Abstract
Purpose
To compare urinary incontinence (UI) severity measures and impact of stress UI in normal, overweight and obese women.
Materials and Methods
Baseline characteristics of subjects in the Stress Incontinence Surgical Treatment Efficacy Trial (SISTEr, N=655) and the TOMUS (N=597) were analyzed. Body mass index [BMI] was defined as normal (<25 kg/m2), overweight (25kg/m2 ≤BMI<30 kg/m2) and obese (≥30 kg/m2). Independent UI severity measures included 3 day diary including incontinence episode frequency (IEF), Urogenital Distress Inventory (UDI) scores, and valsalva leak point pressure (VLPP) from urodynamic testing (UDS). Impact was measured using the Incontinence Impact Questionnaire (IIQ). Multivariable regression models were fit for each severity measures (UDI, IEF, VLPP and IIQ) on weight category. Covariates included age and variables significantly associated with BMI in bivariate analysis.
Results
Mean age (SD) of participants was 51.9 (10.3) in SISTEr and 52.9 (11.0) in TOMUS. In each trial, 45% of subjects were obese. In SISTEr, multivariable regression analyses showed that increasing BMI was independently associated with higher mean UDI scores (p=0.003), IEF (p<0.0001), VLPP (p=0.003) and IIQ score (p=0.0004). In TOMUS, increasing BMI was not associated with UDI scores (p=0.24), but was associated with higher IEF (p=0.0003), VLPP (p=0.0006) and IIQ score (p<0.0001).
Conclusion
Obese women undergoing surgery for stress urinary incontinence report more incontinence episodes, more symptom distress and worse quality of life despite better measure of urethral function (higher VLPP) on urodynamics.
Keywords: obesity, stress incontinence severity and impact, urodynamics
Introduction
Stress urinary incontinence (SUI) is prevalent among women in the United States and has significant quality of life impact1. Consequently, SUI presents tremendous health-related2 and economic3 burdens. Obesity is a modifiable risk factor for the development of urinary incontinence (UI) with numerous epidemiological studies describing the impact of obesity on UI prevalence4–6. The estimated prevalence of obesity, defined as a body mass index (BMI) of ≥ 30 kg/m2, exceeds 30% of the adult population in the United States4. Increased BMI is associated with both prevalent and incident UI, as well as UI severity6. A large cross-sectional study demonstrated that each 5-unit increase in BMI was associated with a 60% increase in daily UI, with obesity having the largest attributable risk for daily UI compared to other factors7. These findings were confirmed in surgical cohorts8, 9. Both behaviorally induced10–12 and surgically induced 13, 14 weight reduction are associated with decreased UI severity.
The pathophysiologic basis posited for the relationship between obesity and UI lies in the significant correlation between BMI and intra-abdominal pressure, suggesting that obesity may stress the pelvic floor secondary to a chronic state of increased pressure15, 16. However, there are limited data on the impact of obesity on patient oriented and urodynamic parameters and on the mechanistic factors that may underlie UI in obese and normal weight women.
To more clearly understand the specific factors that may be associated with signs and symptoms of UI, we sought to compare baseline characteristics between a large number of normal weight, overweight and obese women who enrolled in two randomized comparative effectiveness trials for the surgical treatment of SUI. Specifically, the aim of this study is compare UI severity measures and impact of SUI among obese, overweight and normal weight women planning SUI surgery.
Materials and Methods
The Urinary Incontinence Treatment Network (UITN) performed two large randomized comparative effectiveness trials studying surgical treatment of SUI in women. The first trial, Stress Incontinence Surgical Treatment Efficacy Trial (SISTEr), randomized 655 subjects to either Burch colposuspension or autologous rectus fascial sling in treatment of SUI. The second trial, Trial of Midurethral Slings (TOMUS), randomized 597 subjects to polypropylene midurethral slings placed either in the retropubic or transobturator approach. Primary outcomes for SISTEr have been published17 and will be available for TOMUS in the summer, 2009. Design papers are published for both trials18, 19. This paper represents the analyses of the preoperative data collected from these two trials. World Health Organization definitions of BMI were used to define weight groups: obese, ≥30 kg/m2, overweight, 25kg/m2 ≤BMI<30 kg/m2, and healthy weight, <25 kg/m2.
Demographic variables reported included age, race/ethnicity, education, marital status, and occupational score. Continuous clinical variables included height, weight, BMI, specific parameters from the pelvic organ prolapse quantification examination (POPQ); the most prolapsed portion of the anterior vaginal wall [Ba]; the most prolapsed portion of the posterior vaginal wall [Bp]; and the genital hiatus [gh]), Q-tip test (delta angle), mean muscle strength (Brink) scores, 24-hour pad weight, incontinence episode frequency (IEF) from a 3-day bladder diary and general patient health score. Categorical clinical variables included prior UI surgery, prior prolapse surgery, prior hysterectomy, menopausal status, hormone replacement use (HRT), diabetes, and smoking status. Subjective measures included the Urogenital Distress Inventory (UDI), Incontinence Impact Questionnaire (IIQ), and the Medical, Epidemiologic and Social Aspects of Aging Questionnaire (MESA). Subjective categorical variables included responses to questions about physical accommodation, character of urine stream and fecal incontinence. Continuous urodynamic (UDS) variables included, valsalva leak point pressure (VLPP), intravesical pressure (Pves), intra-abdominal pressure (Pabd), bladder volume at first desire, bladder volume at strong desire, maximal cystometric capacity, and pressure-flow data (maximum flow rate [Qmax], Pves at Qmax, Pabd at Qmax, time to Qmax). The only categorical urodynamic variable was pressure-flow voiding pattern (normal or abnormal).
Analyses were carried out in parallel for the SISTEr and TOMUS subjects as the trials had different inclusion and exclusion criteria representing different populations. Continuous variables were summarized by mean and standard deviation (SD). Distributions of continuous measures were assessed for normality. Although the distribution of some measures were moderately skewed, we elected to conduct and report analyses in the natural scales for ease of interpretation. To investigate the bivariate relationships of demographic, clinical and UDS variables with BMI category, one-way analysis of variance (ANOVA) was used for continuous measures and cross-classification and Chi square test or Fisher’s Exact test for categorical measures as appropriate. In order to assess multi-colinearity among the multiple measures of incontinence a preliminary principal components analysis (PCA) was computed20. The PCA indicated that there were 3 independent dimensions of stress incontinence. One dimension was weighted most heavily by the subjective measures composed of the MESA stress score, UDI stress and IIQ total scores. The second dimension was most heavily weighted by the objective measures of pad weight and mean incontinence episodes/day. The third dimension was weighted by the objective urodynamic measures of composed of VLPP and MUCP (latter in TOMUS only). Based on this analysis we selected independent measures of incontinence for further analysis to reduce the number of redundant hypothesis testing. Within each dimension we selected a single measure to represent that aspect of incontinence, except in the subjective dimension as we wanted to explore both subjective symptom distress and symptom impact. Thus, we report the association of weight category with one objective measure of UI severity (IEF), two subjective measures of UI severity (UDI total score and IIQ), and one urodynamic parameter of UI severity (VLPP)21. To further understand the associations of weight category with severity, we computed an analysis of covariance (ANCOVA) of each severity and impact measure on weight category controlling for clinically important variables and those significantly associated with weight in bivariate analysis.
Analyses were performed using SAS version 9.2 (SAS Institute, Inc. Cary, NC). Because of the large number of hypothesis tests, we defined statistical significance by p=0.01.
Results
Participants in the SISTEr and TOMUS trials had mean ages of 51.9 (SD 10.3) years and 52.9 (SD 11.0) years, respectively. In SISTEr the mean (±SD) BMI of the normal weight women was 22.9(1.6), the overweight women was 27.5(1.4), and the obese women was 35.4(4.8). Similarly, in TOMUS the mean (±SD) BMI of the normal weight women was 22.6(1.7), the overweight women was 27.4(1.2), and the obese women was 36.5(5.0). Seventy three percent of SISTEr subjects and 79% of those in TOMUS were Caucasian. In both trials, compared to normal weight women, obese women were more likely to have less education and report poorer health than normal weight women. Additionally, obese women in SISTEr were more likely to smoke and less likely to use hormone therapy. There were no differences among the groups in age, cesarean deliveries, hysterectomy, prior UI surgery, prior prolapse surgery or POPQ stage (Table 1).
Table 1.
SISTEr Trial | TOMUS Trial | |||||
---|---|---|---|---|---|---|
Variable | Normal | Overweight | Obese | Normal | Overweight | Obese |
N (%) | 142 (22) | 218 (33) | 290 (45) | 137 (23) | 192 (32) | 262 (45) |
Age 1 (mean, SD) | 51.4(10.9) | 52.5(10.1) | 51.7(10.1) | 52.5(11.5) | 54.2(11.3) | 52.1(10.4) |
Race/ ethnicity2 | * | |||||
Non-white | 32(23%) | 53(24%) | 88(30%) | 23(17%) | 31(16%) | 69(26%) |
White | 110(77%) | 165(76%) | 201(70%) | 114(83%) | 161(84%) | 193(74%) |
Education2 | ** | ** | ||||
<High school | 34(24%) | 93(43%) | 98(34%) | 31(23%) | 55(28%) | 96(37%) |
>High school | 58(41%) | 78(36%) | 123(42%) | 44(32%) | 72(38%) | 99(38%) |
Completed college | 50(35%) | 47(21%) | 69(24%) | 62(45%) | 65(34%) | 67(25%) |
Smoking2 | ** | * | ||||
Never smoking | 91(64%) | 120(55%) | 141(49%) | 81(59%) | 100(52%) | 135(52%) |
Former smoking | 37(26%) | 60(28%) | 110(38%) | 47(34%) | 69(36%) | 80(30%) |
Current smoking | 14(10%) | 38(17%) | 39(13%) | 9(7%) | 23(12%) | 47(18%) |
Diabetes2 | 4(3%) | 12(6%) | 29(10%)* | 5(4%) | 8(4%) | 26(10%)* |
Hormone therapy2 | ** | |||||
No | 30(21%) | 89(41%) | 112(39%) | 46(34%) | 76(40%) | 117(45%) |
Yes | 58(41%) | 71(33%) | 92(32%) | 39(28%) | 64(33%) | 67(26%) |
Pre-Menopausal | 54(38%) | 57(26%) | 86(30%) | 52(38%) | 52(27%) | 76(29%) |
Cesarean2 | 10(7%) | 18(8%) | 22(8%) | 13(9%) | 13(7%) | 32(12%) |
Prior hysterectomy2 | 42(30%) | 68(31%) | 91(31%) | 35(26%) | 52(27%) | 78(30%) |
Prior UI surgery2 | 16(11%) | 33(15%) | 44(15%) | 22(16%) | 19(10%) | 36(14%) |
Prior prolapse surgery3 | 5(4%) | 6(3%) | 2(1%) | 4(3%) | 9(5%) | 10(4%) |
General health score2 | *** | *** | ||||
Excellent | 47(33%) | 53(24%) | 45(16%) | 65(47%) | 42(22%) | 43(17%) |
Very good | 56(39%) | 78(36%) | 103(36%) | 54(39%) | 97(51%) | 100(38%) |
Good+Fair+Poor | 39(27%) | 87(40%) | 139(48%) | 18(13%) | 50(27%) | 118(45%) |
N and percent were presented except age which were reported with mean and SD;
Equality of means tested by ANOVA
Equality of frequencies tested by Chi-square
Prior prolapse surgery was tested using Fisher's exact test
0.01≤P< 0.05
0.001≤ P <0.01
P<0.001 by Chi-square test
In both trials (Table 2), obese women had a greater q-tip resting angle and smaller difference between the strain and resting q-tip angles. Other POP-Q points did not differ significantly by weight group.
Table 2.
Variable | SISTER Trial | TOMUS Trial | ||||
---|---|---|---|---|---|---|
Normal | Overweight | Obese | Normal | Overweight | Obese | |
Resting angle 1 | 8.8(15.0) | 14.9(15.6) | 19.0(19.5)*** | 6.7(13.0) | 5.5(11.7) | 11.8(13.5)*** |
Strain angle1 | 59.2(18.8) | 60.0(17.8) | 60.8(18.4) | 46.9(20.2) | 44.7(21.5) | 46.5(20.5) |
Delta1 | 50.5(18.0) | 45.1(17.6) | 41.7(18.1)*** | 40.3(18.7) | 39.2(20.5) | 34.7(17.9)** |
POP-Q [N(%)] 2 | ||||||
Stages 0–I | 33 (23%) | 54 (25%) | 74 (26%) | 64 (47%) | 82 (43%) | 120 (46%) |
Stage II | 85 (60%) | 119 (55%) | 180 (62%) | 60 (44%) | 93 (48%) | 124 (47%) |
Stage III | 24 (17%) | 45 (21%) | 36 (12%) | 13 (9%) | 17 (9%) | 18 (7%) |
Point Ba1 | −0.4(2.1) | −0.4(2.0) | −0.8(1.6)* | −1.2(1.5) | −1.2(1.8) | −1.4 (1.3) |
Point Bp1 | −1.7(1.8) | −1.6(1.7) | −1.7(1.4) | −1.9(1.3) | −1.8(1.8) | −2.0 (1.1) |
Point Gh1 | 3.5(1.0) | 3.5(1.3) | 3.7(1.2) | 3.3(1.0) | 3.4(1.0) | 3.6(1.1)* |
Brink score 1 | 9.1(2.0) | 8.9(2.2) | 8.9(2.0) | 8.9(1.8) | 8.7(2.1) | 8.7 (2.0) |
Mean and SD were presented except POP-Q;
Equality of means tested by ANOVA
Equality of frequencies tested by Chi-square
0.01≤P< 0.05
0.001≤ P <0.01
P<0.001
Sixteen percent of women in SISTEr and 10% in TOMUS reported fecal incontinence as well as UI; the proportion did not differ by weight category (10%, 17% and 17% in SISTEr and 9%, 6%, and 13% in TOMUS for normal weight, overweight and obese women, respectively). Obese women did not differ from their normal weight counterparts in reporting abnormal voiding symptoms, such as slow stream, hesitating, or splinting (data not shown). The baseline UDS measures for each trial are summarized in Table 3. In both trials obese women had higher VLPP, Pves and Pabd at baseline and Pves and Pabd at Qmax than normal and overweight women. Interestingly, there were no differences in the presence of detrusor overactivity among normal, overweight and obese subjects in these trials.
Table 3.
Variable | SISTER Trial | TOMUS | ||||
---|---|---|---|---|---|---|
Mean (SD) | Mean (SD) | |||||
Normal | Overweight | Obese | Normal | Overweight | Obese | |
VLPP | 107.3(31.8) | 115.8(37.1) | 122.2(39.6)*** | 107.9(35.2) | 114.0(39.3) | 130.2(46.1)*** |
Pves baseline | 31.7(10.4) | 35.4(10.8) | 40.3(11.8)*** | 32.3(9.2) | 35.0(11.1) | 39.4(11.9)*** |
Pabd baseline | 30.0(10.5) | 33.5(11.1) | 38.4(12.2) *** | 30.3(9.7) | 33.0(11.2) | 37.8(11.2)*** |
Bladder vol, first desire |
150.1(108.8) | 145.6(96.5) | 135.1(88.7) | 133.4(85.8) | 111.5(85.4) | 111.5(73.1)* |
Bladder vol, strong desire |
276.0(155.9) | 259.2(138.2) | 252.0(126.6) | 250.1(126.4) | 222.1(119.0) | 219.1(111.7)* |
MCC | 399.9(141.0) | 391.8(140.9) | 387.6(134.4) | 371.0(136.4) | 350.3(122.4) | 341.4(114.5)* |
Detrusor Overactivity |
12/139(9%) | 15/217(7%) | 33/285(12%) | 12/133(9%) | 21/190(11%) | 37/260(14%) |
Max Flow (PFS) | 20.8(10.6) | 21.7(9.8) | 21.3(9.8) | 21.9(10.6) | 21.9(11.2) | 22.2(10.5) |
Pves at Qmax | 50.4(18.4) | 54.2(23.8) | 65.5(24.8)*** | 47.5(19.1) | 53.8(28.1) | 64.1(27.2)*** |
Pabd at Qmax | 33.8(18.6) | 36.6(21.7) | 44.6(23.7)*** | 30.2(21.2) | 36.0(28.9) | 42.5(27.0)*** |
Time to max flow, sec |
24.9(33.4) | 19.2(23.3) | 17.5(25.8)* | 20.6(25.6) | 21.7(30.2) | 24.1(48.5) |
Mean and SD were presented. Equality of means tested by ANOVA
0.01≤ P < 0.05
0.001≤ P <0.01
P<0.001
Obese women had poorer scores on all three measures of incontinence severity and impact (Table 4). Specifically, in both trials, obese women experienced more incontinence episodes, reported higher symptom distress, had higher VLPP’s and greater symptom specific impact on quality of life.
Table 4.
Variable | SISTER Trial | TOMUS | ||||
---|---|---|---|---|---|---|
Normal | Overweight | Obese | Normal | Overweight | Obese | |
Unadjusted means (sd) 1 |
||||||
IIQ total score | 132.1(87.0) | 170.5(102.5) | 191.2(101.1)*** | 119.9(78.3) | 132.3(89.7) | 182.7(102.6)*** |
UDI total score | 138.8(43.7) | 146.7(51.4) | 160.0(46.4)*** | 125.2(41.1) | 129.9(44.0) | 143.3(47.1)*** |
UDI urge subscale score |
39.6(22.6) | 45.7(24.5) | 53.3(25.4)*** | 33.7(21.4) | 37.6(25.6) | 48.2(25.5)*** |
UDI stress subscale score |
77.2(19.3) | 74.0(24.6) | 81.4(20.4)*** | 75.7(21.9) | 74.6(21.4) | 73.8(21.4) |
IEF | 2.2(2.1) | 3.3(3.3) | 3.6(3.0)*** | 2.9(3.3) | 2.8(2.2) | 3.9(3.1)*** |
VLPP | 107.3(31.8) | 115.8(37.1) | 122.2(39.6)** | 107.9(35.2) | 114.0(39.3) | 130.2(46.1)*** |
Adjusted means 2 | ||||||
IIQ total score | 151.3 | 175.9 | 189.7*** | 158.2 | 155.0 | 189.8*** |
UDI total score | 144.9 | 147.2 | 159.1 ** | 143.9 | 142.3 | 149.1 |
IEF | 2.8 | 3.8 | 4.2 *** | 2.9 | 2.7 | 3.8 *** |
VLPP | 108.3 | 118.0 | 124.8 ** | 110.8 | 116.6 | 131.9 *** |
Unadjusted Mean and SD were presented Equality of means tested by ANOVA
Means adjusted for age, education race/ethnicity, smoking status, general health HRT use, diabetes using ANCOVA
0.01≤P< 0.05
0.001≤ P <0.01
P<0.001
In order to explore whether the association of these measures of incontinence with weight category remained when covariates were controlled, we computed a multivariable analysis (ANCOVA) of each severity measure on weight category controlling for age, race and ethnicity, education, general patient health score, HRT use, diabetes and smoking. This analysis showed that in SISTEr, weight category remained significantly associated with higher UDI total scores (p=0.003), increasing IEF (p<0.0001), higher VLPP’s (p=0.003) and higher impact (p=0.0004). In TOMUS, weight category was no longer associated with higher UDI scores (p=0.24), but was associated with increased incontinence episodes (p=0.0003), higher VLPP (p=0.0006) and higher impact (p<0.0001) when covariates were controlled. As a check on our decision to conduct analyses utilizing the natural scales of the measures, sensitivity analyses using normalizing transformations were performed and the results were the same as those reported in Table 4.
Discussion
Obese women with SUI participating in two large randomized surgical trials had worse objective and subjective measures of UI severity compared to normal weight women. Obese women report greater symptom distress and impact on quality of life from UI symptoms and experience more incontinent episodes, suggesting they have worse disease and/or experience other factors which increase their symptom burden. As BMI weight categories increased, subjective and objective UI severity seemed to increase. Interestingly, while women in both trials reported greater overall symptom distress from UI, stress-specific symptom distress did not differ among the obese and normal and overweight women. However in these subjects, obese women with SUI did have more concomitant urge incontinence as compared to normal and overweight women which may have contributed to their increased symptoms (Table 4). Clinicians commonly believe that women with mixed UI symptoms (SUI and urge urinary incontinence [UUI]) have more severe UI than those with either pure SUI or UUI. In a large epidemiological study, 38% of women with mixed incontinence had severe incontinence and almost half were bothered by their incontinence. In contrast, only 17% of SUI only women had severe incontinence and only a third were bothered22.
We found that weight group remained significantly associated with higher IEF when other characteristics were held constant, implying that UI severity is not explained by other factors that may be associated with increasing BMI. This is consistent with weight reduction data showing that incontinence episode frequency decreases with significant weight loss7, 10–12. A recent study comparing an intensive 6-month weight loss program (diet, exercise and behavior modification) to a structured education program demonstrated that in the intervention group, a BMI decrease of 8% was associated with 47% fewer incontinence episodes, while in the control group, there was a mean BMI decrease of 1.6% with a 28% decrease in incontinence episode frequency12. In addition, the intervention group had a greater decrease in SUI episodes, but not urge incontinence episodes. These data differ somewhat from our subjective data, which suggest a difference in bother from UUI but not SUI in obese women when compared to normal weight women. We did not differentiate between stress and urge incontinence episodes in our diary data.
Several urodynamic parameters differed between obese and normal and overweight women. Consistent with previous studies, we found that obese women had higher baseline intravesical and abdominal pressures than normal weight women15, 16. Previously, it has been hypothesized that higher abdominal pressures in women with greater BMI may explain the greater prevalence of UI and UI severity in obese women13, 15. In a small cohort of women after surgical weight loss, intravesical pressure decreased13. It seems plausible that the increased UI severity seen in obese women may be in part due to the higher abdominal and vesical pressures which put them closer to their leakage threshold regardless of urethral function. This hypothesis requires further study.
We found that while obese women had worse UI severity than normal weight women, they had higher VLPP values than normal and overweight women. The association between VLPP and obesity in women had been noted in a previous analysis looking at clinical and demographic factors associated with VLPP in the SISTEr population23. We did not measure urethral pressure simultaneously with vesical and abdominal pressures at baseline to determine if higher pressures were transmitted to the urethra in obese women, similar to the higher pressures transmitted to the bladder and abdomen. It seems plausible that at rest, urethral pressures are higher in obese women, but their urethras are unable to “respond” to events, which require quick increases in urethral pressure. Possibly, obese women rely on greater muscle contraction and force at rest, thereby recruiting a larger proportion of their motor unit pool to maintain continence at rest. When a stress event occurs, they are unable to recruit any additional motor units resulting in urinary leakage. Such a hypothesis is consistent with Henneman’s principle for motor unit recruitment in striated muscles which states that as the requirement for greater muscle contraction and force increases, more and larger motor units are recruited24. Research in other fields has demonstrated that obesity is associated with slower median nerve conduction velocities, which further supports a potential neuromuscular etiology for our findings25. Further studies which more precisely assess urethral neuromuscular function in obese and normal weight women are necessary.
Obese women had less urethral mobility with straining (as measured by change in Q-tip angle from rest with straining) than normal weight women. Lack of urethral mobility is associated with poorer outcomes after SUI treatments and may contribute to increased UI severity in obese women despite better measures of intrinsic urethral function. In a case-control study of stress incontinent and continent control women, DeLancey et al recently demonstrated that urethral function, measured as MUCP, was more strongly associated with SUI than urethral mobility/support26. MUCP predicted half the occurrence of SUI; however, urethral support/mobility did predict 16% of SUI cases.
Our analyses are strengthened by inclusion of a large number of stress incontinent women representing all BMI categories from two randomized surgical trials. Study participants are well-characterized using validated subjective and objective measures. In addition, urodynamic techniques were standardized and validated across participating sites27. The consistency of the findings across the two study samples supports the conclusion that the associations found are robust in women with SUI. Our study may have been strengthened by the inclusion of urethral pressure measurements during cystometry and VLPP measurements. Such inclusion may have provided further insight into urethral function. It may also have been more informative if incontinence episodes had been broken down by cause ie associated with stress or urge UI.
The main statistical limitation is of multiple hypothesis testing because this can lead to identification of apparent associations due to chance. However, performing the analysis in parallel across the 2 samples showed consistency, providing evidence of a real association and not just chance. Modeling was performed to assess whether relationships between BMI and incontinence severity measures held controlling for confounders. However, we only partially addressed collinearity, did not test any interaction effects and did not formally test models for goodness of fit. These issues would be more relevant if we were trying to develop an explanatory model for incontinence, which was not the purpose of this report.
Conclusion
In summary, obese women planning incontinence surgery have more severe UI symptom distress, quality of life impact, and objective findings than normal weight women. Surprisingly, obese women also seem to have better urethral function as measured by traditional urodynamic techniques. Factors other than urethral failure may contribute to UI in obese women. Further investigation into urethral function changes with stress events is warranted.
Acknowledgments
Supported by cooperative agreements from the National Institute of Diabetes and Digestive and Kidney Diseases, U01 DK58225, U01 DK58229, U01 DK58234, U01 DK58231, U01 DK60379, U01 DK60380, U01 DK60393, U01 DK60395, U01 DK60397, and U01 DK60401.
Abbreviations
- ANOVA
Analysis of variance
- ANCOVA
Analysis of Covariance
- BMI
Body mass index
- HRT
Hormone replacement therapy
- IEF
Incontinence episode frequency
- IIQ
Incontinence Impact Questionnaire
- MESA
Medical Epidemiologic, Social Aspects of Aging
- MCC
(from Table 4)
- MUCP
Maximum urethral closure pressure
- Pabd
Intra-abdominal pressure
- PFS
Pressure Flow Study
- POPQ
Pelvic organ prolapse quantification
- Pves
Intravesical pressure
- Qmax
Maximum flow rate
- SD
Standard deviation
- SISTEr
Stress Incontinence Surgical Treatment Efficacy Trial
- SUI
Stress urinary incontinence
- TOMUS
Trial of Midurethral Slings
- UDI
Urogenital Distress Inventory
- UDS
Urodynamics
- UI
Urinary incontinence
- UITN
Urinary Incontinence Treatment Network
- UUI
Urge urinary incontinence
- VLPP
Valsalva leak point pressure
APPENDIX A FORMAT FOR CREDITING SITES AND FUNDING IN PUBLICATIONS
STEERING COMMITTEE
Elizabeth A. Gormley, Chair (Dartmouth Hitchcock Medical Center, Lebanon, NH); Larry Sirls, MD, Salil Khandwala, MD (William Beaumont Hospital, Royal Oak, MI and Oakwood Hospital, Dearborn, MI; U01 DK58231); Linda Brubaker, MD, Kimberly Kenton, MD (Loyola University Medical Center, Maywood, IL; U01 DK60379); Holly E. Richter, PhD, MD, L. Keith Lloyd, MD (University of Alabama at Birmingham, Birmingham, AL; U01 DK60380); Michael Albo, MD, Charles Nager, MD (University of California, San Diego, CA; U01 DK60401); Toby C. Chai, MD, Harry W. Johnson, MD (University of Maryland, Baltimore, MD; U01 DK60397); Halina M. Zyczynski, MD, Wendy Leng, MD (University of Pittsburgh, Pittsburgh, PA; U01 DK 58225); Philippe Zimmern, MD, Gary Lemack, MD (University of Texas Southwestern, Dallas, TX; U01 DK60395); Stephen Kraus, MD, Thomas Rozanski, MD (University of Texas Health Sciences Center, San Antonio, TX; U01 DK58234); Peggy Norton, MD, Ingrid Nygaard, MD (University of Utah, Salt Lake City, UT; U01 DK60393); Sharon Tennstedt, PhD, Anne Stoddard, ScD (New England Research Institutes, Watertown, MA; U01 DK58229); Debuene Chang, MD, Marva Moxey-Mims, MD, Rebekah Rasooly, MD (National Institute of Diabetes & Digestive & Kidney Diseases).
CO-INVESTIGATORS
Amy Arisco, MD; Jan Baker, APRN; Diane Borello-France, PT, PhD; Kathryn L. Burgio, PhD; Ananias Diokno, MD; Melissa Fischer MD; MaryPat Fitzgerald, MD; Chiara Ghetti, MD; Patricia S. Goode, MD; Robert L. Holley, MD; Margie Kahn, MD; Jerry Lowder, MD; Karl Luber, MD; Emily Luckacz, MD; Alayne Markland, DO, MSc; Shawn Menefee, MD; Pamela Moalli, MD; Elizabeth Mueller, MD; Pradeep Nagaraju MD; Kenneth Peters, MD; Elizabeth Sagan, MD; Joseph Schaffer, MD; Amanda Simsiman, MD; Robert Starr, MD; Gary Sutkin, MD; R. Edward Varner, MD.
STUDY COORDINATORS
Laura Burr, RN; JoAnn Columbo, BS, CCRC; Tamara Dickinson, RN, CURN, CCCN, BCIAPMDB; Rosanna Dinh, RN, CCRC; Judy Gruss, RN; Alice Howell, RN, BSN, CCRC; Chaandini Jayachandran, MSc; Kathy Jesse, RN; D. Lynn Kalinoski, PhD; Barbara Leemon, RN; Kristen Mangus; Karen Mislanovich, RN; Elva Kelly Moore, RN; Caren Prather, RN; Sylvia Sluder, CCRP; Mary Tulke, RN; Robin Willingham, RN, BSN; Kimberly Woodson, RN, MPH; Gisselle Zazueta-Damian.
DATA COORDINATING CENTER:
Kimberly J. Dandreo, MSc; Liyuan Huang, MS; Rose Kowalski, MA; Heather Litman, PhD; Marina Mihova, MHA; Anne Stoddard, ScD (Co-PI); Kerry Tanwar, BA; Sharon Tennstedt, PhD (PI); Yan Xu, MS.
DATA SAFETY AND MONITORING BOARD
J. Quentin Clemens MD, (Chair) Northwestern University Medical School, Chicago IL; Paul Abrams MD, Bristol Urological Institute, Bristol UK; Diedre Bland MD, Blue Ridge Medical Associates, Winston Salem NC; Timothy B. Boone, MD, The Methodist Hospital, Baylor College of Medicine, Houston, TX; John Connett PhD, University of Minnesota, Minneapolis MN; Dee Fenner MD, University of Michigan, Ann Arbor MI; William Henderson PhD, University of Colorado, Aurora CO; Sheryl Kelsey PhD, University of Pittsburgh, Pittsburgh PA; Deborah J. Lightner, MD, Mayo Clinic, Rochester, MN; Deborah Myers MD, Brown University School of Medicine, Providence RI; Bassem Wadie MBBCh, MSc, MD, Mansoura Urology and Nephrology Center, Mansoura, Egypt; J. Christian Winters, MD, Louisiana State University Health Sciences Center, New Orleans, LA
Footnotes
Financial interest and/or other relationship with Xanodyne and Pfizer.
Financial interest and/or other relationship with Intuitive Surgical.
Financial interest and/or other relationship with Pfizer and Laborie Medical Technologies.
Financial interest and/or other relationship with Pfizer, Allergan and National Institutes of Health.
Financial interest and/or other relationship with Pfizer, Astellas, Novartis and Allergan.
Financial interest and/or other relationship with Elan Corporation, Johnson & Johnson, Stryker, Bristol-Myers Squibb and Procter & Gamble.
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