Zusammenfassung
Ösophagus, Magen und Pankreas stellen primäre Zielorgane alkoholinduzierter Erkrankungen
dar. Ethanol verursacht im Ösophagus und Magen dosisabhängig Motilitätsstörungen und
Mukosaläsionen, die unter akuten Bedingungen reversibel sind. Chronischer Alkoholkonsum
ist mit einer deutlichen Risikosteigerung für Plattenepithelkarzinome des Ösophagus
vergesellschaftet. Diese Wirkungen werden hauptsächlich durch direkten Mukosakontakt
mit Ethanol oder seines Metaboliten Azetaldehyd verursacht. Einige Wirkungen von alkoholischen
Getränken, beispielsweise die maximale Stimulation der Magensäuresekretion durch vergorene
Alkoholika, werden durch nichtalkoholische Begleitstoffe hervorgerufen. Am exokrinen
Pankreas induziert Alkohol sekretorische Veränderungen, die von der Verabreichungsart
und -dauer, der zusätzlichen Gabe von Mahlzeiten, der Getränkeart oder dem basalen
Sekretionszustands des Organs abhängig sind. Für die Sekretionsveränderungen sind
hauptsächlich systemische und cholinerg-vagale Mechanismen verantwortlich, da das
Pankreas keiner topischen Ethanolexposition unterliegt. Chronischer Alkoholabusus
kann über subklinische rezidivierende Entzündungsschübe zur chronischen alkoholischen
Pankreatitis führen, wobei zusätzlich genetische Prädispositionen diskutiert werden.
Anders als beim kardiovaskulären System existieren bei diesen Alkoholzielorganen keine
gesundheitsförderlichen moderaten Alkoholmengen. Weiterer Forschungsbedarf besteht
bei der Klärung der genauen molekularen Mechanismen und möglichen genetischen Prädispositionen
von Alkoholfolgeerkrankungen sowie den Wirkungen nichtalkoholischer Substanzen in
alkoholischen Getränken.
Abstract
The oesophagus, stomach and pancreas are primary target organs for ethanol-related
diseases. In the oesophagus and stomach, ethanol induces motility disorders and mucosal
lesions that are dose-dependent and reversible under acute conditions. Chronic consumption
of alcohol causes a significant increase in the risk for squamous carcinoma of the
oesophagus. All of these effects are mainly caused by direct contact of alcohol or
its metabolite acetaldehyde with the mucosa. Non-alcoholic components are responsible
for many effects of alcoholic beverages, including the powerful stimulation of gastric
acid secretion by beverages that are produced by fermentation. In the exocrine pancreas,
alcohol induces secretory alterations that are mainly affected by the manner and duration
of alcohol exposure, the additional administration of food, the type of beverage or
the basal secretory state of the gland. Because the pancreas is not topically exposed
to ethanol, these ethanol effects on pancreatic secretion are primarily caused by
systemic cholinergic mechanisms of the vagus nerve. Chronic alcohol abuse may cause
chronic alcoholic pancreatitis after recurrent subclinical inflammatory episodes.
Genetic predispositions are believed to play an additional role in the pathomechanism
of the disease. In contrast to the cardiovascular system, moderate consumption of
alcoholic beverages does not have any beneficial health effects on the oesophagus,
stomach or pancreas. Future research needs to define the exact molecular mechanisms
and the role of different genetic predispositions for alcohol-induced diseases as
well as the effects of the non-alcoholic components of alcoholic beverages.
Schlüsselwörter
Alkohol - Ethanol - alkoholinduzierte Erkrankungen - Ösophagus - Magen - Pankreas
Key words
Alcohol - ethanol-alcohol-related diseases - oesophagus - stomach - pancreas
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Prof. Dr. med. Dr. h. c. M. V. Singer
II. Medizinische Universitätsklinik (Gastroenterologie/Hepatologie/Infektionskrankheiten),
Fakultät für Klinische Medizin der Universität Heidelberg, Universitätsklinikum Mannheim
Theodor-Kutzer-Ufer 1-3
68135 Mannheim
Phone: 06 21/3 83-32 84
Fax: 06 21/3 83-38 05
Email: manfred.v.singer@med.ma.uni-heidelberg.de