal part of the stomach) seems to be equally frequent in patients with and without GERD. The authors conclude that it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's associated adenocarcinoma. 1 figure. 100 references.
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Surgical Management of Gastrointestinal Bleeding. Gastroenterology Clinics of North America. 29(1): 189-222. March 2000.
The role of surgery in gastrointestinal (GI) bleeding has recently diminished because of the development of effective endoscopic and interventional radiologic therapies. Nevertheless, operation remains an important salvage strategy for failure of less invasive interventions and is required in most patients with bleeding GI neoplasms other than small benign polyps. This article reviews the surgical management of GI bleeding. Operations for upper tract bleeding are often designed to address the specific pathophysiology responsible for the bleeding lesion. Operations for lower GI tract bleeding more commonly entail simple segmental bowel resections that encompass the bleeding lesion. The combined application of endoscopic and laparoscopic techniques now provides a minimally invasive alternative to treat a highly selected group of patients with GI bleeding. The authors review surgical strategies for hemorrhagic gastritis, esophageal and gastric varices, esophageal ulcers and erosions, Mallory-Weiss tears, Dieulafoy's lesion, angiodysplasia, neoplastic lesions, hemobilia, pancreatic pseudocysts and pseudoaneurysms, aortoenteric fistula, diverticular disease, arteriovenous malformations, inflammatory bowel disease (IBD), tumors of the colon and rectum, anorectal disease, and Meckel's and other small intestinal diverticula. The authors conclude that, despite the less frequent need for surgical intervention, traditional operative approaches, such as suture ligation, lesion or organ excision, vagotomy, portasystemic anastomosis, and devascularization procedures, continue to be life saving in many instances. 8 figures. 2 tables. 156 references.
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Treatment of Helicobacter Pylori: An Overview. Alimentary Pharmacology and Therapeutics. 14(Supplement 3): 1-6. October 2000.
Helicobacter pylori is recognized to be a serious pathogen, but there is still controversy as to who should be treated. This article reviews the arguments and some of the data advanced to support the differing views; the author briefly considers the currently used therapies and how they may best be employed. There is consensus for treatment of patients with H. pylori positive peptic ulcer and B cell lymphoma. Patients with lymphcytic gastritis and giant fold gastritis (Menetrier's disease) may also respond to treatment. Patients with functional dyspepsia have a 20 percent placebo response with a 5 to 10 percent 'eradication' response, results not dissimilar from empirical treatment with a proton pump inhibitor (PPI). A 'test and treat' policy for patients with uninvestigated dyspepsia remains controversial. Some clinicians have suggested that eradication of the H. pylori may increase the patient's risk of gastroesophageal reflux disease (GERD) or predispose patients to adenocarcinoma at the gastroesophageal junction (stomach cancer). However, PPI treatment without H. pylori eradication induces greater inflammation in the gastric corpus; this is the phenotype associated with non-cardia gastric cancer. A minority of clinicians believe the H. pylori should be eradicated in all individuals. The author concludes that, when choosing treatment, it is logical to start with a combination of antibiotics that, in the event of failure, will allow a second combination to be used without overlap. The author recommends the use of amoxycillin, clarithromycin, and a PPI for the first treatment, which then leaves the option of ranitidine bismuth citrate, tetracycline, and metronidazole, in the event of first line failure. 37 references.
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Trend Toward a Reduced Prevalence of Helicobacter Pylori Infection, Chronic Gastritis, and Gastric Cancer in Japan. Gastroenterology Clinics of North America. 29(3): 623-631. September 2000.
Although there has been a remarkable decline in the prevalence and mortality (death) rates of gastric (stomach) cancer in developed countries, gastric cancer is one of the common malignancies in the world and is still the main cause of death in Japan. This article investigates the trends in Helicobacter pylori infection and gastritis in Japan over the past few decades. The author notes that it is important to investigate the relationship between H. pylori infection and gastric cancer and gastritis to understand better the mechanisms for carcinogenesis (the development of cancer) in the stomach. The author speculates that declines in H. pylori infection and gastritis over the past few decades may lead to a decline in gastric cancer in Japan, supplemented by excellent procedures for the early detection of gastric cancer. H. pylori infection rarely is acquired in adult life, so once it is eradicated, reinfection is not expected in adult patients. The author concludes that adequate treatment of H. pylori provides long term protection against gastric cancer.
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Understanding H. Pylori. Nurse Practitioner. 25(8): 48. August 2000.
This patient education handout reviews Helicobacter pylori, the most common chronic bacterial infection in the world, colonizing the stomachs of more than 50 percent of the human population. Many people have no signs that they are infected, but others may have a burning stomach pain, nausea, vomiting, and reduced appetite. The infection weakens the lining of the stomach and may lead to an ulcer. H. pylori infection has been associated with gastritis, ulcers, stomach tumors, and iron deficiency anemia. In the United States, approximately 20 percent of the population may be infected. Children and adults can be infected with H. pylori, although infection rates increase as one gets older. H. pylori testing is done through a blood test, a breath test, or by endoscopy. H. pylori is treated with a combination of drugs that kill bacteria (antibiotics) and drugs that suppress the acid in the stomach. Reinfection rarely occurs after successful treatment of H. pylori. If symptoms remain after treatment, the patient is usually referred to a gastroenterologist (a digestive specialist). The fact sheet concludes with the contact address for the National Digestive Diseases Information Clearinghouse (NDDIC), for patients wishing to obtain additional information.
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