Résumé
Helicobacter pylori (HP) a été retrouvé au niveau de l’œsophage, uniquement sur un épithélium de type gastrique dans l’œsophage de Barrett, et presque exclusivement chez des patients porteurs d’une contamination gastrique par HP. L’infection de l’œsophage de Barrett par HP n’a aucune influence sur sa sévérité, ses complications ou son histoire naturelle. La contamination gastrique par HP n’est pas un facteur de risque de reflux gastro-œsophagien et au contraire la présence de HP au niveau gastrique, l’inflammation de la partie fundique et la gastrite atrophique pourraient jouer un rôle protecteur contre l’œsophagite par reflux. L’éradication de HP chez les patients porteurs d’un ulcère duodénal expose ceux-ci à un risque de développement d’œsophagite par reflux. HP influence l’efficacité du traitement antisécrétoire: les inhibiteurs de pompe à protons et la ranitidine procurent une réduction de l’acidité gastrique supérieure chez les sujets contaminés par HP par rapport aux sujets HP négatifs. Au cours d’un traitement par inhibiteur de pompe à protons, on constate un déplacement de HP de l’antre vers le fundus. Les traitements prolongés par inhibiteur de pompe à protons provoquent une gastrite atrophique chez les sujets positifs pour Helicobacter pylori, ce qui constitue un argument majeur en faveur de l’éradication de HP chez les patients soumis à une inhibition sécrétoire acide de longue durée.
Summary
HP may be found in the oesophagus only on gastric type epithelium in Barrett’s oesophagus, and almost only in patients with gastric HP infection. There is no indication that HP infection of Barrett’s oesophagus has any influence on its severity, complications, or natural history. HP infection of the stomach is not a risk factor for reflux oesophagitis, and the consequence of the presence of HP in the stomach, body inflammation and atrophic gastritis, may protect against reflux oesophagitis. There is a risk for developing reflux oesophagitis after HP eradication in duodenal ulcer patients. HP influences the efficacy of acid-lowering treatment: proton pump inhibitors and ranitidine produce a greater decrease in gastric acidity in subjects with H. pylori infection than those H. pylori negative. During proton pump inhibitor treatment, there is a shift of HP from antrum to body mucosa. Long term proton pump inhibitor treatment induces atrophic gastritis in Helicobacter pylori positive patients, which is the strongest argument in favour of eradicating HP in patients receiving long term potent acid inhibition.
Article PDF
Avoid common mistakes on your manuscript.
Références
WALKER S.J., BIRCH P.J., STEWART M., STODDARD C.J., HART C.A., DAY D.W. — Patterns of colonisation of Campylobacter pylori in the oesophagus, stomach and duodenum.Gut. 1989,30, 1334–1338.
CHENG E.H., BERMANSKI P., SILVERSMITH M., VALENSTEIN P., KAWANISHI H. — Prevalence of Campylobacter pylori in esophagitis, gastritis, and duodenal disease.Arch. Intern. Med. 1989,149, 1373–1375.
AGNHOLT J., FALLINGBORG J., MOLLER-PETERSEN J., LOMBORG S., CHRISTENSEN L.A., SONDERGAARD G., TEGLBJAERG P.S., RASMUSSEN S.N. — The occurrence ofHelicobacter pylori in the oesophagus. Eur. J. Gastroenterol.-Hepatol. 1991,3, 685–688.
COOPER B.T., GEARTY J.C. — Helicobacter pylori in Barrett’s oesophagus.Gullet. 1991,1, 173–176.
O’CONNOR H.J., CUNNANE K. — Helicobacter pylori and gastro-oesophageal reflux disease a prospective study.Ir. J. Med. Sci. 1994,163, 369–373
ABBAS Z., HUSSAINY A.S., IBRAHIM F., JAFRI S.M.W., SHAIKH H., KHAN A.H. — Barrett’s oesophagus and Helicobacter pylori.J. Gastroenterol. Hepatol. 1995,10, 331–333.
JONES D.M., ELDRIDGE J., FOX A.J.et al. — Antibody to the gastric campylobacter-like organism (‘Campylobacter pyloridis’): Clinical correlations and distribution in the normal population.J. Med. Microbiol. 1986,22, 57–62.
BOIXEDA D., GISBERT J.P., CANTON R., ALVAREZ-BALERIOLA I., GIL-GRANDE L.A., MARTIN-DEARGILA C. — Existe alguna relacion entre la infeccion por Helicobacter pylori y la esofagitis peptica? [Is there any association betweenHelicobacter pylori infection and gastroesophageal reflux disease?]Medicina Clinica, 1995,105, 774–777.
DE KOSTER E, FERHAT M., DEPREZ C., DELTENRE M. —Helicobacter pylori, gastric histology and gastro-esophageal reflux disease.Gut, 1995,37 Suppl 1, A36.
LEE J., BRESLIN N., O’MORAIN C. —Helicobacter pylori (HP) infection, cigarette smoking and alcohol consumption in reflux oesophagitis.Gut, 1996,39 Suppl 2, A29.
LISTON R., PITT M.A., BANERJEE A.K. — Reflux oesophagitis andHelicobacter pylori infection in elderly patients.Postgraduate Medical Journal, 1996,72, 221–223.
ROSIORU C., GLASSMAN M.S., HALATA M.S., SCHWARZ S.M. — Esophagitis andHelicobacter pylori in children: Incidence and therapeutic implications.Am. J. Gastroenterol. 1993,88, 510–513.
PEITZ U., AYGEN S., HENNEMANN O., TILLENBURG B., BORSCH G., GORDUNA C., STOLTE M., LABENZ J. —Helicobacter pylori infection in young dyspeptic patients referred for upper gastrointestinal endoscopy.Gut, 1995,37 (Suppl 1), A25.
LOFFELD R.J.L.F., WERDMULLER B.F.M. —Helicobacter pylori and reflux oesophagitis.Gut, 1996,39 (Suppl 2), A89.
MIHARA M., HARUMA K., KAMADA T.et al. — Low prevalence ofHelicobacter pylori infection in patients with reflux oesophagitis.Gut, 1996,39 (Suppl 2), A94.
EL-OMAR E., PENMAN I., DORRIAN C.A., ARDILL J.E., McCOLL K.E. — EradicatingHelicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer.Gut, 1993,34, 060–5.
EL-OMAR E., PENMAN I., ARDILL JES, CHITTAJALLU R.S., HOWIE C., McCOLL KEL. — Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease.Gastroenterology, 1995,109, 681–691.
EL-OMAR E., PENMAN I., ARDILL J.E.S., McCOLL KEL. A. — Substantial proportion of non-ulcer dyspepsia patients have the same abnormality of acid secretion as duodenal ulcer patients.Gut, 1995,36, 534–538.
YASUNAGA Y., SHINIMURA Y., KANAYAMA S., YABU M., NAKANISHI T., MIYAZAKA Y., MURAYAMA Y., BONILLA-PALACIOS J.J., MATSUZAWA Y. — Improved fold witdth and increased acid secretion after eradication of the organism inHelicobacter pylori associated enlarged fold gastritis.Gut, 1994,35, 1571–1574
OHARA S., SEKINE H., HJIMA K.et al. — Gastric mucosal atrophy and prevalence ofHelicobacter pylori in reflux esophagitis of the elderly.Japanese Journal of Gastroenterology, 1996,93, 235–239.
SOLCIA E., FIOCCA R., VILLANI L., CARLSSON J., RUDBACK A., ZEIJLON L. — Effects of permanent eradication or transient clearance ofHelicobacter pylori on histology of gastric mucosa using omeprazole with or without antibiotics.Scand. J. Gastroenterol. 1996,31 Suppl 215, 105–110.
HIRSCHL A.M., SCHUTZE K., HENTSCHEL E., DRAGOSICS B. — Serological, microbiological and clinical results of a 43 months follow-up after successful eradication ofH. pylori in duodenal ulcer patients.Am. J. Gastroenterol. 1994,89, 1374.
LABENZ J., TILLENBURG B., PEITZ U., BORSCH G. — Long-term consequences ofHelicobacter pylori eradication: Clinical aspects.Scandinavian Journal of Gastroenterology 1996,31 Supplement 215, 111–115.
LABENZ J., TILLENBURG B., PEITZ U., SOLLBOHMER M., STOLTE M., BORSCH G. — Long-term clinical course of ulcer disease and incidence of reflux esophagitis in a large cohort of duodenal ulcer patients followed after eradication of Helicobacter pylori.Gut, 1995,37 Suppl 1, A6.
SACCA N., DE MEDICI A., RODINO S., DE SIENA M., GIGLIO A. — Reflux esophagitis: a complication ofHelicobacter pylori eradication therapy?Gut, 1996,39 Suppl 2, A91.
LABENZ J., MONTBRIAND J.R., APPLEMAN H.D., COTNER E.K., NOSTRAND T.T., ELTA GH.et al. — Treatment of Campylobacter pylori does not alter gastric acid secretion.Am. J. Gastroenterol., 1989,84, 1513–1516.
ALLESCHER H.D., STOSCHUS B., WUNSCH E., SCHUSDZIARRA V., CLASSEN M. — Effect of human gastrin-17 with and without acid suppression on human esophageal motility.Z Gastroenterol. 1995,33, 385–391.
VERDU E.F., ARMSTRONG D., FRASER R., VIANI F., IDSTROM J., CEDERBERG C., BLUM A.L. — Effect ofHelicobacter pylori status on intragastric pH during treatment with omeprazole.Gut, 1995,36, 539–543.
LABENZ J., TILLENBURG B., PEITZ U., IDSTROM J.-P., VERDU E.F., STOLTE M., BORSCH G., BLUM A.L. —Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcer.Gastroenterology, 1996,110, 725–732.
LABENZ J., TILLENBURG B., PEITZ U., IDSTROM J.-P., VERDU E., STOLTE M., BORSCH G., BLUM A.L. — Efficacy of omeprazole one year after cure ofH. pylori infection in duodenal ulcer patients.Gut, 1996,39 Suppl 2, A98.
TILLENBURG B., BLUM A.L., PEITZ U., VERDU E., BORSCH G., STOLTE M., LABENZ J. — Cure ofH. Pylori infection decreases the antisecretory effect of ranitidine in duodenal ulcer patients.Gut, 1996,39 Suppl 2, A98.
LOGAN R.P.H., WALKER M.M., MISIEWICZ J.J., GUMMETT P.A., KARIM Q.N., BARON J.H. — Changes in the intragastric distribution ofHelicobacter pylori during treatment with omeprazole.Gut, 1995,36, 12–16.
KUIPERS E.J., UYTERLINDE A.M., PENA A.S., HAZENBERG H.J.A., BLOEMENA E., LINDEMAN J., KLINKENBERG-KNOL E.C., MEUWISSEN S.G.M. — Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: Implications for long-term safety.American Journal of Gastroenterology, 1995,90, 1401–1406.
BERSTAD A.E., HATLEBAKK J.G., MAARTMANNMOE H., BERSTAD A., BRANDTZAEG P. —Helicobacter pylori-infected patients show increased inflammation in gastric body mucosa during long-term treatment with lansoprazoleGut, 1996,39 Suppl 2, A104.
MAAROOS H.I., KEKKI M., VOROBJOVA T., SALUPERE V., SIPPONEN P. — Risk of recurrence of gastric ulcer, chronic gastritis, and grade ofHelicobacter pylori colonization. A long term follow-up study of 25 patients.Scand. J. Gastroenterol. 1994,29, 532–536.
KUIPERS E.J., LUNDELL L., KLINKENBERG-KNOL E.C., HAVU N., FESTEN H.P.M., LIEDMAN B., LAMERS CBHW, JANSEN J.B.M.J., DALENBACK J., SNEL P., NELIS G.F., MEUWISSEN S.G.M. — Atrophic gastritis andHelicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.New England Journal of Medicine 1996,334, 1018–1022.
KUIPERS E.J., UYTERLINDE A.M., PENA A.S.et al. — Long-term sequelae ofHelicobacter pylori gastritis.Lancet 1995,345, 1525–1528.
IHAMAKI T., SAUKKONEN M., SIURALA M. — Long-term observation of subjects with normal gastric mucosa and with superficial gastritis: results of 23–27 years follow-up examinations.Scand. J. Gastroenterol. 1978,13, 771–775.
CORREA P., HAENSZEL W., CUELLO C.et al. — Gastric precancerous process in a high risk population: cohort follow-up.Cancer Res. 1990,50, 4737–4740.
VILLAKO K., KEKKI M., MAAROOS H.I.et al. — Chronic gastritis: progression of inflammation and atrophy in a six year endoscopic follow-up of a random sample of 142 Estonian urban subjects.Scand. J. Gastroenterol. Suppl. 1991,186, 135–141.
MAAROOS H.I., SALUPERE V., UIBO R., KEKKI M., SIPPONEN P. — Seven-year follow-up study of chronic gastritis in gastric ulcer patients.Scand. J. Gastroenterol. 1985,20, 198–204.
JONSSON L.A., STROM M., BODEMAR G., NORRBY K. — Histologic changes in the gastroduodenal mucosa after long-term medical treatment with cimetidine or parietal cell vagotomy in patients with juxtapyloric ulcer disease.Scand. J. Gastroenterol. 1988,23, 433–441.
LAMBERTS R., CREUTZFELDT W., STRUBER H.G., BRUNNER G., SOLCIA E. — Long-term omeprazole therapy in peptic ulcer disease: gastrin, endocrine cell growth, and gastritis.Gastroenterology, 1993,104, 1356–1370.
SOLCIA R., FIOCCA R., HAVU N., DALVAG A., CARLSSON R. — Gastric endocrine cells and gastritis in patients receiving long-term omeprazole treatment.Digestion, 1992,51 Suppl 1, 82–92.
E. DE KOSTER, M. BUSET, E. FERNANDES, M. DELTENRE. —Helicobacter pylori and cancer prone lesions of the stomach.Acta Endoscopica, 1995,25, 33–44.
STALNIKOWICZ R., BENBASSAT J. — Risk of gastric cancer after gastric surgery for benign disorders.Arch. Int. Med. 1990,150, 2022–2026.
VOUILLAMOZ D., BLUM A.L. — Esophagite peptique.Médecine et Hygiène, 1996,54, 169–70+172.
Author information
Authors and Affiliations
About this article
Cite this article
de Koster, E., Jonas, C.L., Ferhat, M. et al. Helicobacter pylori doit-il être éradiqué avant de prescrire un traitement à long terme par un inhibiteur de pompe à protons pour une œsophagite par reflux?. Acta Endosc 27, 201–211 (1997). https://doi.org/10.1007/BF02969051
Issue Date:
DOI: https://doi.org/10.1007/BF02969051
Mots clés
- Helicobacter pylori
- éradication
- gastrite atrophique
- Lansoprazole
- œsophagite par reflux
- œsophage de Barrett
- reflux gastroœsophagien
- traitement par inhibiteur de pompe à protons
- Ranitidine