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Differences in Clinical Features and Histopathology in BPS/IC with and without Hunner Lesions

  • Christina Kåbjörn-GustafssonEmail author
  • Ralph Peeker
Chapter
  • 462 Downloads

Abstract

The understanding of interstitial cystitis (IC) has changed a lot since the term was first introduced by Skene as early as in 1887 [1]. Guy L. Hunner described a symptom complex of bladder pain associated with an elusive cystoscopic feature, the Hunner ulcer, almost exactly 100 years ago [2]. A couple of decades later things became a lot more confusing when John Hand presented a large series of IC patients noticing that IC did not comprise just one single entity [3]. Some 40 years ago Messing and Stamey believed that there might be an early form of the disease, displaying the so-called submucosal glomerulations, potentially progressing into the well-known classic disease [4]. This notion has subsequently been considered unrealistic since progression from the so-called ‘early form’ to the classic ulcerous form or end stage disease (bladder contracture) actually never has been reported. Conversely, during the recent decades it has become increasingly clear that the different forms of IC indeed represent completely different pathological entities, despite sharing similar symptomatology and the same chronic course [5–8]. In a recent report, Killinger et al. failed to reveal any significant differences in pain patterns between the two subtypes [9].The differences between the two subtypes are reflected in clinical manifestation and age distribution [7, 8]. It has also been reported that the two subtypes respond differently to many treatment procedures [8]. Koziol et al. supported the contention of heterogeneity of interstitial cystitis by observations based on epidemiological data relating to demographics, risk factors, symptoms, pain and psychosocial factors [6], and, more recently, Peters et al. demonstrated notable differences between the two subtypes in the number of comorbid diagnoses as well as symptoms [10]. In these reports, subjects with Hunner disease were significantly older.

Notes

Acknowledgments

We would like to thank Ulric Pedersen for his contribution to the preparation of included figures.

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Copyright information

© Springer International Publishing AG 2018

Authors and Affiliations

  1. 1.Institute of BiomedicineGothenburg UniversityLandvetterSweden
  2. 2.Department of Urology, Institute of Clinical SciencesSahlgrenska Academy at the University of GothenburgGöteborgSweden

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