Terminologie und Pathophysiologie der Überaktiven Harnblase (ÜAB)

Zusammenfassung

Der Begriff Überaktive Blase (ÜAB) wurde als Symptomen-Syndrom in 2002 von der International Continence Society definiert, das mit Drangsymptomatik mit oder ohne Harninkontinenz, Pollakisurie und Nykturie einhergeht. Harnwegsinfektionen und andere nachweisbare Pathologien müssen ausgeschlossen sein.

Die Pathophysiologie der ÜAB ist noch nicht bis ins Detail geklärt und Gegenstand laufender Forschungen, sodass Hypothesen existieren, sich teilweise überlappen. In der Urothel-Hypothese werden sowohl funktionelle Veränderungen der urothelialen Rezeptoren als auch der Sensitivität und Kopplung suburothelialer Myofibroblasten diskutiert, die letztlich zu einer ansteigenden Aktivität von afferenten Signalen führen. Die myogene Hypothese basiert auf der Annahme, dass instabile Detrusor-Kontraktionen durch Veränderungen ihrer Erregbarkeit und Kopplung mit anderen Myozyten oder Myofibroblasten ausgelöst werden können. Instabile Detrusor-Kontraktionen erzeugen eine vermehrte afferente Aktivität und generieren auf diesem Weg Symptome einer überaktiven Blase. Die Hypothese einer abnormen Verarbeitung von afferenten Signalen nimmt an, dass Schäden an zentralen hemmenden Bahnen und/oder Sensibilisierung der afferenten Nerven zur Aktivierung des Miktionsreflexes führen, was wiederum instabile Detrusorkontraktionen auslöst. Darüber hinaus werden hormonelle und psychische Einflüsse diskutiert.

Abstract

In 2002, the International Continence Society defined the term overactive bladder (OAB) as a symptom syndrome that is accompanied by urgency with or without urge incontinence, frequency and nocturia. A proven urinary tract infection or other obvious pathologies must be excluded.

The pathophysiology of OAB has not been clarified in detail and is the subject of ongoing research, so partially overlapping hypotheses exist. The urothelium-based hypothesis suggests functional changes of urothelial receptors as well as functional changes regarding the sensitivity and coupling of the suburothelial myofibroblasts, which ultimately lead to increasing activity of afferent signals and urgency. The myogenic hypothesis is based on the assumption that unstable detrusor contractions may be triggered by changes in their excitability and coupling with other myocytes or myofibroblasts. Unstable detrusor contractions generate increased afferent activity followed by symptoms of overactive bladder. The hypothesis of abnormal processing of afferent signals assumes that damage to central inhibitory pathways and/or sensitisation of afferent nerves lead to the activation of the micturition reflex, which, in turn, induces unstable detrusor contractions. In addition, hormonal and psychological influences are discussed.

Schlüsselworter

Überaktive Blase - Terminologie - Pathophysiologie

Key words

overactive bladder - terminology - pathophysiology

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