Overactive BladderNCT00868621
Urinary Cytokines in Patients With Overactive Bladder (OAB)
An observational study of Overactive Bladder and Urinary Tract Infection, run by The Cleveland Clinic at 1 site in United States.
Trial summary
Overactive bladder (OAB) is a widespread condition characterized by urgency, urge incontinence, nocturia and excessive urinary frequency, affecting millions of people worldwide. In two epidemiological studies, OAB was found in about 17% of American and European populations. Read more about this study
- Who is it for?
- Ages 18 years and older, women onlyHealthy volunteers can take part
- Conditions the study is for
- Overactive Bladder, Urinary Tract Infection
- How many people
- 60 participants
- Where
- 1 siteUnited States
- Study dates
- Mar 2007to Aug 2009
- Phase
- Observational
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- Women only
- Healthy volunteers accepted
- Adult, Older adult
Study population: Twenty healthy women (control), 20 women suffering from overactive bladder and other 20 women suffering from UTI will be selected for the study. Each control will be age matched within +/- 5 years to patients.
Who may be able to join
- Group I (OAB patients)
- Women with OAB, ≥18 years and premenopausal non-menstruating, not on any anticholinergic for at least two weeks before enrollment in the study.
- Significant urgency,i.e., having moderate or severe urgency score.
- Having a score > 8 on the OAB-V8 questionnaire.
- Urinary frequency of more than 8/day, with urgency of urination, with or without urge incontinence.
- Negative screening urinalysis one month after documented UTI.
Show all 14Show fewer
- Group II (Control)
- Age-matched normal volunteers (≥18 years and premenopausal non-menstruating)
- No Urgency.
- OAB-8 score < 8.
- No UTI.
- Group III (UTl)
- Age-matched
- ≥18 years and premenopausal non-menstruating women with culture proven UTI.
Who cannot join
- Treatable genitourinary conditions that could cause incontinence
- Hematuria
- Obstructive uropathy
- Patients diagnosed with vaginitis
- History of urothelial carcinoma
- Urinary tract infection (except group III)
Show all 12Show fewer
- Pelvic radiation.
- Neurogenic bladder.
- Renal pathology.
- Stress urinary incontinence.
- Medications.
- Recent history of Botox injection in the bladder (Within the last year).
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Identification of Urinary Cytokines in Patients With Overactive Bladder (OAB)
Overactive bladder (OAB) is a widespread condition characterized by urgency, urge incontinence, nocturia and excessive urinary frequency, affecting millions of people worldwide. In two epidemiological studies, OAB was found in about 17% of American and European populations. This accounts for an estimated 33 million patients suffering from OAB in the USA. The disorder constitutes a psychological stress that impacts the patient's social life.
Read the detailed description
Overactive bladder (OAB) is a widespread condition characterized by urgency, urge incontinence, nocturia and excessive urinary frequency, affecting millions of people worldwide.(1) In two epidemiological studies, OAB was found in about 17% of American and European populations.(2)(3). This accounts for an estimated 33 million patients suffering from OAB in the USA. The disorder constitutes a psychological stress that impacts the patient's social life.
The luminal surface of the bladder is covered by the urothelium, which functions as a highly efficient barrier to the movement of water and ionized substances across the bladder wall.(4) Urothelial cells also have specialized sensory and signaling properties that allow them to respond to their chemical and physical environment, and engage in reciprocal chemical communication with neighboring nerves in the bladder wall. These properties are 1) nicotinic, muscarinic, tachykinin, adrenergic and capsaicin (TRPV1) receptor expression, 2) sensitivity to transmitters released from afferent and efferent nerves, 3) mechanosensitivity, 4) close physical association with afferent nerves and 5) the ability to release chemical mediators such as ATP and NO, which can regulate the activity of adjacent nerves and, thereby, trigger local vascular changes and/or reflex bladder contractions.(5)
Transmitter release from urothelial cells appears to be mediated by a calcium dependent exocytotic mechanism that is similar to the mechanism involved in transmitter release from nerve terminals. Transmitters released from urothelial cells can act in an autocrine/paracrine manner in the urothelium, or on subepithelial myofibroblasts, nerves or blood vessels to influence various functions, including the urothelial barrier, local blood flow and sensory mechanisms.(6)
Urine cytokine assays have been studied in various bladder and kidney disorders with the hope of understanding the pathophysiology and developing a noninvasive, reliable predictor of disease progression and evaluate the response to treatment.
Interstitial cystitis (IC) is a severely debilitating syndrome of unknown etiology affecting the urinary bladder that is mainly associated with urgency, frequency and pain. Pro-inflammatory molecules and neuroinflammation are suggested in the patho-mechanism of IC. Abdel Mageed and Ghoniem found out the activation of the nuclear factor kappa B (NF-k B) in the bladder biopsy of IC patients. NF-k B is a transcription factor found in some inflammatory diseases like rheumatoid arthritis, bronchial asthma, and inflammatory bowel diseases. NF-k B has a role in induction of pro inflammatory cytokines IL-6, IL-2, IL-1β and TNF-α. Activation of NF-k B was associated with 27, 8, 10 and 7 fold increase in TNF-α, IL-10, IL-6 and IL-8 transcripts respectively.(7,8) Keay et al determined that the urine of IC patients specifically contains a factor that inhibit primary bladder epithelial proliferation, anti proliferative factor (APF) and it has significantly decreased heparin binding epidermal growth factor like factor (HBEGF) and increased epidermal growth factor (EGF) levels compared to urine from normal subjects.(9) Chai et al compared urine levels of APF and HB-EGF before and after bladder distention and neurostimulation.(10,11) Both of urine markers changed toward normal levels after hydrodistention or neuromodulation treatment of IC.
Urinary cytokines have also been studied in patients undergoing intravesical bacillus Calmette Guerin (BCG) therapy for superficial bladder cancer.(12) BCG is thought to cause local immunostimulation, resulting in infiltration of T-lymphocytes in the bladder wall. After treatment, IL-1, IL-2, IL-6, and TNF are significantly elevated in the urine. It is thought that BCG induced cytokines may generate bladder tumor killing cells, and an elevation of urine cytokines may correlate clinical response to BCG therapy.
Recently, there have been studies that have attempted to identify specific measurable urinary factors that lead to the progression of chronic renal disease. Cytokines are involved in the recruitment of inflammatory cells, leading to infiltration in the diseased kidney, ultimately resulting in renal scarring. Elevated levels of urinary IL-6 and TNF receptor-1 are identified in children with vesicoureteral reflux associated with reflux nephropathy and renal scarring.(13)
Acute renal allograft rejection is a result of the recipient's immune response to the donor kidney, and 35% of these patients experience an episode of acute rejection the first year after surgery. Elevated urinary cytokines have been measured in patients who have biopsy proven renal allograft acute rejection.(14)
Urinary cytokines and markers have been identified in different urological disorders. They are used to understand the pathophysiology, diagnosis and evaluation of the treatment of these disorders. We hypothesize that there is urothelial abnormality in cases of overactive bladder that leads to elaboration of certain kinds of urinary cytokines. To our knowledge, no study has been published evaluating urinary markers in patients with OAB.
- Conditions
- Overactive Bladder, Urinary Tract Infection
- Medical subject headings
- Urinary Bladder, Overactive, Urinary Tract Infections
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| 1 | Control Group(CG)- Healthy age-matched volunteers with no urinary symptoms. | |
| 2 | Overactive Bladder Patients Group(OAB)- Patients with urgency of urination. | |
| 3 | Urinary Tract Infection Group(UTI)- Symptomatic patients with dysuria, urgency and frequency of urination with proven urine cultures of infection. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Number of Participants With Elevated Cytokines (Levels of Pro-inflammatory)
Used commercial human cytokine chip. If the study proved that certain cytokines are significantly present (p<0.05 compared to a standard) in the urine of OAB patients, further research to study the effect of anticholinergic drugs on the level of these cytokines in urine will be conducted.
Measured: 18 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Mar 2009 (estimated)
- Study startMar 2007
- Primary completionSep 2008
- Study completionAug 2009
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (12)Papers the sponsor has linked to this study.
- Other trials for Overactive BladderStudies of the same condition, open and under way.
- More trials run by The Cleveland ClinicThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Other
- Time perspective
- Prospective
- Enrolment
- 60 participants (actual)
Sponsor and investigators
- Lead sponsor
- The Cleveland Clinic
- Sponsor type
- University, hospital or other
- Collaborators
- Astellas Pharma US, Inc.
- Responsible party
- Sponsor
- Investigators
- Gamal Ghoniem, MD, Principal investigator, Cleveland Clinic Florida
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00868621
- Sponsor's protocol ID
- IRB 8848
- Status last verified
- Jul 2024
- First submitted
- 23 Mar 2009
- Last updated
- 29 Jul 2024
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- Yes
- Individual data sharing
- No
Publications
Abdel-Mageed AB, Bajwa A, Shenassa BB, Human L, Ghoniem GM. NF-kappaB-dependent gene expression of proinflammatory cytokines in T24 cells: possible role in interstitial cystitis. Urol Res. 2003 Oct;31(5):300-5. doi: 10.1007/s00240-003-0339-9. Epub 2003 Jul 11.
PubMed 14574533de Reijke TM, de Boer EC, Kurth KH, Schamhart DH. Urinary cytokines during intravesical bacillus Calmette-Guerin therapy for superficial bladder cancer: processing, stability and prognostic value. J Urol. 1996 Feb;155(2):477-82.
PubMed 8558640Ninan GK, Jutley RS, Eremin O. Urinary cytokines as markers of reflux nephropathy. J Urol. 1999 Nov;162(5):1739-42.
PubMed 10524926Lewis SA. Everything you wanted to know about the bladder epithelium but were afraid to ask. Am J Physiol Renal Physiol. 2000 Jun;278(6):F867-74. doi: 10.1152/ajprenal.2000.278.6.F867.
PubMed 10836974Chopra B, Barrick SR, Meyers S, Beckel JM, Zeidel ML, Ford AP, de Groat WC, Birder LA. Expression and function of bradykinin B1 and B2 receptors in normal and inflamed rat urinary bladder urothelium. J Physiol. 2005 Feb 1;562(Pt 3):859-71. doi: 10.1113/jphysiol.2004.071159. Epub 2004 Dec 2.
PubMed 15576455Kanai A, de Groat W, Birder L, Chai T, Hultgren S, Fowler C, Fry C. Symposium report on urothelial dysfunction: pathophysiology and novel therapies. J Urol. 2006 May;175(5):1624-9. doi: 10.1016/S0022-5347(05)00977-8.
PubMed 16600715Kim JC, Park EY, Seo SI, Park YH, Hwang TK. Nerve growth factor and prostaglandins in the urine of female patients with overactive bladder. J Urol. 2006 May;175(5):1773-6; discussion 1776. doi: 10.1016/S0022-5347(05)00992-4.
PubMed 16600756Yokoyama O, Yusup A, Miwa Y, Oyama N, Aoki Y, Akino H. Effects of tolterodine on an overactive bladder depend on suppression of C-fiber bladder afferent activity in rats. J Urol. 2005 Nov;174(5):2032-6. doi: 10.1097/01.ju.0000176793.50410.9e.
PubMed 16217388Yokoyama O, Yusup A, Oyama N, Aoki Y, Tanase K, Matsuta Y, Miwa Y, Akino H. Improvement of bladder storage function by alpha1-blocker depends on the suppression of C-fiber afferent activity in rats. Neurourol Urodyn. 2006;25(5):461-7. doi: 10.1002/nau.20253.
PubMed 16673377Thongboonkerd V, McLeish KR, Arthur JM, Klein JB. Proteomic analysis of normal human urinary proteins isolated by acetone precipitation or ultracentrifugation. Kidney Int. 2002 Oct;62(4):1461-9. doi: 10.1111/j.1523-1755.2002.kid565.x.
PubMed 12234320Townsend JC, Sadler WA, Shanks GM. The effect of storage pH on the precipitation of proteins in deep frozen urine samples. Ann Clin Biochem. 1987 Jan;24 ( Pt 1):111-2. doi: 10.1177/000456328702400118. No abstract available.
PubMed 3827174Tadros Y, Ruiz-Deya G, Crawford BE, Thomas R, Abdel-Mageed AB. In vivo proteomic analysis of cytokine expression in laser capture-microdissected urothelial cells of obstructed ureteropelvic junction procured by laparoscopic dismembered pyeloplasty. J Endourol. 2003 Jun;17(5):333-6. doi: 10.1089/089277903322145530.
PubMed 12885361
Study at a glance
From the registry record, last updated by the sponsor on 29 Jul 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Identification of Urinary Cytokines in Patients With Overactive Bladder (OAB)
- ClinicalTrials.gov ID
- NCT00868621
- Acronym / sponsor ID
- IRB 8848
- Conditions
- Overactive Bladder, Urinary Tract Infection
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 60 participants (actual)
- Lead sponsor
- The Cleveland ClinicUniversity, hospital or other
- Collaborators
- Astellas Pharma US, Inc.
- Study start
- Mar 2007
- Primary completion
- Sep 2008 (actual)
- Study completion
- Aug 2009 (actual)
- First posted
- 25 Mar 2009 (estimated)
- Results
- Posted 29 Jul 2024
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Overactive bladder (OAB) is a widespread condition characterized by urgency, urge incontinence, nocturia and excessive urinary frequency, affecting millions of people worldwide. In two epidemiological studies, OAB was found in about 17% of American and European populations. This accounts for an estimated 33 million patients suffering from OAB in the USA. The disorder constitutes a psychological stress that impacts the patient's social life.
Detailed description
Overactive bladder (OAB) is a widespread condition characterized by urgency, urge incontinence, nocturia and excessive urinary frequency, affecting millions of people worldwide.(1) In two epidemiological studies, OAB was found in about 17% of American and European populations.(2)(3). This accounts for an estimated 33 million patients suffering from OAB in the USA. The disorder constitutes a psychological stress that impacts the patient's social life.
The luminal surface of the bladder is covered by the urothelium, which functions as a highly efficient barrier to the movement of water and ionized substances across the bladder wall.(4) Urothelial cells also have specialized sensory and signaling properties that allow them to respond to their chemical and physical environment, and engage in reciprocal chemical communication with neighboring nerves in the bladder wall. These properties are 1) nicotinic, muscarinic, tachykinin, adrenergic and capsaicin (TRPV1) receptor expression, 2) sensitivity to transmitters released from afferent and efferent nerves, 3) mechanosensitivity, 4) close physical association with afferent nerves and 5) the ability to release chemical mediators such as ATP and NO, which can regulate the activity of adjacent nerves and, thereby, trigger local vascular changes and/or reflex bladder contractions.(5)
Transmitter release from urothelial cells appears to be mediated by a calcium dependent exocytotic mechanism that is similar to the mechanism involved in transmitter release from nerve terminals. Transmitters released from urothelial cells can act in an autocrine/paracrine manner in the urothelium, or on subepithelial myofibroblasts, nerves or blood vessels to influence various functions, including the urothelial barrier, local blood flow and sensory mechanisms.(6)
Urine cytokine assays have been studied in various bladder and kidney disorders with the hope of understanding the pathophysiology and developing a noninvasive, reliable predictor of disease progression and evaluate the response to treatment.
Interstitial cystitis (IC) is a severely debilitating syndrome of unknown etiology affecting the urinary bladder that is mainly associated with urgency, frequency and pain. Pro-inflammatory molecules and neuroinflammation are suggested in the patho-mechanism of IC. Abdel Mageed and Ghoniem found out the activation of the nuclear factor kappa B (NF-k B) in the bladder biopsy of IC patients. NF-k B is a transcription factor found in some inflammatory diseases like rheumatoid arthritis, bronchial asthma, and inflammatory bowel diseases. NF-k B has a role in induction of pro inflammatory cytokines IL-6, IL-2, IL-1β and TNF-α. Activation of NF-k B was associated with 27, 8, 10 and 7 fold increase in TNF-α, IL-10, IL-6 and IL-8 transcripts respectively.(7,8) Keay et al determined that the urine of IC patients specifically contains a factor that inhibit primary bladder epithelial proliferation, anti proliferative factor (APF) and it has significantly decreased heparin binding epidermal growth factor like factor (HBEGF) and increased epidermal growth factor (EGF) levels compared to urine from normal subjects.(9) Chai et al compared urine levels of APF and HB-EGF before and after bladder distention and neurostimulation.(10,11) Both of urine markers changed toward normal levels after hydrodistention or neuromodulation treatment of IC.
Urinary cytokines have also been studied in patients undergoing intravesical bacillus Calmette Guerin (BCG) therapy for superficial bladder cancer.(12) BCG is thought to cause local immunostimulation, resulting in infiltration of T-lymphocytes in the bladder wall. After treatment, IL-1, IL-2, IL-6, and TNF are significantly elevated in the urine. It is thought that BCG induced cytokines may generate bladder tumor killing cells, and an elevation of urine cytokines may correlate clinical response to BCG therapy.
Recently, there have been studies that have attempted to identify specific measurable urinary factors that lead to the progression of chronic renal disease. Cytokines are involved in the recruitment of inflammatory cells, leading to infiltration in the diseased kidney, ultimately resulting in renal scarring. Elevated levels of urinary IL-6 and TNF receptor-1 are identified in children with vesicoureteral reflux associated with reflux nephropathy and renal scarring.(13)
Acute renal allograft rejection is a result of the recipient's immune response to the donor kidney, and 35% of these patients experience an episode of acute rejection the first year after surgery. Elevated urinary cytokines have been measured in patients who have biopsy proven renal allograft acute rejection.(14)
Urinary cytokines and markers have been identified in different urological disorders. They are used to understand the pathophysiology, diagnosis and evaluation of the treatment of these disorders. We hypothesize that there is urothelial abnormality in cases of overactive bladder that leads to elaboration of certain kinds of urinary cytokines. To our knowledge, no study has been published evaluating urinary markers in patients with OAB.
Study design
- Observational model
- Other
- Time perspective
- Prospective
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| 1 | – | –Control Group(CG)- Healthy age-matched volunteers with no urinary symptoms. |
| 2 | – | –Overactive Bladder Patients Group(OAB)- Patients with urgency of urination. |
| 3 | – | –Urinary Tract Infection Group(UTI)- Symptomatic patients with dysuria, urgency and frequency of urination with proven urine cultures of infection. |
Who may qualify
- Ages
- 18 years and older
- Sex
- Female only
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Twenty healthy women (control), 20 women suffering from overactive bladder and other 20 women suffering from UTI will be selected for the study. Each control will be age matched within +/- 5 years to patients.
Key inclusion criteria (14 listed)
- Group I (OAB patients)
- Group II (Control)
- Group III (UTl)
Key exclusion criteria (12 listed)
- Treatable genitourinary conditions that could cause incontinence
- Hematuria
- Obstructive uropathy
- Patients diagnosed with vaginitis
- History of urothelial carcinoma
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Number of Participants With Elevated Cytokines (Levels of Pro-inflammatory)
Time frame: 18 months
Used commercial human cytokine chip. If the study proved that certain cytokines are significantly present (p<0.05 compared to a standard) in the urine of OAB patients, further research to study the effect of anticholinergic drugs on the level of these cytokines in urine will be conducted.
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 29 Jul 2024.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Background: PubMed 14574533Abdel-Mageed AB, Bajwa A, Shenassa BB, Human L, Ghoniem GM. NF-kappaB-dependent gene expression of proinflammatory cytokines in T24 cells: possible role in interstitial cystitis. Urol Res. 2003 Oct;31(5):300-5. doi: 10.1007/s00240-003-0339-9. Epub 2003 Jul 11.
- Background: PubMed 8558640de Reijke TM, de Boer EC, Kurth KH, Schamhart DH. Urinary cytokines during intravesical bacillus Calmette-Guerin therapy for superficial bladder cancer: processing, stability and prognostic value. J Urol. 1996 Feb;155(2):477-82.
- Background: PubMed 10524926Ninan GK, Jutley RS, Eremin O. Urinary cytokines as markers of reflux nephropathy. J Urol. 1999 Nov;162(5):1739-42.
- Background: PubMed 10836974Lewis SA. Everything you wanted to know about the bladder epithelium but were afraid to ask. Am J Physiol Renal Physiol. 2000 Jun;278(6):F867-74. doi: 10.1152/ajprenal.2000.278.6.F867.
- Background: PubMed 15576455Chopra B, Barrick SR, Meyers S, Beckel JM, Zeidel ML, Ford AP, de Groat WC, Birder LA. Expression and function of bradykinin B1 and B2 receptors in normal and inflamed rat urinary bladder urothelium. J Physiol. 2005 Feb 1;562(Pt 3):859-71. doi: 10.1113/jphysiol.2004.071159. Epub 2004 Dec 2.
- Background: PubMed 16600715Kanai A, de Groat W, Birder L, Chai T, Hultgren S, Fowler C, Fry C. Symposium report on urothelial dysfunction: pathophysiology and novel therapies. J Urol. 2006 May;175(5):1624-9. doi: 10.1016/S0022-5347(05)00977-8.
- Background: PubMed 16600756Kim JC, Park EY, Seo SI, Park YH, Hwang TK. Nerve growth factor and prostaglandins in the urine of female patients with overactive bladder. J Urol. 2006 May;175(5):1773-6; discussion 1776. doi: 10.1016/S0022-5347(05)00992-4.
- Background: PubMed 16217388Yokoyama O, Yusup A, Miwa Y, Oyama N, Aoki Y, Akino H. Effects of tolterodine on an overactive bladder depend on suppression of C-fiber bladder afferent activity in rats. J Urol. 2005 Nov;174(5):2032-6. doi: 10.1097/01.ju.0000176793.50410.9e.
- Background: PubMed 16673377Yokoyama O, Yusup A, Oyama N, Aoki Y, Tanase K, Matsuta Y, Miwa Y, Akino H. Improvement of bladder storage function by alpha1-blocker depends on the suppression of C-fiber afferent activity in rats. Neurourol Urodyn. 2006;25(5):461-7. doi: 10.1002/nau.20253.
- Background: PubMed 12234320Thongboonkerd V, McLeish KR, Arthur JM, Klein JB. Proteomic analysis of normal human urinary proteins isolated by acetone precipitation or ultracentrifugation. Kidney Int. 2002 Oct;62(4):1461-9. doi: 10.1111/j.1523-1755.2002.kid565.x.
- Background: PubMed 3827174Townsend JC, Sadler WA, Shanks GM. The effect of storage pH on the precipitation of proteins in deep frozen urine samples. Ann Clin Biochem. 1987 Jan;24 ( Pt 1):111-2. doi: 10.1177/000456328702400118. No abstract available.
- Background: PubMed 12885361Tadros Y, Ruiz-Deya G, Crawford BE, Thomas R, Abdel-Mageed AB. In vivo proteomic analysis of cytokine expression in laser capture-microdissected urothelial cells of obstructed ureteropelvic junction procured by laparoscopic dismembered pyeloplasty. J Endourol. 2003 Jun;17(5):333-6. doi: 10.1089/089277903322145530.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Gamal Ghoniem, MD principal investigator
Cleveland Clinic Florida
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Overactive Bladder and Urinary Tract Infection, run by The Cleveland Clinic at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 14 inclusion and 12 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 29 Jul 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Yes. Results are posted in the registry (first posted 29 Jul 2024). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Number of Participants With Elevated Cytokines (Levels of Pro-inflammatory) (time frame: 18 months). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00868621, which also lists 12 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 29 Jul 2024.