Abstract
ABSTRACTObjectives:To evaluate the expression of sphingosine kinase 1 (SPK1) in the bladder wall in patients with neurogenic lower urinary tract dysfunction and its association with clinical, urodynamic and pathological features.Materials and Methods:The expression of SPK1 was studied in bladder wall specimens obtained from cystectomy using immunohistochemistry in ten patients with spinal cord injury (n=8) or multiple sclerosis (n=2) with urodynamically proven neuropathic bladder dysfunction, and in controls (n=5). Inflammation and fibrosis were analysed with histological criteria and SPK1 expression was determined by individual immunohistochemical staining.Results:Significant increased SPK1 urothelial immunoreactivity was shown in patients compared to control group (p=0.03). By contrast, SPK1 immunoreactivity in patients was significantly decreased in the sub-urothelium, muscles and nerves, p=0.02; 0.01 and 0.003, respectively. Patients with neurogenic detrusor overactivity (NDO) had higher SPK1 urothelium expression than those without any DO (p=0.04).Conclusions:SPK1 is expressed in the human bladder wall, specifically the urothelium, in bladder specimens from patients with NDO. The role of SPK1 in the pathophysiology of NDO needs further elucidation.
Highlights
Lower urinary tract dysfunction (LUTD) is common following neurological disorders such as spinal cord injury and multiple sclerosis
Inflammatory lymphocytic/plasma cell infiltration was observed in all patients specimen with predominance in the deep layers of the bladder wall
There were no significant differences in inflammation or fibrosis in the patient group regarding age, aetiology and bladder localization
Summary
Lower urinary tract dysfunction (LUTD) is common following neurological disorders such as spinal cord injury and multiple sclerosis. The commonest manifestation is an overactive bladder syndrome, characterized by urinary urgency, frequency and urge incontinence due to neurogenic detrusor overactivity (NDO). One pathophysiological hypothesis is an increase in afferent input from the bladder where nonadrenergic noncholinergic mechanisms become predominant [1]. A shift from A delta-fibers to abnormal C-fibers activity is observed. There is good evidence that the main transmitter contraction is ATP and that nitric oxid (NO) is responsible for the main part of inhibitory NANC responses [2]. The mechanisms of altered excitability are not totally understood and the role of many others substances such as neuropeptides need to be fully established
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