Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Helicobacter pylori and the oesophagus
Autore:
Zerbib, F; De Koster, E; Galmiche, JP;
Indirizzi:
Bordeaux Univ Hosp, Hop St Andre, Dept Gastroenterol & Hepatol, Bordeaux, France Bordeaux Univ Hosp Bordeaux France oenterol & Hepatol, Bordeaux, France
Titolo Testata:
CURRENT OPINION IN GASTROENTEROLOGY
fascicolo: 6, volume: 16, anno: 2001, supplemento:, 1
pagine: S33 - S38
SICI:
0267-1379(2001)16:6<S33:HPATO>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
GASTROESOPHAGEAL REFLUX DISEASE; GASTRIC-ACID SECRETION; INTESTINAL METAPLASIA; DUODENAL-ULCER; ESOPHAGOGASTRIC JUNCTION; ATROPHIC GASTRITIS; NONULCER DYSPEPSIA; CORPUS GASTRITIS; INFECTION; ESOPHAGITIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Galmiche, JP CHU Nantes, Hotel Dieu, Dept Gastroenterol & Hepatol, F-44035Nantes, France CHU Nantes Nantes France F-44035 ol, F-44035 Nantes, France
Citazione:
F. Zerbib et al., "Helicobacter pylori and the oesophagus", CURR OPIN G, 16(6), 2001, pp. S33-S38

Abstract

The relationship between H. pylori and gastroesophageal reflux disease (GERD) continues to remain an area of active research. Epidemiological studiesdo not support an important role of H. pylori in the pathogenesis of GERD. However, recent papers suggest that inflammation may sensitize the gastroesophageal junction to acid in non-erosive GERD. Otherwise, the impact of H.pylori infection on intragastric pH depends primarily on the distribution (antral versus pangastritis) and severity of gastritis. When GERD develops,corpus gastritis and gastric atrophy may reduce the severity of oesophagitis. In contrast there is no evidence that H. pylori infection can influencethe underlying motor pattern responsible for the occurrence of reflux episodes. Several studies have contributed to the clarification of the relationships between H. pylori and the cardia. It is becoming more and more obvious that carditis has at least two aetiologies namely H. pylori and GERD. Carditis with unremarkable Z-line is more frequently associated with H. pyloriwhile short or long segment of Barrett's oesophagus are more likely related to GERD. In the absence of Barrett's aspect there is no evidence that intestinal metaplasia associated with H. pylori-related carditis is a premalignant lesion which deserves endoscopic surveillance. While H. pylori infection can accelerate the healing of oesophagitis and the speed of symptom relief in patients treated with PPI, there is no evidence that H. pylori influences the therapeutic needs in the long-term. Conflicting results have been published regarding the effects of eradicating H. pylori on the developmentof GERD. Studies in duodenal ulcer (DU) patients or healthy volunteers maynot be relevant to the situation of GERD. The central role of the patient's inflammatory response to H. pylori infection has been demonstrated by a study showing a polymorphism in interleukin 1 beta gene and an association between some alleles and the risk of hypochlorhydria and gastric cancer. A 3-year prospective randomized study did not confirm that patients receiving maintenance with PPI progress more frequently to corpus inflammation, atrophy or intestinal metaplasia than controls treated surgically. Finally, it is our opinion that the diagnosis of GERD should not influence the decision whether to eradicate H. pylori which is more related to the risk of gastriccancer. Curr Opin Gastroenterol 16 (suppl 1):S33-S38 (C) 2000 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 11:24:29