Abstract
ObjectivesRecent studies have shown that chronic inflammation is involved in overactive bladder (OAB) syndrome. OAB could be a subtype of neurogenic inflammation. This pilot study investigated serum adipokine levels in patients with OAB refractory to antimuscarinic therapy.MethodsThirty consecutive patients with OAB-dry (n = 16) or OAB-wet (n = 14) refractory to previous antimuscarinic treatment were prospectively enrolled in this study, a group of 26 normal subjects without lower urinary tract symptoms served as controls. Concentrations of serum C-reactive protein (CRP), nerve growth factor (NGF), and adipokines including interleukins ([IL], IL-1β, IL-6, IL-8), tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1, insulin, and leptin were quantified using a bead-based human serum adipokine panel B kit. Data were analyzed using the LX 200 platform. Patients were further classified as having dry or wet OAB and having medical diseases or not. The serum CRP, NGF, and adipokine levels were compared between OAB patients and the controls, and between OAB subgroups.ResultsThe serum concentrations of CRP, NGF, IL-1β, IL-6, IL-8, and TNF-α in OAB-dry and OAB-wet patients were significantly higher than among the controls. There was no significant difference in adipokine levels between OAB-dry and OAB-wet, or between OAB patients with and without medical diseases. Serum CRP and NGF levels were significantly higher only in OAB-wet or OAB patients with medical diseases than among controls. The MCP-1 levels, on the other hand, were significantly higher in OAB-dry or OAB patients with disease, than the controls.ConclusionsBoth OAB-dry and OAB-wet patients showed increased serum CRP, NGF, and adipokine levels compared with the controls, suggesting chronic inflammation of the bladder involving both peripheral and central mechanisms in all OAB patients refractory to antimuscarinic therapy. The increased serum adipokine levels were not relevant to medical diseases.
Highlights
The clinical presentations of overactive bladder syndrome (OAB) are symptoms of urgency with or without urgency incontinence, and it is usually associated with frequency and nocturia [1]
Both OAB-dry and OAB-wet patients showed increased serum C-reactive protein (CRP), nerve growth factor (NGF), and adipokine levels compared with the controls, suggesting chronic inflammation of the bladder involving both peripheral and central mechanisms in all OAB patients refractory to antimuscarinic therapy
The serum concentrations of NGF, CRP, IL-1b, IL6, IL8, and tumor necrosis factor (TNF)-a in OAB-dry and OAB-wet patients were significantly higher than for the control subjects. (Fig. 1) There were no significant differences in the adipokine levels between OAB-dry and OABwet, or between OAB patients with and without medical diseases
Summary
The clinical presentations of overactive bladder syndrome (OAB) are symptoms of urgency with or without urgency incontinence, and it is usually associated with frequency and nocturia [1]. A high percentage of non-urological conditions overlap in patients with OAB, which implies possible common pathophysiology between them [4]. Histological investigations of the bladder urothelium and suburothelium have shown that chronic inflammation is present in 60% of baseline biopsies of patients with OAB [5]. The inflammatory responses triggered by the activation of primary sensory neurons induce overexpression of transient receptor potential vanilloid receptor subfamily type 1 (TRPV1) in the suburothelium as well as c-fos protein in the dorsal root ganglia, which have been demonstrated in rat models of OAB and in human bladder biopsies [6,7]
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