Abstract

In this review, we focused on putatively interesting biomarkers of interstitial cystitis/bladder pain syndrome (IC/BPS) in relation to the etiopathology of this disease. Since its etiopathology is still under discussion, the development of novel biomarkers is critical for the correct classification of the patients in order to open personalized treatment options, on the one hand, and to separate true IC/BPS from the numerous confusable diseases with comparable symptom spectra on the other hand. There is growing evidence supporting the notion that the classical or Hunner-type IC (HIC) and the non-Hunner-type IC (NHIC) are different diseases with different etiopathologies and different pathophysiology at the full-blown state. While genetic alterations indicate close relationship to allergic and autoimmune diseases, at present, the genetic origin of IC/BPS could be identified. Disturbed angiogenesis and impairment of the microvessels could be linked to altered humoral signaling cascades leading to enhanced VEGF levels which in turn could enhance leucocyte and mast cell invasion. Recurrent or chronic urinary tract infection has been speculated to promote IC/BPS. New findings show that occult virus infections occurred in most IC/BPS patients and that the urinary microbiome was altered, supporting the hypothesis of infections as major players in IC/BPS. Environmental and nutritional factors may also influence IC/BPS, at least at a late state (e.g., cigarette smoking can enhance IC/BPS symptoms). The damage of the urothelial barrier could possibly be the result of many different causality chains and mark the final state of IC/BPS, the causes of this development having been introduced years ago. We conclude that the etiopathology of IC/BPS is complex, involving regulatory mechanisms at various levels. However, using novel molecular biologic techniques promise more sophisticated analysis of this pathophysiological network, resulting in a constantly improvement of our understanding of IC/BPS and related diseases.

Highlights

  • Interstitial cystitis/bladder pain syndrome (IC/BPS) is a disabling disease, with a reported prevalence of 52—500/100,000 in the female and 8—41/100,000 in the male population [1,2,3]

  • interstitial cystitis/bladder pain syndrome (IC/BPS) comprises the classic IC/BPS, presenting cystoscopically identifiable Hunner lesions of the urothelium (HIC), contrasting that the non-Hunner-type interstitial cystitis (NHIC) [5,6] and other molecular subtypes may emerge in the future

  • Cellular crosstalk with immune system has greatly improved our view in IC/BPS

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Summary

Introduction

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a disabling disease, with a reported prevalence of 52—500/100,000 in the female and 8—41/100,000 in the male population [1,2,3]. The full-blown disease has a significant social impact since participation in social activities is severely hampered. No specific biomarkers have been found, allowing unequivocal diagnosis of the disease. Diagnosis largely relies on the exclusion of confusable diseases [4]. IC/BPS comprises the classic IC/BPS, presenting cystoscopically identifiable Hunner lesions of the urothelium (HIC), contrasting that the non-Hunner-type interstitial cystitis (NHIC) [5,6] and other molecular subtypes may emerge in the future. We summarize the current knowledge on potential biomarkers, linking them to potential etiopathology of IC/BPS

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