Painful Bladder Syndrome (Including Interstitial Cystitis)
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CHAPTER 23 Committee 21 Painful Bladder Syndrome (including interstitial cystitis) Chairman P. H ANNO (USA), Members A. BARANOWSKI (U.K), M. FALL (SWEDEN), J. GAJEWSKI (CANADA), J. NORDLING (DENMARK), L. NYBERG (USA), V. R ATNER (USA), A. ROSAMILIA (AUSTRALIA), T. UEDA (JAPAN) Consultant T. HORN (DENMARK), S. JOHANSSON (SWEDEN), C. PAYNE (USA), J. SCURRY (AUSTRALIA), J.J WYNDAELE (BELGIUM) 1455 CONTENTS ABBREVIATIONS I. DEFINITION APF antiproliferative factor BCG Bacille Calmette-Guerin BDI Beck Depression Inventory II. AETIOLOGY OF INTERSTITIAL BOO bladder outlet obstruction CYSTITIS BPI Brief Pain Inventory BTX-A Botulinum toxin type A CIS carcinoma in situ III. EPIDEMIOLOGY OF PAINFUL DMMCR detrusor to mucosa mast cell ratio BLADDER SYNDROME / DMSO dimethyl sulfoxide EM electron microscopy INTERSTITIAL CYSTITIS EMDA electromotive drug administration FDA Food and Drug Administration (USA) GAG glycosaminoglycan IV. INTERSTITIAL CYSTITIS/ GRA Global Response Assessment PAINFUL BLADDER - PATHOLOGY HADS Hospital Anxiety and Depression Scale HB-EGF heparin-binding epidermal growth factor-like growth factor V. DIAGNOSIS HPF high power field IC interstitial cystitis ICA Interstitial Cystitis Association ICDB Interstitial Cystitis Data Base VI. CLINICAL SYMPTOM SCALES ICS International Continence Society Ig immunoglobulin IL interleukin VII. ASSESSING OUTCOMES IMMPACT Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials mEQ milliequivalents VIII. CONSERVATIVE THERAPY OF MPI Multidimensional Pain Inventory MPQ McGill Pain Questionnaire INTERSTITIAL CYSTITIS / PAINFUL NHS Nurses Health Study BLADDER DISEASE NIDDK National Institute of Diabetes, Digestive, and Kidney Diseases NIH National Institutes of Health NO nitric oxide IX. ORAL THERAPY OF INTERSTI- NOS nitric oxide synthase TIAL CYSTITIS / PAINFUL NRS numerical rating scales BLADDER DISEASE NSAIDS nonsteroidal anti-inflammatory drugs OAB overactive bladder PBS painful bladder syndrome PBS/IC painful bladder syndrome/interstitial cystitis X. INTRAVESICAL THERAPY PDI Pain Disability Index PORIS Patient’s Overall Rating of Improvement of Symptoms XI. SURGERY FOR INTERSTITIAL PPI present pain intensity CYSTITIS/PAINFUL BLADDER PPS pentosanpolysulfate SYNDROME PST potassium sensitivity test PUF Pelvic Pain and Urgency/Frequency Scale QIAM quantitative image analysis and morphometry XII. FUTURE DIRECTIONS IN RCT randomized controlled trial RESEARCH: INTERSTITIAL RNA ribosomal nucleic acid RTX resiniferatoxin CYSTITIS / PAINFUL BLADDER SF36 Short Form 36 of Medical Outcomes Study SYNDROME SIP Sickness Impact Profile TB tuberculosis UK United Kingdom REFERENCES UW University of Wisconsin VAS visual analogue scale 1456 Painful Bladder Syndrome (including interstitial cystitis) P. H ANNO, A. BARANOWSKI, M. FALL, J. GAJEWSKI, J. NORDLING, L. NYBERG, V. RATNER, A. ROSAMILIA, T. UEDA In practice, patients with symptoms of PBS/IC are I. DEFINITION screened to exclude other relevant diagnoses and a focused evaluation is performed at the discretion of Interstitial Cystitis (IC) is a clinical diagnosis pri- the physician or centre. This evaluation might inclu- marily based on symptoms of urgency/ frequency de cystoscopy under local or general anaesthesia, and pain in the bladder and or pelvis. The Inter- bladder distension with registration of bladder capa- national Continence Society [1] (ICS) prefers the city and/or the presence of glomerulations and Hun- term Painful Bladder Syndrome (PBS) defined as ner’s ulcer. Bladder wall biopsies might be obtained “ the complaint of suprapubic pain related to and evaluated for inflammation, ulcer, fibrosis, mast bladder filling, accompanied by other symptoms cells etc. The evaluation might also include urodyna- such as increased daytime and night-time fre- mics with registration of bladder capacity, complian- quency, in the absence of proven urinary infection ce and bladder stability [2]. One view of the rela- or other obvious pathology”. ICS reserves the dia- tionship of PBS/IC with OAB is graphically depicted gnosis IC to patients with “typical cystoscopic and in figure 1 [3]. The 14% incidence of urodynamic histological features”, without further specifying detrusor overactivity in the PBS/IC [4] patients is these. The condition will therefore in the remain- probably close to what one might expect in the gene- der of this chapter be referred to as PBS/IC. This ral population if studied urodynamically [5]. seems to be a usable way ahead until more specific In the end, these investigations might prove to be criteria can be established. As the terminology is in normal, but because no other diagnosis is available, flux, some of the older literature will be discussed the patients are identified as having PBS/IC as a dia- using the original terminology in the interests of cla- gnosis of exclusion. The relevance of urodynamic, rity. Logically IC should include some form of cystoscopic and histological findings is further obs- demonstrable inflammation in the bladder wall, cured, because the methodology by which these while PBS should include pain in the region of the results is obtained is not standardised making it dif- bladder. The diagnosis of PBS/IC is often based on ficult or impossible to compare studies. exclusion of other diseases in the bladder, urethra, and other pelvic organs including the musculoskele- The committee believes that the Oxford system for tal system. As with other diseases without diagnostic categorizing levels of evidence is relevant only for criteria or pathophysiological explanation, countless the sections on treatment, which follow. While the theories have been put forward without adding much committee’s opinions will be expressed, where to the delineation or understanding of the disease. applicable, regarding evidence and conclusions for other areas, including diagnosis, aetiology, and pathophysiology, use of the Oxford system would be inappropriate. 1457 Figure 1 8 II. AETIOLOGY OF INTERSTITIAL mine, leucotrienes, serotonins and cytokines . These CYSTITIS cells are thus the repositories of many potent inflam- matory factors, all of which are of importance in chronic inflammatory diseases. Many of the symp- Despite extensive scientific effort, the precise toms and findings in ulcerative IC, such as pain, fre- aetiology of PBS/IC is still an enigma. Much data quency, oedema, fibrosis and the production of new has been compiled resulting in an abundance of theo- vessels in the lamina propria, could possibly be ries concerning aetiology and pathogenesis. Since ascribed to the release of mast cell-derived factors. aetiology is unknown, hypotheses abound with spar- Hence, the mast cell-IgE system and its interaction se evidence. A fact that hampers studies on PBS/IC with other inflammatory cells and the nervous sys- is that, in clinical practice, there is no general tem [9] seems to be of importance when it comes to consensus on how to define and classify this condi- etiology and pathogenesis. There is a ten-fold increa- tion. se in mast cell count in bladder tissue from patients 1. INFLAMMATION would seem an essential featu- with ulcerative IC as compared to controls. In non- re since the term cystitis refers to an inflammatory ulcer IC, however, the mast cell count is normal or process. Still, inflammation is a non-disputable fea- only slightly increase [8,10,11]. Activation of mast ture only in the classic or ulcerative form of intersti- cells has been described as a characteristic and tial cystitis. Histological examination of bladder essential feature in IC [12]. lesions has revealed pan-cystitis and perineural Other mechanisms have also been put forward. Leu- inflammatory infiltrates of lymphocytes and plasma kotriene E4, the end product of cysteinyl containing cells. Inflammation is scant in non-ulcer IC [6,7]. leukotrienes, and eosinophil protein X are markers of The cause of a documented inflammatory response is the activation of mast cells and eosinophils. Bouche- a central issue and has been subject to repeated louche [13] compared the urinary excretion of leuko- investigations and much speculation. triene E4 and eosinophil protein X in patients with interstitial cystitis and in healthy controls and 2. MAST CELL ACTIVATION concluded that patients with interstitial cystitis and Mast cells are thought to have a pivotal role in IC. detrusor mastocytosis had increased urinary leuko- They are multifunctional immune cells that contain triene E4 and eosinophil protein X. Urinary leuko- highly potent inflammatory mediators such as hista- triene E4 and eosinophil protein X may be useful 1458 markers for assessing the grade of activation of mast urine of patients with IC but not most others, and cells and eosinophils in patients with interstitial cys- these findings open up new avenues for development titis and/or for confirming the diagnosis. of urine markers for IC. 3. UROTHELIAL DYSFUNCTION/GAG-LAYER 5. AUTOIMMUNE MECHANISMS DEFECTS There are numerous reports on autoantibodies in A defect in the glycosaminoglycane- (GAG) –layer patients with IC [20-23]. However, the precise iden- is a pathogenetic explanation to IC that has been pro- tity of these autoantibodies is not yet determined. posed by Parsons and co-workers [14]. By such a Some of the common clinical and histopathological defect the sub-mucosal nerve filaments might beco- characteristics present in IC patient show certain me accessible to noxious substances of urine, which similarities with other known autoimmune phenome- may explain pain and