Abstract
Chornic spinal cord injury (SCI) will induce bladder urothelium dysfunction. This study investigated the therapeutic effects on urothelial dysfunction after repeated detrusor injections of onabotulinumtoxinA (BoNT-A) in SCI patients with neurogenic detrusor overactivity (NDO). Twenty chronic suprasacral SCI patients with NDO were enrolled. The patients received 300 U BoNT-A injection into the detrusor every six months. The urothelium was assessed by cystoscopic biopsy at baseline and six months after each BoNT-A treatment. Immunofluorescence staining for urothelial dysfunction, including E-cadherin, zonula occludens-1 (ZO-1), tryptase for mast cell activity, and urothelial apoptosis were investigated. The outcome of urothelial dysfunction parameters after BoNT-A injection were compared between baseline and six months after each treatment. Repeated 300 U BoNT-A injections showed a sustained decrease of detrusor pressure compared with baseline. After three repeated BoNT-A detrusor injections, significantly greater distributions of E-cadherin (p = 0.042) and ZO-1 (p = 0.003) expressions, but no significant changes, of urothelial apoptosis and mast cell activation were found after repeated BoNT-A therapy. Urothelial dysfunction, such as adhesive and junction protein concentrations in SCI patients’ bladders, recovered after three repeated cycles of BoNT-A treatment. The therapeutic effects sustained. However, urothelial inflammation and apoptosis after SCI were not significantly improved after three repeated BoNT-A injections.
Highlights
Spinal cord injury (SCI) is a significant cause of morbidity and mortality in developing countries, with the worldwide incidence of SCI reported in the literature ranges from 12.1 to 57.8 per million [1].In chronic SCI patients, the main problems of neurogenic lower urinary tract dysfunction (NLUTD)are failure to store due to detrusor overactivity (DO), or urethral incompetence
A total of 20 patients with chronic SCI and 10 controls were enrolled in this study
The injury level was at cervical spinal cord in seven patients, thoracic cord in 11, and lumbar cord in two
Summary
In chronic SCI patients, the main problems of neurogenic lower urinary tract dysfunction (NLUTD). Are failure to store due to detrusor overactivity (DO), or urethral incompetence Another problem is failure to empty due to detrusor areflexia, bladder neck dysfunction, or detrusor sphincter dyssynergia (DSD), and a usually-combined failure to store and empty, such as due to DSD or DO and impaired contractility [2]. High intravesical pressure may damage the upper urinary tract, causing renal scarring and chronic renal insufficiency, which greatly impairs the quality of life [3]. SCI leads to rapid disruption of the uroepithelial barrier This manifests in a loss of cell–cell interactions, decrease in transepithelial resistance, and increases in water and urea permeability [4]
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