Résumé
Des données récentes ont permis de redéfinir la gastrite. Des entités nouvelles ont été décrites (gastrite lymphocytaire, gastrite par reflux) et surtout un nouveau germe, à tropisme gastrique, a été décrit :Helicobacter pylori. Ce germe répond aux postulats de Koch sans répondre entièrement encore aux postulats associés (relation chronologique, spécificité, relation dose-réponse, plausibilité).
Helicobacter pylori est done une cause, sans doute la principale, de gastrite chronique active. L’histoire naturelle de cette infection et les études thérapeutiques devraient nous aider à préciser son rôle exact dans les maladies du tractus digestif supérieur.
Summary
Recent developments have redefined gastritis with the description of newly recognised entities such as lymphocytic gastritis and reflux gastritis and especially with the discovery ofHelicobacter pylori. This microorganism fulfills Koch’s postulates but extended causality postulates (time-order, specificity, doseresponse relationship and plausibility) are not completely fulfilled.
ThusHelicobacter pylori is a cause, probably the main cause, of chronic active gastritis. The natural history of this infection and therapeutic studies should help us delineate it’s exact role in diseases of the foregut.
Resumen
Existen datos de reciente conocimiento que han permitido una redefinitión de la gastritis. Se han descrito nuevas tntidades (Gastritis linfocitaria, gastritis por reflujo) y, en especial un nuevo germen con tropismo gastrico se ha vista involucrado en la enfermedad : el Helicobacter pylori. Este germen responde a los postulados de Koch aun sin responder por completo a los postulados asociados (relatión cronológica, especificidad, relatión dosis-respuesta, plausibilidad).
El Helicobacter pylori es pues una causa, sin duda la más importante, de la gastritis crónica activa. La historia natural de ésta infectión y los estudios terapeúticos deberían ayudarnos a precisar su verdadero protagonismo en las enfermedades del tracto digestivo superior.
De|Référence
ANDERSEN L.P., HOLCK S., POULSEN CO., ELSBORG L., JUSTESEN T. —Campylobacter pyloridis in peptic ulcer disease.Scand. J. Gastroenterol, 1987,22, 219–224.
ANDERSEN L.P., ELSBORG L., JUSTESEN T. —Campylobacter pylori in peptic ulcer disease III Symptoms and paraclinical and epidemiologic finding.Scand. J. Gastroenterol., 1988,23, 347–350.
BARBOSA A.J.A., QUEIROZ D.M.M., MENDEZ E.N., ROCHA G.A., LIMA G.F., OLIVEIRA C.A. — Immu-nocytochemical identification ofCampylobacter pylori in gastritis and correlation with culture.Arch. Pathol. Lab. Med., 1988,112, 523–525.
BASKERVILLE A., NEWELL D.G. — Naturally occu-ring chronic gastritis and C.pylori infection in the Rhesus monkey: a potential model for gastritis in man.Gut, 1988,29, 465–472.
BERSTAD A., ALEXANDER B., WEBERG R., SERCK-HANSSEN A., HOLLAND S., HIRSCHOWITS. — Antacids reduceCampylobacter pylori colonization without healing the gastritis in patients with non ulcer dyspepsia and erosive prepyloric changes.Gastroenterology, 1988,95, 619–624.
BIZZOZERO G. — Über die schlauchformigen drusen des magendarmkanals und die beziehungen ihres epithets zu dem oberflachenepithel der schleimhaut.Arch. F. Mikr. Anat., 1893,42, 82–152.
BLOMBERG B., JARNEROT G., KJELLANDER J., DANIELSSON D., KRAAZ W. — Prevalence ofCampylobacter pylori in an unselected Swedish population of patients referred for gastroscopy.Scand. J. Gastroenterol., 1988,23, 358–362.
BODE G., MALFERTHEIMER P., DITSCHUNEIT H. — Pathogenic implications of ultrastructural finding inCampylobacter pylori related gastroduodenal disease.Scand. J. Gastroenterol., 1988,23S142, 25–39.
BUCK G.E., GOURLEY W.K., LEE W.K., SUBRAMA-MYAN K., LATIMER J.M., DI MUZZO A.R. — Relation ofCampylobacter pyloridis to gastritis and peptic ulcer.J. Infect. Dis., 1986,153, 664–669.
CARRICK J., LEE A., HAZELL S., RALSTON M., DASKALOPOULOS G. —Campylobacter pylori, duodenal ulcer and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis.Gut, 1989,30, 790–797.
COELHO L.G.V., DAS S.S., PAYNE A., KARIM Q.H., BARON J.H., WALKER M.M. —Campylobacter pylori association with antral and fundic mucosal histology and diagnosis by serology in patients with upper gastrointestinal symptoms.Am. J. Gastroenterol., 1989,84, 367–371.
DEBONGNIE J.C., LEGROS G., BEYAERT C. — La gastrite àCampylobacter pylori. Comparaison de plusieurs méthodes diagnostiques.Acta Gastroent. Belg., 1987,50, 666–673.
Dupebongnie J.C., Bupeyaert C, Lupegros G. — A large follow-up study of patients with and without itCampylobacter pylori. A retrospective analysis. In gastroduodenal pathology and itCampylobacter, pylori. Ed. Megraud F., La-mouliatte H., Excerpta Medical, 1989. Amsterdam, 459-462.
DELTENRE M., NYST J.F., GLUPCZYNSKI Y., BURETTE A. — Donnees cliniques, endoscopiques et histologiques chez 1 100 patients dont 574 colonisés parCampylobacter pylori. Gastroenterol. Clin. Biol., 1989,13, 89B-95.
DOOLEY C.P., McKENNA D., HUMPHREYS H., BOURKE S., DEANE C.T., SWEENEY E., O’MORAIN C. — Histological gastritis in duodenal ulcer: Relationship toCampylobacter pylori and effect of ulcer therapy.Am. J. Gastroenterol., 1988,83, 278–282.
DOOLEY C.P., COHEN H., FITZGIBBONS PL., BAUER M., APPLEMAN M., PEREZ-PEREZ G., BLA-SER M.J. — Prevalence ofHelicobacter pylori infection and histologic gastritis in asymptomatic persons.New Engl. J. Med., 1989,321, 1362–1366.
DROY-LEFAIX M.T. — Mecanismes de defense de l’esto-mac etCampylobacter pylori. Gastroenterol. Clin. Biol., 1989,13, 13B-17B.
FOX J.G., CORREA P., TAYLOR M.C, ZAVALA D., FONTHAM E., JANNEY F., RODRIGUEZ E., HUNTER F., DIAVOLITSIS S. —Campylobacter pylori-asso ciated gastritis and immune response in a population at increased risk of gastric carcinoma.Amer. J. Gastroent., 1989,84, 775–781.
GAD A., HRADSKY M., FURUGARD K., MALMO-DIN B., NYBERG O. —Campylobacter pylori and non-ulcer dyspepsia.Scand. J. Gastroenterol., 1989,24 (Suppl. 167), 44–48.
GOODWIN C.S., ARMSTRONG J.A., CHIVERS T., PETERS M., COLLINS D., SLY L., MCCONNEL W., HARPER W.E.S. — Transfer ofCampylobacter pylori andCampylobacter mustelac toHelicobacter gen now asHelicobacter pylori comb. nov. and Helicobacter mustelac comb, nov. respectively.Int. J. Syst. Bacterial, 1989,39, 397–405.
GRAHAM ETY., ALPERT L.C., SMITH L., YOSHI-MURA H.H. — IatrogenicCampylobacter pylori infection is a cause of epidemic achlorhydria.Amer. J. Gastroent., 1988?,83, 974–980.
HAOT J., DELOS M., WALLEZ L., HARDY N., LEN-ZEN B., JOURET-MOURIN A. — Intraepithelial lymphocytes in inflammatory gastric pathology.Acta en-doscop., 1986,16, 61–67.
HAOT J., JOUREZ A., WILLETTE M., GOSSUIN A., MAINGUET P. — Lymphocytic gastritis — prospective study of its relationship with varioliform gastritis.Gut, 1990,31, 282–285.
HAZELL S.L., BORODY T.J., GAL A., LEE A. —Campylobacter pyloridis Gastritis I: Detection of urease as a marker of bacterial colonization and gastritis.Am. J. Gastroent., 1987,82, 292–296.
HAZELL S.L., HENNESSY W.B., BORODY T.J., CARRICK J., RALSTON M., BRADY L., LEE A. —Campylobacter pyloridis Gastritis II: Distribution of bacteria and associated inflammation in the gastroduodenal environment.Am. J. Gastroent., 1987,82, 297–301.
HESSEY S.J., SPENCER J., WYATT J.I., SOBALA G., RATHBONE B.J., AXON ATR., DIXON M.F. — Bacterial adhesion and disease activity inHelicobacter associated chronic gastritis.Gut, 1990,31, 134–138.
HUMPHREYS H., BOURKE S., DOOLEY C, MCKENNA D., POWER D., KEANE C.T., SWEENEY E.C., O’SMORAIN C. — Effect of treatment onCampylobacter pylori in peptic disease: a randomised prospective trial.Gut, 1988,29, 279–283.
JIANG S.J., LIU W.Z., ZHANG D.Z., SHI Y., XIAO S.D., ZHANG Z.H., LU D.Y. —Campylobacter-like organisms in chronic gastritis, peptic ulcer and gastric carcinoma.Scand. J. Gastroenterol, 1987,22, 553–558.
JOHNSTON B.J., REED P.I., ALI M.H. —Campylobac-ter-tike organisms in duodenal and antral endoscopic biopsies: relationship to inflammation.Gut, 1986,027, 1132–1137.
JOHNSTON B.J., REED P.I., ALI M.H. — Prevalence ofCampylobacter pylori in duodenal and gastric mucosa -Relationship to inflammation.Scand. J. Gastroenterol, 1988,23S142, 69–75.
JONES D.M., CURRY A., FOX A.J. — An ultrastructural study of the gastriccampylobacter-Like organisms « Campylobacter pyloridis ».J. Gen. Micro Biol, 1985,131, 2535–2541.
JONSSON K.A., GOTTHARD R., BODEMAR G., BRODIN U. — The clinical relevance of endoscopic and histologic inflammation of gastroduodenal mucosa in dyspepsia of unknown origin.Scand. J. Gastroenterol, 1989,24, 385–395.
JONSSON K.A., STROM M., BODEMAR G., MOR-RBY 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., 1989,23, 433–441.
KANG J.Y., TAY H.H., WEE A., GUAN R., MATH M.V., YAP I. — Effect of colloïdal bismuth subcitrate on symptoms and gastric histology in non ulcer dyspepsia. A double blind placebo controlled study.Gut, 1990,31, 476–480.
KRAKOWA S., MORGAN D.R., KRAFT W.G., LEUNK R.D. — Establishment of gastricCampylobacter pylori infection in the neonatal gnotabiotic piglet.Infect. Immun., 1987,55, 2789–2796.
LAMBERT JR., DONN K., BORROMEO M., KOR-MAY M.G., HANSKY J., SMITH A.C. —Campylobacter pylori — a role in non-ulcer dyspepsia?Scand. J. Gastroenterol., 1989,24S160, 14–18.
LAMOULIATTE H., MEGRAUD F., DE MASGAREL A., ROUX D., QUINTON A. —Campylobacter pyloridis and epigastric pain: endoscopic, histological and bacteriological correlations.Gastroenterol. Clin. Biol, 1987,II, 212–216.
LANZA F.L., SKOGLUND M.L., RACK M.F., YARD-LEY J.Y. — The effect of bismuth subsalicylate on the histologic gastritis seen with Campylobacter pylori: A placebo-controlled randomized study. Amer. J. Gastroent., 1989,84, 1060–1064.
LE BODIC M.F., BARRE P., FREGAND C., LE BODIC L., GALMICHE J.P. —Campylobacter pyloridis et muqueuse gastrique: étude histologique, bactériologique et résultats préliminaires d’une enquête épidémiologique dans la région nantaise.Gastroenterol. Clin. Biol, 1987,11, 376–381.
LOFFELD R.J.L.F., POTTERS H.V.J.P., STOBBE-RINGH E., FLENDRIG J.A., VAN SPREEUWEL J.P., ARENDS J.W. —Campylobacter associated gastritis in patients with non-ulcer dyspepsia: a double blind placebo controlled trial with colloidal bismuth subcitrate.Gut, 1989,30, 1206–1212.
MANGANARO M., CASALE V., ACETI A., ATTANA-SIO R., CITARDA F., CONTI EMS., CUNEGO A., FERRO S., GRASSI A., PENNI A., SCIARRETTA F., SCINICARIELLO F. —Campylobacter pylori et gastrite: etude biologique, immunologique, histologique et en-doscopique.Acta endosc, 1988,18, 91–96.
MARCHEGIANNO A., IANOMMI C., AGNELLO M., PAOLUZZI P., PALLONE F. —Campylobacter-like organisms in the human gastric mucosa. Relationship to type and extent of gastritis in different clinical groups.Gastroenterol. Clin. Biol., 1987,II, 376–381.
MARSHALL B. — Unindentifed curved bacilli on gastric epithelium in active chronic gastritis.Lancet, 1983,1, 1273–1275.
MARSHALL B.J., ROYCE H., ANNEAR D.J., GOODWIN C.S., PEARMAN J.W., WARREN J.R., ARMSTRONG J.A. — Original isolation ofCampylobacter pyloridis from human gastric mucosa.Microbios. Letters, 1984,25, 83–88.
MARSHALL B.J., ARMSTRONG J.A., MCGECHIE D.B., GLANCY R.J. — Attempt to fulfill Koch’s postulates forCampylobacter pyloridis.Med. J. Aust., 1985,142, 436–439.
MARSHALL B.J., WARREN J.R., FRANCIS G.J., LANGTON S.R., GOODWIN C.S., BLINCOW E. — Rapid urease test in the management ofCampylobacter pyloridis-associated gastritis.Am. J. Gastroent., 1987,82, 200–210.
MARSHALL B.J. — Etudein vivo deCampylobacter pylori — Modeles experimentaux.Gastroenterol. Clin. Biol., 1989?,13, 50B-52.
MARSHALL B.J., WARREN R.J., BLINCOW E.D., PHILLIPS M., GOODWIN C.S., MURRAY R., BLACK-BOURN S.J., WATERS T.H.J., SANDERSON C.R. — Prospective double-blind trial of duodenal ulcer relapse after eradication ofCampylobacter pylori.Lancet, 1988,2, 1437–1442.
MCNULTY C.A.M., DENT J.C., UFF J.S., GEAR M.W.L., WILKINSON S.P. — Detection onCampylobacter pylori by the biopsy urease test: an assessment in 1 445 patients.Gut, 1989,30, 1058–1062.
MILLER N.M., NARAN A., SIMJEE A.E., SPITAELS J.M., PETTENGELL K.E., VANDEN ENDE J., MA-NION G. — Incidence ofCampylobacter pylori in patients with upper gastro-intestinal symptoms.South Afr. Med. J., 1988,74, 563–566.
MITCHELL H.M., LEE A., BERKOWICZ J., BORODY T. — The use of serology to diagnose activeCampylobacter pylori infection.Med. J. Austr., 1988,149, 604–609.
MORRIS A., MICHOLSON G. — Ingestion ofCampylobacter pyloridis causes gastritis and raised fasting gastric pH.Am. J. Gastroent., 1987,82, 192–199.
MORRIS A., BROWN P., ALI R., LANE M., PALMER R. — Treatment ofCampylobacter pylori gastritis: a pilot study using pirenzepine dihydrochloride (Gastrozepin) and three formulations of colloidal bismuth subcitrate (De Nol).NZ Med. J., 1988,101, 651–654.
MORVAN J., TEYSSOU R., BOTTON A., VIALETTE G., MEGRAUD F. —Campylobacter pylori et gastrites: Resultats a propos de 95 biopsies gastriques.Med. Mai. Inf., 1987,10, 543–548.
MUSGROVE C, BOLTON J., KRYPCZYK A.M., TEM-PERLEY J.M., CAIRNS S.A., OWEN W.G., HUTCHINSON D.M.Campylobacter pylori: clinical, histological and serological studies.J. Clin. Pathol., 1988,41, 1316–1321.
NEWELL D.G., JOHNSTON B.J., ALI M.H., REED P.I. — An enzyme-linked immunosorbent assay for the serodiagnosis ofCampylobacter pylori associated gastritis.Scand. J. Gastroenterol., 1988,23S142, 53–57.
O’CONNOR H.J., WYATT J.J., DIXON M.F., AXON A.T.R. —Campylobacter-like organisms and reflux gastritis.J. Clin. Pathol., 1986,39, 531–534.
PAULL G., YARDLEY J.H. — Gastric and esophagealCampylobacter pylori in patients with Barret’s esophagus.Gastroenterology, 1988,95, 216–218.
PETTROSS C.W., APPLEMAN M.D., COHEN H., VA-LENZUELA J.E., CHANDRASOMA P., LAINE L.A. — Prevalence ofCampylobacter pylori and association with antral mucosal histology in subjects with and without upper gastrointestinal symptoms.Dig. Dis., 1988,33, 649–653.
PRICE A.B., LEVI J., DOLBY J.M., DUNCOMBE PL., SMITH A., CLARK J., STEPHENSON M.L. —Campylobacter pyloridis in peptic ulcer disease: microbiology, pathology and scanning electon microscopy.Gut, 1985,26, 1183–1188.
QUEIROZ D.M.M., BARBOSA A.J.A., MENDES E.N., ROCHA G.A., CISALPINO E.O., LIMA G.F., OLIVEI-RA C.A. — Distribution ofCampylobacter pylori and gastritis in the stomach of patients with and without duodenal ulcer.Amer. J. Gastroent., 1988,83, 1368–1370.
RASKOV H., LANNG G., GAARSLEV K., FISHER HANSEN B., HAUCH O. — Screening forCampylobacter pyloridis in patients with upper dyspepsia and the relation to inflammation of the human gastric antrum.Scand. J. Gastroenterol., 1987,22, 568–572.
RATHBONE B.J., WYATT J.I., WORSLEY et at. — Systemic and local antibody responses to gastricCampylobacter pyloridis in non-ulcer dyspepsia.Gut, 1986,27, 642–647.
RAUWS E.A.J., LANGENBERG W., HOUTHOFF H.J., ZANEN J.C., TYTGAT G.M.J. —Campylobacter pylori-dis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment.Gastroenterology, 1988,94, 33–40.
Rupauws E.A.J., Tupytgat G.N.J., Lupangenberg W., Rupoyen E.V. — Experience with 14 c-urea breath test in detecting itCampylobacter pylori. In itCampylobacter pylori. Ed. Menge Springer Verlag, 1988, pp. 151-156.
RIARD PH., HOSTEIN J., CROIZE J., BOURGUI-GNON G., LEMARC HADOUR F., FAURE H., FOURNET J. — LeCampylobacter pylori: valeur dia-gnostique de l’uréase test pratiqué en salle d’endoscopie.Gastroenterol. Clin. Biol., 1989,13, 8–13.
ROKKAST., PURSEYC, VZOECHINA E., DOR-RINGTON L., SIMMONS N.A., FILIPE M.J., SLADEN G.E. —Campylobacter pylori and non-ulcer dyspepsia.Am. J. Gastroent., 1987,82, 1149–1152.
SIURALA M., SIPPONEN P., KEKKI M. —Campylobacter pylori in a sample of Finnish population: relations to morphology and functions of the gastric mucosa.Gut, 1988,29, 909–915.
SPILKER B. — Concept of cause and effect. In: Spliker B. Guide to clinical interpretation of date. New York Raven Press, 1986, 19–26.
VAIRA D., HOLTON J., OSBORN J., DOWSETT J., McNEIL I., HATFIELD A. — Use of endoscopy in patients with dyspepsia.Br. Med. J., 1989,299, 237.
VON WULFFEN H., HEESEMANN J., BUTZOW G.H., LOMING T., LAUFS R. — Detection ofCampylobacter pyloridis in patients with antrum gastritis and peptic ulcers by culture, complement fixation test and immunoblot.J. Clin. Microbiol., 1986,24, 716–720.
WHITEHEAD R., TRUELOVE S.C., GEAR M.W.L. — The histological diagnosis of chronic gastritis in fibreoptic gastroscope biopsy specimens.J. Clin. Pathol., 1972,25, 1–11.
WORMSLEY K.G. —Campylobacter pylori and ulcer disease — A causal connection?Scand. J. Gastroentero0l., 1989,24 (Suppl. 160), 53–58.
WYATT J.I., DIXON M.F. — Chronic gastritis — a pathogenetic approach.J. Pathology., 1988,154, 113–124.
WYATT J.I., RATHBONE B.J. — Immune response of the gastric mucosa to Campylobacter pylori.Scand. J. Gastroenterol., 1988,23 (Suppl. 142), 44–49.
WYATT J.I., RATHBONE B.J., DIXON M.F., HEAT-LEY R.V. —Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis.J. Clin. Pathol., 1987,80, 841–848.
YARDLEY J.H. — Pathology of chronic duodenitis and gastritis. In gastrointestinal pathology. Ed. Goldmann H., Appelman D. Williams & Wilkins, Baltimore, 1990.
Author information
Authors and Affiliations
About this article
Cite this article
Debongnie, J.C. La gastrite type B: une gastrite bactérienne: réalité ou fantaisie ?. Acta Endosc 20, 415–425 (1990). https://doi.org/10.1007/BF02977550
Issue Date:
DOI: https://doi.org/10.1007/BF02977550