Detrusor Mast Cells in Refractory Idiopathic Instability

Moore, Kate H.; Nickson, Paul; Richmond, D. H.; Sutherst, J. R.; Manasse, Paul; Helliwell, T. R.

doi:10.1111/j.1464-410x.1992.tb16136.x

Cited by 7 publications

(5 citation statements)

References 17 publications

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“…The terminology problem was considered by a previous ICI‐RS “Think Tank,” but no firm definition was decided upon. At the present meeting, it was suggested that refractory DO should be defined as proven idiopathic DO (no features of outflow obstruction or neurological disorder) in patients who have failed to respond to at least two anticholinergic drugs with detailed bladder training for at least 12 months, as evidenced by persisting frequency >8 voids per day, disabling urgency, with or without nocturia and urgency incontinence, as documented on a frequency volume Chart . In patients not having had urodynamic testing, the above requirement for proof of persistent symptomatic OAB related disability should remain.…”

Section: Definition Of Refractory Idiopathic Oab/domentioning

confidence: 99%

What is the role of covert infection in detrusor overactivity, and other LUTD? ICI-RS 2013

Moore

Malykhina

2014

Neurourol. Urodynam.

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A think tank was convened at the fourth ICI-RS meeting, which took place June 5-7, 2013 in Bristol UK, to consider current evidence and controversies surrounding the possible role of 'covert infection' in the pathophysiology of refractory detrusor overactivity (DO) and other lower urinary tract disorders (LUTD). The topic was chosen because several authors from different centers worldwide have recently published evidence which supports this concept. However, to date there is inconsistency regarding terminology and microbiological definitions, which were discussed by the participants. The mechanisms whereby infection/inflammation could actually promote aberrant detrusor contractions in the human remain controversial, and are more fully described in this report. Future requirements for research into this topic were outlined.

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Section: Definition Of Refractory Idiopathic Oab/domentioning

confidence: 99%

What is the role of covert infection in detrusor overactivity, and other LUTD? ICI-RS 2013

Moore

Malykhina

2014

Neurourol. Urodynam.

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“…13, 20-23]. Detursor mast cell counts as high as or higher than those described in IC have been observed in other conditions, including bladder cancer and refractory detrusor instabili ty [3,22,24]; abundant mast cells have also been described in suburothclium of the bladder in association with urinary infection [25]. Mast cells do exist in both suburothclium and muscularis of the normal bladder [6]; there is also evidence that they become increasingly abun dant in the bladder with natural aging [26].…”

Section: Introductionmentioning

confidence: 99%

Distinctive Ultrastructural Pathology of Nonulcerative Interstitial Cystitis

Jk²

1996

Urol Int

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Ultrastructural study of the bladder in interstitial cystitis has, so far, been limited, mainly to the urothelium. The present study was conducted first to study in detail the ultrastructural features of all tissue components of the bladder wall in nonulcerative interstitial cystitis and second to derive clues from the observed changes to pathogenesis of the disease. Endoscopic biopsies of urothelium with attached suburothelium, and muscularis, were obtained from both lesional and nonlesional areas in 5 female patients with unequivocal clinical diagnosis of interstitial cystitis. The specimens were processed for electron microscopic study by standard methods and subjected to comprehensive ultrastructural study of urothelium, suburothelium, detrusor muscle cells, intrinsic blood vessels, and intrinsic nerves. A distinctive combination of peculiar muscle cell profiles, injury of intrinsic vessels and nerves in muscularis and suburothelium, and discohesive urothelium was observed in lesional and less markedly in nonlesional samples of all specimens. Marked edema of various tissue elements and cells appeared to be a common denominator of many observed changes. Edema of muscle cells resulted in characteristic querciphylloid profiles, so designated because of peripheral bosselation of cell sarcoplasm with a lobed perimeter resembling that of an oak leaf. Urothelial changes disrupted the true permeability barrier, consisting of asymmetric unit membrane and triple epithelial junctions of surface (umbrella) cells. Vascular lesions included endothelial cell injury and suggested sluggishness of intrinsic microcirculation. Neural changes included a combination of degenerative and regenerative features, some expressing neural plasticity. The observed ultrastructural changes appear to be sufficiently distinctive to be diagnostic in specimens submitted for pathologic confirmation of nonulcerative interstitial cystitis. The changes do not support a primary pathogenetic role of mast cells or a selectively deficient glycosaminoglycan layer. They do suggest, however, a pathogenesis based on a potentially self-perpetuating process of neurogenic inflammation that can trigger a biologically potent cascade of events, including a leaky urothelium and mast cell activation. As proposed, neurogenic inflammation consolidates various proposals advanced as the pathogenesis of interstitial cystitis and can readily accommodate infectious, immunologic, and autoimmunologic mechanisms as factors that contribute to development or chronicity of the disease.

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“…Definition of non response comprised at least six urgency incontinence episodes per 3-day diary. Similarly, Moore et al 23 defined "refractory" as: (1) detrusor overactivity on medium fill cystometry without evidence of voiding difficulty on free uroflowmetry; (2) duration of symptoms >4 years; (3) failure to respond to at least two anticholinergic drugs coupled with out-patient bladder training for more than 1 year; and (4) persistent disabling symptoms of frequency/urgency/incontinence documented on a frequency volume chart. It would seem that a standard definition of the term "refractory OAB" would facilitate research in this area.…”

Section: The Refractory Oab Patientmentioning

confidence: 97%

Can we predict which patient will fail drug treatment for overactive bladder? A think tank discussion

Νitti

Kopp

Lin

et al. 2010

Neurourology and Urodynamics

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The treatment of overactive bladder (OAB) has evolved over the past 20 years to include a number of behavioral, pharmacological, and minimally invasive treatments. After behavioral therapy, pharmacological therapy with antimuscarinics remains the mainstay of treatment. Despite this, a large number of patients will "fail" or be unsatisfied with drugs therapy. It would be extremely helpful to patients and clinicians to be able to predict who those patients are. However, there are a number of barriers. First and foremost are defining "success" and "failure" and this can vary dramatically from one patient to another. Endpoints other than the traditional variables used in clinical trials may be more effective in evaluating treatments and helping to predict outcomes. Along similar lines, there are various definitions for OAB that is "refractory" to conventional treatments and this term needs clarification. In many cases, response to therapy may be affected by factors such as comorbidities, metabolism of drugs, concurrent therapies, etc. These factors are sometimes obvious and sometimes not, and for a variety of reasons it can be quite difficult to predict or determine their effect on outcome. Finally, many patients with OAB include have mixed (stress and urgency) symptoms. It is important to sort out the OAB component of mixed symptoms and mixed urinary incontinence (MUI) when determining effects of therapy.

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Detrusor Mast Cells in Refractory Idiopathic Instability

Cited by 7 publications

References 17 publications

What is the role of covert infection in detrusor overactivity, and other LUTD? ICI-RS 2013

What is the role of covert infection in detrusor overactivity, and other LUTD? ICI-RS 2013

Distinctive Ultrastructural Pathology of Nonulcerative Interstitial Cystitis

Can we predict which patient will fail drug treatment for overactive bladder? A think tank discussion

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