Ignite Creation Date:
2024-05-06 @ 12:40 AM
Last Modification Date:
2024-10-26 @ 10:53 AM
Study NCT ID:
NCT01629433
Status:
COMPLETED
Last Update Posted:
2012-06-27
First Post:
2012-06-20
Brief Title:
Onabotulinumtoxina Intradetrusorial Injections and NGF Expression
Sponsor:
University Of Perugia
Organization:
University Of Perugia
Study Overview
Official Title:
PHASE IV STUDY ON THE EFFECTS OF ONABOTULINUMTOXINA INTRADETRUSORIAL INJECTIONS ON BLADDER EXPRESSION OF NGF TRKA P75 AND TRPV1 IN PATIENTS WITH DETRUSOR OVERACTIVITY
Status:
COMPLETED
Status Verified Date:
2012-06
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
OnabA-NGF
Brief Summary:
In the last years botulinum toxin type A onabA has been increasingly used as a treatment option for overactive bladder symptoms in patients affected by either neurogenic and idiopathic detrusor overactivity DO How onabA injected into the detrusor muscle improves overactive bladder symptoms in neurologic patients has been only partially investigatedSome evidence suggested that the neurotoxin probably reduces detrusor muscle contraction blocking detrusor muscle cholinergic innervation However recent experimental observations indicated that onabA determines more complex effects on bladder activity acting on afferent innervations as well as on the efferent one Only few experimental studies have investigated the activity of onabA on bladder afferent nervous transmission Experimental studies in animals showed that Nerve Growth Factor NGF elicits increased sensation urgency and DO Although there are some evidence on the ability of onabA to improve DO and to reduce bladder and urinary content of NGF how onabA influences NGF expression and the expression of TrKa p75 and TRPV1 receptors is still unclear The hypothesis is that onabA reduces NGF bladder tissue levels and in the same time it modulates the gene expression of NGF associated receptors TrkA p75 and TRPV1
Detailed Description:
NGF has been suggested to modulate neurotransmitters release induces synaptic reorganization and influences neuronal excitability acting on TrkA and p75 associated receptors Moreover recent observations indicated that NGF-induced DO and noxious input depend on the interaction of NGF with TRPV1 that is over-expressed in overactive bladders and interstitial cystitispainful bladder syndrome From a clinical point of view a decrease in urinary NGF levels has been detected in patients with DO treated with onabA Although there are some evidence on the ability of onabA to improve DO and to reduce bladder and urinary content of NGF how onabA influences NGF expression and the expression of TrKa p75 and TRPV1 receptors is still unclear
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None