Platelet Activating Factor Stability in Urine
| Status: | Completed |
|---|---|
| Conditions: | Other Indications, Urology, Urology |
| Therapuetic Areas: | Nephrology / Urology, Other |
| Healthy: | No |
| Age Range: | 18 - 80 |
| Updated: | 7/20/2018 |
| Start Date: | January 27, 2017 |
| End Date: | February 28, 2017 |
The investigator's hypothesis is that smoking induces inflammation in the bladder wall. This
may predispose to the development of Interstitial cystitis(IC) / bladder pain syndrome(BPS).
Previous research has linked one the Platelet Activating Factor - PAF to interstitial
cystitis. The investigators will study a limited number of patients to determine whether PAF
is stable in urine and whether special precautions (for example - immediate freezing in
liquid nitrogen) is necessary for accurate measurement of PAF in the urine.
Patients who are presenting for an office visit will be asked to donate at least 50 ml of
urine.
A separate group of patients who are scheduled for surgery, are also being asked to donate
around 25 ml of urine during surgery.
No patient data other than group assignment, whether they smoke or if they have or not have
interstitial cystitis will be recorded.
may predispose to the development of Interstitial cystitis(IC) / bladder pain syndrome(BPS).
Previous research has linked one the Platelet Activating Factor - PAF to interstitial
cystitis. The investigators will study a limited number of patients to determine whether PAF
is stable in urine and whether special precautions (for example - immediate freezing in
liquid nitrogen) is necessary for accurate measurement of PAF in the urine.
Patients who are presenting for an office visit will be asked to donate at least 50 ml of
urine.
A separate group of patients who are scheduled for surgery, are also being asked to donate
around 25 ml of urine during surgery.
No patient data other than group assignment, whether they smoke or if they have or not have
interstitial cystitis will be recorded.
Interstitial cystitis/bladder pain syndrome (IC/BPS) is a severe, chronic bladder condition
that is extremely painful and disruptive. Incidence of the disease has increased dramatically
in recent years, primarily due to enhanced awareness and better defined inclusion criteria.
Difficulty in diagnosis arises from the diversity of symptoms and severity between patients
and in the same patient at different times. IC/BPS is generally accepted as a disease of
exclusion in which a diagnosis is reached after ruling out other conditions. A firm diagnosis
is only mildly assuring for patients because there are very few therapeutic approaches that
can alleviate the symptoms. Several risk factors are associated with IC/BPS, including age,
sex and race [5] and modifiable risk factors such as diet and smoking. This proposal is to
test the hypothesis that cigarette smoking contributes directly to changes in the bladder
that are indicative of, or predispose to, IC/BPS. In preliminary studies, the investigators
have exposed mice to cigarette smoke and observed breaks in the urothelium, decreased
urothelial tight junction protein expression, increased vascularity and inflammatory cells in
the bladder wall. This lab has previously demonstrated that cigarette smoke inhibits
endothelial cell platelet activating factor acetylhydrolase (PAF-AH), which is responsible
for the hydrolysis of PAF, resulting in increased PAF, a membrane phospholipid-derived
inflammatory mediator. The investigators have also shown that calcium-independent
phospholipase A2β (iPLA2β) is responsible for the majority of PAF production in endothelial
and urothelial cells. PAF has been shown to increase matrix metalloproteinases (MMP) which in
turn inhibit anti-angiogenic pigment epithelium-derived factor (PEDF), thus promoting
angiogenesis. These studies indicate a direct relationship between PAF accumulation and PEDF
expression in the bladder that may contribute to inflammation in smokers.
PAF stability in urine has not been established in the literature. This study is proposing to
assess PAF and PAF-AH activity in urine after using various handling methods of the urine
specimen. Better understanding of PAF stability will allow for better design of future
experiments involving PAF in interstitial cystitis patients.
The investigators have exposed mice to cigarette smoke and examined changes in the bladder.
they have observed thinning and sloughing of the urothelium, plus increased vascularization.
These changes are observed in the bladder wall of IC/BPS patients. We have measured increased
PAF accumulation and decreased expression of PEDF in the bladder wall.
that is extremely painful and disruptive. Incidence of the disease has increased dramatically
in recent years, primarily due to enhanced awareness and better defined inclusion criteria.
Difficulty in diagnosis arises from the diversity of symptoms and severity between patients
and in the same patient at different times. IC/BPS is generally accepted as a disease of
exclusion in which a diagnosis is reached after ruling out other conditions. A firm diagnosis
is only mildly assuring for patients because there are very few therapeutic approaches that
can alleviate the symptoms. Several risk factors are associated with IC/BPS, including age,
sex and race [5] and modifiable risk factors such as diet and smoking. This proposal is to
test the hypothesis that cigarette smoking contributes directly to changes in the bladder
that are indicative of, or predispose to, IC/BPS. In preliminary studies, the investigators
have exposed mice to cigarette smoke and observed breaks in the urothelium, decreased
urothelial tight junction protein expression, increased vascularity and inflammatory cells in
the bladder wall. This lab has previously demonstrated that cigarette smoke inhibits
endothelial cell platelet activating factor acetylhydrolase (PAF-AH), which is responsible
for the hydrolysis of PAF, resulting in increased PAF, a membrane phospholipid-derived
inflammatory mediator. The investigators have also shown that calcium-independent
phospholipase A2β (iPLA2β) is responsible for the majority of PAF production in endothelial
and urothelial cells. PAF has been shown to increase matrix metalloproteinases (MMP) which in
turn inhibit anti-angiogenic pigment epithelium-derived factor (PEDF), thus promoting
angiogenesis. These studies indicate a direct relationship between PAF accumulation and PEDF
expression in the bladder that may contribute to inflammation in smokers.
PAF stability in urine has not been established in the literature. This study is proposing to
assess PAF and PAF-AH activity in urine after using various handling methods of the urine
specimen. Better understanding of PAF stability will allow for better design of future
experiments involving PAF in interstitial cystitis patients.
The investigators have exposed mice to cigarette smoke and examined changes in the bladder.
they have observed thinning and sloughing of the urothelium, plus increased vascularization.
These changes are observed in the bladder wall of IC/BPS patients. We have measured increased
PAF accumulation and decreased expression of PEDF in the bladder wall.
Inclusion Criteria:
- Patient presenting for routine care in the UroGynecology division or
- Patient undergoing gynecologic or urogynecologic surgery exceeding 60 minute operating
time.
Exclusion Criteria:
- Age less than 18 or more than 80
- Unable to provide informed consent
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