Aktuelle Gastroenterologie -- Campylobacter Pylori
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Vor nunmehr 5 Jahren gelang in PerthlWestaustralien der Nachweis von gekrümmten oder spiraligen begei elten Bakterien auf der Magenschleim- haut des Menschen. Die Form des Bakteriums und der Ort der Kolonisation veranla ten die Bezeichnung: Campylobacter pylori. Inzwischen liegen mehr als 200 Publikationen über dieses Bakterium vor. Zielzellen des Campylobacter pylori sind offensichtlich Oberflächenepithe- lien der Antrumschleimhaut, die im Rahmen entzündlicher Metaplasie (bei peptischer Bulbitis) sehr häufig auch im Bulbus duodeni angetroffen werden (antrale Metaplasie). Elektronenmikroskopische Analysen lie en eine reversible Schädigung der Oberflächenepithelien durch Campylobacter pylori erkennen, bioptische histologische und kulturelle Untersuchungen deckten eine hohe Assoziation der Campylobacter-Besiedelung im Antrum mit der primär im Antrum lokalisierten Gastritis (Typ B-Gastritis) und dem Ulcus duodeni und, in geringerem Ma e, auch mit dem Ulcus ventriculi auf. Diese Assoziationen lassen noch nicht auf kausale Zusammenhänge schlie- en, sie werden eher durch Regression des Aktivitätsgrades der Antrumga- stritis parallel zu Eradikation des Campylobacter py 10 ri und durch Beschleu- nigung der Ulkusheilung durch Wismutsalze und/oder Antibiotika wahr- scheinlich gemacht; von besonderer Bedeutung ist die geringere Rezidivrate nach Ulkusheilung durch Wismutsalze im Vergleich zu anderen Ulkusthera- peutika. Viele Fragen blieben offen, vor allem die nach der pathogenetischen Bedeutung des Campylobacter für das Ulcus duodeni und das Magen- ulkus. Während des 1. Münchener Campylobacter pylori Symposiums am 5. Dezember 1987 sollten neue Resultate aufgezeigt und diskutiert werden. Wir hoffen, da diese dazu beigetragen haben, die Rolle des Campylobacter in der Entstehung der Typ-B-Gastritis und anderer Gastritiden und des peptischen Ulkus zu klären.
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