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DOI: 10.12687/phleb2413-2-2018
Adipositas und chronische Inflammation bei phlebologischen und lymphologischen Erkrankungen
Article in several languages: deutsch | EnglishPublication History
Eingereicht:
08 February 2018
Angenommen:
12 February 2018
Publication Date:
02 April 2018 (online)
![](https://www.thieme-connect.de/media/10.1055-s-00034913/201802/lookinside/thumbnails/10-12687-phleb2413-2-2018_de-1.jpg)
Zusammenfassung
Die Prävalenz der Adipositas ist in den letzten 15 Jahren weiter stark angestiegen. Dabei fällt besonders die deutliche Zunahme der morbiden Adipositas auf, die wiederum bei den Älteren besonders ausgeprägt ist. Da mit dem Alter auch venöse Thromboembolien, chronisch venöse Insuffizienz und sekundäre Lymphödeme zunehmen, steigt die Zahl der Patienten mit venösen oder lymphatischen Erkrankungen, die gleichzeitig schwer adipös und häufig multimorbide sind, überproportional an. Die Adipositas, vor allem die viszerale, verschlechtert alle Ödemerkrankungen, erhöht das Risiko für thromboembolische Erkrankungen und postthrombotisches Syndrom und kann alleinige Ursache sein für die Adipositas-assoziierte funktionelle Veneninsuffizienz ohne Nachweis von Obstruktion oder Reflux. Das Adipositasassoziierte Lymphödem stellt inzwischen den größten Anteil unter den sekundären Lymphödemen. Mehr als 50 Prozent der Lipödempatientinnen sind adipös, die bei ihnen im Verlauf zu beobachtenden sekundären Lymphödeme in der Regel Folge der Adipositas, nicht des Lipödems. Die Symptomatik wird bei allen Krankheitsbildern durch Gewichtsreduktion gebessert. Neben mechanischen Faktoren wie der Erhöhung des intraabdominalen und intertriginösen Drucks, der wiederum zu einer venösen Drucksteigerung in den Beingefäßen führt, sind es vor allem die durch die Zunahme des viszeralen Fettgewebes verursachten metabolischen, chronisch inflammatorischen und prothrombotischen Prozesse, die für diese Zusammenhänge verantwortlich sind, erkennbar an niedrigen Spiegeln von Adiponektin und hohen von Leptin, Insulin, intaktem Proinsulin, PAI-1 sowie proinflammatorischen Zytokinen (Il-6, Il-8, TNF-α). Therapeutische Maßnahmen müssen also in erster Linie auf die Reduktion der viszeralen Adipositas und damit der Hyperinsulinämie bzw. der Insulinresistenz sowie auf die Bekämpfung der chronischen Entzündung abzielen.
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