Zusammenfassung
Rauchen ist der wesentliche Risikofaktor für das Auftreten der chronisch-obstruktiven Lungenerkrankung (COPD) sowie des Lungenkarzinoms. Als chronische Erkrankung ist die COPD mit erheblicher Einschränkung der Lebensqualität verbunden. Das Lungenkarzinom stellt in Deutschland bei Männern die führende und bei Frauen die dritthäufigste Krebs-Todesursache dar. Die vorliegende Übersicht vermittelt Daten zur Primärprävention beider Erkrankungen und die positiven Effekte der Tabakentwöhnung auf den Verlauf bei bestehender Diagnose. Tabakrauch führt über oxidativen Stress zu einer chronischen Entzündung, die im Mittelpunkt der Pathogenese der COPD steht. Onkogene Mutationen sowie durch Tabakrauch abgeschaltete Tumor-Suppressorgenen führen zur Entstehung eines Lungenkarzinoms. Frauen tragen im Vergleich zu Männern bei gleicher Exposition ein höheres Risiko für die Entwicklung beider Erkrankungen. Die Tabakentwöhnung ist die einzige therapeutische Maßnahme, die bei Patienten mit COPD die Exazerbationen sowie die Mortalität reduziert und zu einer nachhaltigen Besserung der Lungenfunktion führt. Aufgrund des hohen Abhängigkeitsgrades von Rauchern mit COPD müssen bei der Entwöhnung dieser Patienten multimodale Konzepte mit Pharmakotherapie und psychosozialer Intervention verfolgt werden. Bei Patienten mit Lungenkarzinom sind positive Effekte des Rauchstopps auf Körpergewicht, Performancestatus, postoperative Komplikationen und Mortalität gesichert. Entsprechend sollte die Tabakentwöhnung integraler Bestandteil der Lungenkarzinom-Therapie sein. Weitere Untersuchungen sind allerdings notwendig, um die Tabakentwöhnung in Relation zu etablierten Therapieansätzen besser einzuordnen.
Abstract
Smoking is the main risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Being a chronic disease, COPD severely impairs the quality of life. Lung cancer is the leading cause of death among German males and the third most important cause of death among German females. This review gives data on the primary prevention of both diseases and the beneficial effects of smoking cessation following disease manifestation. Smoking-induced oxidative stress triggers a chronic inflammation which is central to the pathogenesis of COPD. Smoking causes lung cancer by oncogenic mutations as well as inhibition of tumour-supressor genes. Women have an increased risk to develop COPD and lung cancer as compared to men when exposed to the same amounts of tobacco smoke. Smoking cessation is the only treatment capable of reducing exacerbations and mortality as well as sustainedly improving lung function. The high level of nicotine dependence in COPD patients mandates an intensive smoking cessation treatment including pharmacotherapy and psychosocial intervention. In patients with lung cancer, smoking cessation has confirmed favourable effects on body weight, performance status, postoperative complications and mortality. Thus, smoking cessation should be an integral part of lung cancer treatment. Further research is needed to better delineate the effects of smoking cessation in relation to other treatment modalities.
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Prof. Dr. med. Stefan Andreas
Lungenfachklinik Immenhausen
Robert-Koch-Straße 3
34376 Immenhausen
eMail: sandreas@lungenfachklinik-immenhausen.de
