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      Biomarkers in Overactive Bladder: A New Objective and Noninvasive Tool?

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          Abstract

          Overactive bladder syndrome (OAB) is a highly prevalent urinary dysfunction, with considerable economic and human costs. Clinical diagnosis of OAB is still based on subjective symptoms. A new accurate, objective and noninvasive test to diagnose OAB and assess therapeutic outcome is lacking. Recent studies in lower urinary tract (LUT) dysfunctions, particularly in OAB patients, indicate that urinary proteins (neurotrophins, prostaglandins, and cytokines), serum C reactive protein, and detrusor wall thickness are altered, and such changes could be used as biomarkers of the disease. Nowadays, increasing emphasis has been given to the role of urinary neurotrophins, namely nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF), as key players in some urinary dysfunctions. Although recently considered to be a bladder dysfunction biomarker, urinary NGF presents low sensitivity and specificity. Preliminary results suggest that BDNF may serve as a more efficient biomarker. Even though we have to wait for future studies to confirm the potential role of NGF and BDNF as OAB biomarkers, it is already clear that neurotrophins will contribute to elucidate the physiopathological basis of OAB. Herein are reviewed the latest advances in this new and exciting field, the detection and clinical application of emerging OAB biomarkers.

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          Brain-derived neurotrophic factor modulates nociceptive sensory inputs and NMDA-evoked responses in the rat spinal cord.

          B J Kerr, E. J. Bradbury, D L H Bennett … (1999)
          Central sensitization, the hyperexcitability of spinal processing that often accompanies peripheral injury, is a major component of many persistent pain states. Here we report that the neurotrophin, brain-derived neurotrophic factor (BDNF), is a modulator of excitability within the spinal cord and contributes to the mechanism of central sensitization. BDNF, localized in primary sensory neuron cell bodies and central terminals, potentiates nociceptive spinal reflex responses in an in vitro spinal cord preparation and induces c-fos expression in dorsal horn neurons. NMDA receptor-mediated responses, known as a major contributor to central sensitization, were significantly enhanced by exogenous BDNF. Systemic NGF treatment, a procedure that mimics peripheral inflammatory states, raises BDNF levels in sensory neurons and increases nociceptive spinal reflex excitability. This increased central excitability is reduced by trkB-IgG, a BDNF "antagonist." We also show directly that inflammatory pain-related behavior depends on BDNF release in vivo. Thus behavioral nociceptive responses induced by intraplantar formalin and by intraplantar carageenan are significantly attenuated by trkB-IgG. Hence BDNF is appropriately localized and regulated in inflammatory states and is sufficient and necessary for the expression of central sensitization in the spinal cord. We propose that BDNF may function as a modulator of central sensitization in pathological states, and our results suggest that pharmacological antagonism of BDNF may prove an effective and novel analgesic strategy for the treatment of persistent inflammatory pain states.
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            Mechanisms of disease: involvement of the urothelium in bladder dysfunction.

            Lori A. Birder, Henrica de Vet (2006)
            Although the urinary bladder urothelium has classically been thought of as a passive barrier to ions and solutes, a number of novel properties have been recently attributed to urothelial cells. Studies have revealed that the urothelium is involved in sensory mechanisms (i.e. the ability to express a number of sensor molecules or respond to thermal, mechanical and chemical stimuli) and can release chemical mediators. Localization of afferent nerves next to the urothelium suggests that urothelial cells could be targets for neurotransmitters released from bladder nerves or that chemicals released by urothelial cells could alter afferent nerve excitability. Taken together, these and other findings highlighted in this article suggest a sensory function for the urothelium. Elucidation of mechanisms that influence urothelial function might provide insights into the pathology of bladder dysfunction.
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              Increased nerve growth factor levels in the urinary bladder of women with idiopathic sensory urgency and interstitial cystitis.

              G. Terenghi, Nicholas J Osborne, D Sinicropi … (1997)
              To determine whether nerve growth factor (NGF) is elevated in painful conditions of the urinary bladder (idiopathic sensory urgency, interstitial cystitis and painful chronic cystitis). Sixteen women patients were recruited from the Urodynamic Clinic at The Elizabeth Garrett Anderson Hospital, London. Four each had idiopathic sensory urgency (mean age 34 years, range 24-51), chronic cystitis (mean age 51 years, range 40-79) and interstitial cystitis (mean age 41 years, range 29-53). Four women who had genuine stress incontinence on cystometry but with no irritative symptoms were used as controls (mean age 45 years, range 35-54). The levels of NGF were determined in bladder biopsies from all women and biopsy sections were immunostained to detect NGF. The levels of NGF were higher in samples from all three painful bladder conditions than in samples from controls. Immunostaining showed increased NGF expression in the urothelium, most marked in patients with idiopathic sensory urgency. The increased level of NGF may explain several clinical and pathological features in these conditions, including sensitization of nociceptor fibres and increased numbers of mast cells. We propose that anti-NGF treatment may be a rational and effective treatment in intractable bladder pain.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Adv Urol
                Journal ID (publisher-id): AU
                Title: Advances in Urology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1687-6369
                ISSN (Electronic): 1687-6377
                Publication date (Print): 2011
                Publication date (Electronic): 29 May 2011
                Volume: 2011
                Electronic Location Identifier: 382431
                Affiliations
                1Department of Urology, Hospital de S. João, 4200-319 Porto, Portugal
                2Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal
                3Instituto de Biologia e Molecular e Celular (IBMC), University of Porto, 4150-180 Porto, Portugal
                4Institute of Histology and Embryology, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal
                Author notes

                Academic Editor: Ervin Kocjancic

                Article
                DOI: 10.1155/2011/382431
                PMC ID: 3113283
                PubMed ID: 21687625
                SO-VID: f0efc089-be25-4ff4-ae45-0ae5d8e4f363
                Copyright © Copyright © 2011 Tiago Antunes-Lopes et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 March 2011
                Date accepted : 28 March 2011
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Urology
                Data availability:
                ScienceOpen disciplines: Urology

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