Interstitielle Zystitis: Was gibt es Neues zur Ätiopathogenese?

Zusammenfassung

Neue Erkenntnisse bringen Fortschritte in das Verständnis der komplizierten Ätiopathogenese der Interstitiellen Zystitis/Bladder Pain Syndrom (IC/BPS), deren Kausalitäten bisher nur in Fragmenten entschlüsselt wurden. Dabei zeigt sich ein immer komplexeres Netzwerk von Pathomechanismen, in denen die oft genannten Mastzellen und Urothelveränderungen nur ein Fragment der pathologischen Veränderungen zu sein scheinen. Neueste Erkenntnisse für eine mögliche genetische und epigenetische Veranlagung basieren auf Stammbaumanalysen, Nachweisen von Einzelnukleotid-Polymorphismen und eindeutigen Veränderungen bei Differentiell Exprimierten Genen. Multiple Veränderungen lassen sich auf molekularer Ebene nachweisen. Der Plättchenaktivierende Faktor, VEGF, das Corticotropin Releasing Hormone und das Inflammasom sind wichtige Player im Verständnis der Erkrankung. Der Pathomechanismus der „Aktivierung“ der IC/BPS bleibt immer noch ungeklärt. Neue Ansatzpunkte könnten Virusnachweise (Epstein-Barr Virus, BK Polyomaviren) oder bakterielle Entzündungen durch in Standardkulturen nicht nachweisbaren Erregern geben.

Abstract

New findings provide progress in the understanding of the complicated aetiopathogenesis of interstitial cystitis/bladder pain syndrome (IC/BPS), whose causalities have only been deciphered in fragments so far. An increasingly complex network of pathomechanisms is emerging, in which the frequently mentioned mast cells and urothelial changes seem to be only a fragment of the pathological changes. The latest findings regarding a possible genetic and epigenetic predisposition are based on pedigree analyses, detection of single nucleotide polymorphisms and significant changes in differentially expressed genes. Multiple alterations can be detected at the molecular level. Platelet-activating factor, VEGF, corticotropin-releasing hormone and the inflammasome are important players in understanding the disease, but the pathomechanism underlying the „activation“ of IC remains unclear. New starting points could be the detection of viruses (Epstein-Barr virus, BK polyomaviruses) or bacterial inflammation by pathogens that cannot be detected in standard cultures.

Schlüsselwörter

Interstitielle Zystitis - Ätiopathogenese - Genetik - VEGF - Inflammasom

Keywords

genetics - VEGF - inflammasome - aetiopathogenesis - interstitial cystitis

Publication History

Received: 09 June 2021

Accepted after revision: 16 September 2021

Article published online:
30 November 2021

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