Helicobacter Pylori: Basic Mechanisms to Clinical Cure 2000

ISBN-13: 9780792387640 / Angielski / Twarda / 2000 / 689 str.

Guido N. J. Tytgat; Richard H. Hunt; G. N. J. Tytgat

Opis

The fourth meeting in the very successful series Helicobacter pylori: Basic Mechanisms to Clinical Cure was held on the island of Bermuda in late March 2000. This was only some two years after the third meeting in San Diego and it seemed hardly possible that there would be so much new information. However, as the contributions in this volume testify, there was plenty of exciting new information with important implications for both understanding this infection and for clinical management. Some of this information was of a fundamental nature, such as the role of the acid sensitive urel channel in regulating the influx of urea and the formation of ammonia transported back in the microbial periplasmic space to neutralize acid; the observation of genetic polymorphism of the IL-1 gene as an explanation of achlorhydria and gastric cancer risk in the first-degree relatives of gastric cancer patients; and the peculiar biochemical and physio logical consequences of the genome of the microorganisms. The format of the meeting, with short fifteen-minute state-of-the-art pre sentations by world experts closely involved in Helicobacter research fol lowed by ample time for panel discussions, was again followed this year. Traditional aspects included detailed study of the microbial characteristics, the novel Helicobacters, the interaction with the human host, the peculiarities of the inflammatory immune response, the short and long-term mucosal consequences, the effects on acid secretion, the problem of gastric malignancy and the therapeutic possibilities."

Recenzje

`This book provides an extensive compendium of information(with an index) on the recent developments in the broad range of investigations into H.pylori and its varions manifestations. It will be a valuable, up-to-date resource for gastroentelogists, microbiologists, and anyone interested in H.pylori.'
Helicobacter pylori: Basic Mechanisms to Clinical Cure 200 (2000)

Spis treści

Section I: Helicobacter pylori — The Organism.- 1 What are the biochemical and physiological implications of the new genetic information?.- 2 The urease system of Helicobacter pylori.- 3 The amphibiotic relationship of Helicobacter pylori and humans.- 4 Helicobacter pylori is pathogenic flora.- 5 Disease-specific Helicobacter pylori virulence factors: the role of cagA, vacA, iceA, babA2 alone or in combination.- Section II: Helicobacter pylori — Epidemiology.- 6 Factors associated with disappearance of Helicobacter pylori in the West.- 7 Factors associated with disappearance of Helicobacter pylori in the Far East.- 8 Differences in prevalence of Helicobacter pylori and disease outcomes according to race/environmental factors in Southeast Asia.- Section III: Novel Helicobacters.- 9 Infection with Helicobacter heilmannii (formerly Gastrospirillum hominis): characterization, epidemiology and therapy.- 10 Hepatobiliary Helicobacters: recognized animal pathogens with suspected pathogenic potential in humans.- 11 Novel Helicobacter species in the intestine.- Section IV: Diagnosis of Helicobacter pylori Infection.- 12 Diagnosis of Helicobacter pylori infection: faecal antigen determination.- 13 Pitfalls in Helicobacter pylori diagnosis.- Section V: Inflammation and the Immune Response to Helicobacter pylori Infection.- 14 Overview of immune and inflammatory changes due to Helicobacter infection.- 15 Interaction of Helicobacter pylori with gastric epithelium.- 16 Helicobacter pylori and the epithelial barrier: role of oxidative injury.- 17 Immuno-inflammatory response to Helicobacter pylori in children.- 18 Severity and reversibility of mucosal inflammation in children and adolescents infected with Helicobacter pylori.- 19 Elimination of Helicobacter pylori is dependent on a Th2 response.- 20 Elimination of Helicobacter pylori is not dependent on a Th2 cytokine response.- 21 The inflammatory activity in Helicobacter pylori infection is predominantly organism related.- 22 The inflammatory activity in Helicobacter pylori infection is predominantly host-related.- Section VI: Helicobacter pylori and Gastritis.- 23 Helicobacter pylori gastritis — a global view.- 24 Unusual forms of gastric inflammation and their relationship to Helicobacter pylori infection.- 25 Can atrophic gastritis be diagnosed in the presence of Helicobacter pylori infection?.- 26 Mechanisms involved in gastric atrophy.- 27 Intestinal metaplasia: types, mechanisms of origin, and role in gastric cancer histogenesis.- 28 Long-term proton pump inhibitor therapy accelerates the onset of atrophic gastritis in Helicobacter pylori-positive patients.- 29 Proton pump inhibitors do not accelerate the development of gastric atrophy in Helicobacter pylori gastritis.- 30 Autoimmune gastritis via mimicking does occur.- 31 Autoimmune gastritis and antigenic mimicking.- 32 Carditis and intestinal metaplasia of the cardia is reflux related.- 33 Carditis and cardia intestinal metaplasia are Helicobacter pylori-related.- 34 Is gastric metaplasia in Helicobacter pylori really gastric?.- Section VII: Helicobacter pylori and Clinical Consequences.- 35 Extragastric manifestations of Helicobacter pylori — are they relevant?.- 36 Peptic ulcer disease — the transitional zones are important.- 37 What causes Helicobacter pylori-negative non-NSAID-related ulcers?.- 38 From the pump to the helix.- 39 Mechanisms involved in the development of hypochlorhydria and pangastritis in Helicobacter pylori infection.- 40 Effect of Helicobacter pylori infection on gastric acid control using proton pump inhibitors.- 41 Rebound acid hypersecretion after acid-suppressive therapy.- 42 Gastric consequences of proton pump therapy and Helicobacter pylori eradication.- Section VIII: Helicobacter pylori, Dyspepsia and NSAIDs.- 43 Current concepts of dyspepsia: the role of the nervous system.- 44 How to explain outcome differences in dyspepsia studies.- 45 Helicobacter pylori eradication for dyspepsia is clinically useful.- 46 Dyspepsia is no indication for Helicobacter pylori eradication.- 47 Role of Helicobacter pylori infection in NSAID-associated gastropathy.- 48 Role of Helicobacter pylori in NSAID gastropathy: can Helicobacter pylori infection be beneficial?.- 49 Helicobacter pylori and non-steroidal anti-inflammatory drugs.- Section IX: Helicobacter pylori and ‘Test-and-Treat’ Strategies.- 50 The impact of a ‘test-and-treat’ strategy for Helicobacter pylori: the United States perspective.- 51 Test-and-treat strategy in dyspepsia — the European perspective.- 52 The impact of the ‘test-and-treat’ strategies for Helicobacter pylori infection — an Asian perspective?.- Section X: Helicobacter pylori and Gastric Malignancy.- 53 Rodent models for Helicobacter-induced gastric cancer.- 54 Helicobacter pylori and gastric cancer: the risk is real.- 55 Helicobacter pylori in gastric malignancy: role of oxidants, antioxidants and other co-factors.- 56 Gastric markers of pre-malignancy are not reversible.- 57 The case for the reversibility of gastric dysplasia/neoplasia.- 58 Evaluation of the long-term outcome of Helicobacter pylori-related gastric mucosa-associated lymphoid tissue (MALT) lymphoma.- Section XI: Treatment of Helicobacter pylori Infection.- 59 Current state-of-the-art management for Helicobacter pylori infection: global perspective.- 60 Guidelines for therapy of Helicobacter pylori infection — a world perspective.- 61 Bismuth triple and quadruple studies for Helicobacter pylori eradication in Canada.- 62 Approach to Helicobacter pylori infection in children.- 63 What role for clarithromycin in the treatment of Helicobacter pylori infection?.- 64 What is the role of bismuth in Helicobacter pylori antimicrobial resistance?.- 65 Risk factors for failure of Helicobacter pylori eradication therapy.- 66 Strategies for therapy failures: choice of ‘back-up’ regimen determined by primary treatment for Helicobacter pylori infection.- 67 Quadruple should be first-line therapy for Helicobacter pylori infection.- 68 Quadruple therapy should be secondline treatment for Helicobacter pylori infection.- 69 Helicobacter pylori infection: expectations for future therapy.- 70 A Helicobacter pylori vaccine is essential.- Section XII: Helicobacter Infections and the Future.- 71 The agenda for the microbiologist.- 72 The agenda for the immunologist.- 73 The agenda for the histopathologist.- 74 Helicobacter infections in the new millennium: the challenge for the clinician.