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Keywords:

  • nocturia;
  • lower urinary tract symptoms;
  • exercise therapy;
  • adrenergic α-blockers;
  • muscarinic antagonists

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

What's known on the subject? and What does the study add?

  • Nocturia is a common and bothersome lower urinary tract symptom, particularly in men. Many single drug therapies have limited benefit.
  • For men who have persistent nocturia despite alpha-blocker therapy, the addition of behavioural and exercise therapy is statistically superior to anticholinergic therapy.

Objective

  • To compare reductions in nocturia resulting from adding either behavioural treatment or antimuscarinic drug therapy to α-adrenergic antagonist (α-blocker) therapy in men.

Patients and Methods

  • Participants were men who had continuing urinary frequency >8 voids/day) and urgency after 4 weeks of α-blocker therapy run-in and who had ≥1 nightly episode of nocturia.
  • Participants received individually titrated drug therapy (extended-release oxybutynin) or multicomponent behavioural treatment (pelvic floor muscle training, delayed voiding and urge suppression techniques).
  • Seven-day bladder diaries were used to calculate reductions in mean nocturia.

Results

  • A total of 127 men aged 42–88 years with ≥1 nocturia episode per night were included in the study.
  • There were 76 men who had a mean of ≥2 nocturia episodes.
  • Among those with ≥1 nocturia episode, behavioural treatment reduced nightly nocturia by a mean of 0.97 episodes and was significantly more effective than drug therapy (mean reduction = 0.56 episodes; P = 0.01).
  • Participants with ≥2 episodes nocturia at baseline also showed larger changes with behavioural treatment compared with antimuscarinic therapy (mean reduction = 1.26 vs 0.61; P = 0.008).

Conclusions

  • Both behavioural treatment and drug therapy reduced nocturia in men with ≥1 episode of nocturia/night when added to α-blocker therapy.
  • These results were similar even when only those with ≥2 episodes of nocturia were considered.
  • The addition of behavioural treatment was statistically better than bladder-relaxant therapy for nocturia.

Abbreviation
MOTIVE

Male Overactive Bladder Treatment in Veterans

Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

Nocturia, defined as waking from sleep at night to void [1], is highly prevalent and bothersome [2-4]. Nocturia prevalence rises dramatically with increasing age [5] and to a greater extent in older men than in older women [6]. Nocturia is associated with poor sleep [3], higher absenteeism from work [7], a greater risk of accidental falls [8], and higher mortality [9].

Because nocturia is known to be related to many other diseases and conditions (overactive bladder, benign prostatic enlargement, obstructive sleep apnoea, congestive heart failure), treatment involves identifying the relevant conditions that are present and tailoring therapy accordingly [10, 11]. Because reductions in nocturia are usually modest with a single drug [12], recent studies have focused on the efficacy of combining multiple drugs or drugs with other interventions to determine whether outcomes can be improved [13-15]. One uncontrolled trial used a multicomponent approach to treating nocturia in men, including behavioural interventions and medications, and demonstrated significant improvements [11].

Recent guidelines have noted the low number of studies conducted on behavioural treatment for nocturia and suggested the need to further evaluate the benefits of such treatment [16]. In one randomized controlled trial that compared behavioural and drug therapy for urgency-predominant urinary incontinence in older women, secondary analyses examined their impact on nocturia. Among women who had concomitant nocturia at baseline, biofeedback-assisted pelvic floor muscle training and urge suppression strategies reduced nocturia by a mean of 0.5 episodes/night, which was significantly more than antimuscarinic drug therapy (mean 0.3) or placebo (mean 0.0) [17]. A similar trial, the Male Overactive Bladder Treatment in Veterans (MOTIVE) trial, compared the efficacy of adding either behavioural treatment or titrated antimuscarinic therapy for men whose urinary urgency and frequency persisted after 4 weeks of run-in with α-blocker therapy [18]. The purpose of this planned secondary analysis was to examine the impact of behavioural treatment on nocturia in the subgroup of participants who met the definition of having nocturia ≥1 episode of nocturia/night and in those likely to have clinically meaningful nocturia [2] (≥2 episodes/night) despite standard α-blocker therapy.

Materials and Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

The parent trial for this current analysis was the MOTIVE trial. This two-site, randomized clinical trial examined the effects of adding behavioural treatment or antimuscarinic therapy in men whose urinary frequency persisted after 4 weeks of α-blocker therapy. All participants provided written informed consent. The institutional review boards at each institution approved the study. Details of participant flow, recruitment and selection, inclusion/exclusion and the relation of the current analysis to the parent trial is shown in the CONSORT diagram (Fig. 1). Full details of the MOTIVE study appear elsewhere [18].

figure

Figure 1. CONSORT diagram showing flow through MOTIVE study and analysis set for the current study.

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Briefly, parent trial participants who had urinary urgency with frequent urination (>8 voids/24-h) were eligible. Full details regarding participant eligibility are available elsewhere [18], but exclusion criteria for the parent trial specifically relevant to nocturia in this current analysis included: haematuria (>5 cells/hpf); UTI (>100 000 cfu); diabetes mellitus with HgbA1c >9.0; uncompensated heart failure; urinary flow rate <5 mL/s; being given a diagnosis of sleep apnoea, or current or past treatment with continuous positive airway pressure; and a post-void residual urine volume ≥150 mL.

All participants not previously on α-blocker therapy were prescribed tamsulosin 0.4 mg for a 4-week run-in period. Participants who were on an optimum dose of an alternate α-blocker were not required to switch to tamsulosin. At the end of 4 weeks, those participants whose urinary frequency persisted after prescription of α-blocker therapy were randomized to receive additional treatment with 8 weeks of behavioural treatment or antimuscarinic drug therapy, provided that they had a post-void residual urine volume <150 mL.

During the baseline assessment, participants were identified as having diabetes mellitus based upon patient self-report of having the condition or the presence of a prescription of an oral medication for diabetes or insulin therapy. Congestive heart failure and peripheral oedema were determined by patient self-report. Nocturnal polyuria was determined through evaluation of a baseline 24-h voided volume. Participants were asked to record the time they arose in the morning on 2 consecutive days, and the time they went to bed with the intention of sleeping during the intervening night. The calculated daytime urine volume did not include the first void of the first day, but did include all other daytime voids up until a void within 15 min of bedtime. The nocturnal urine volume included all voids from overnight (except within 15 min of bedtime) as well as the first void of the subsequent morning when the participant arose for the day. The 24-h voided volume was calculated as {[(total volume in daytime and nighttime)/no. of h recorded]*24}. The percentage of nocturnal urine produced overnight was calculated as the (nighttime urine volume/24-h voided volume *100). Nocturnal polyuria was defined as nocturnal urine volume ≥33% of 24-h total urine volume. We did not use polysomnography or wrist actigraphy in the present study to gather information about sleep.

Intervention

In the parent trial, participants in each treatment group had four clinic visits over 8 weeks. All kept daily bladder diaries throughout the trial and received a fluid management handout.

For those randomized to behaviour, the treatment included pelvic floor muscle training, monitoring and coaching using the bladder diaries, and delayed voiding and urge suppression techniques to reduce urgency, frequency, nocturia and incontinence [19]. Each site's interventionalist initiated training by giving a verbal explanation on how to properly perform a pelvic floor muscle contraction. She then verified the participant's technique during the physical assessment by using a finger examination of the anus (for contraction) and palpating the abdomen with the opposite hand (for absence of contraction). If the participant could not demonstrate proper pelvic floor muscle contraction, he would be given verbal feedback for correction by the interventionalist until proper technique was demonstrated. Behavioural techniques specific to nocturia included: not drinking fluids after 6 pm and use of the urge suppression strategy to defer the need to void when awakening with urinary urgency [19]. If nighttime urinary urgency resolved with repeated pelvic floor muscle contractions, participants could go back to sleep; if not, they could void and return to bed. Full details of this teaching protocol are described in the parent article [18] and shown in Appendix S1.

In the parent trial, participants allocated to receive antimuscarinic therapy received individually titrated, extended-release oxybutynin with an initial starting dosage of 10 mg daily and titration through a range of 5–30 mg/day. Dosages were increased if urinary frequency persisted and side effects were tolerable. Post-void residual urine volume >150 mL or intolerable side effects resulted in a decrease in oxybutynin dosage. Pill counts were used to monitor drug adherence.

Minor side effects of all study drugs were treated symptomatically. An inability to tolerate the drug or a participant's request to stop the drug was allowed (without then being excluded from the study). In the parent study >95% of the participants continued on an α-blocker (for 75% of the participants, this was tamsulosin) [18].

Outcome Assessment

For the current analysis, the primary outcome measure was mean no. of episodes of nocturia per night as documented by 7-day bladder diaries. Nocturia was defined as number of voids between the time the participant recorded that he went to bed and morning awakening (the first morning void was not counted). Baseline nocturia was defined as after α-blocker run-in and after randomization, and post-treatment nocturia was defined as occurring at 8 weeks after prescription of either behavioural treatment or drug therapy (oxybutynin). A research assistant blinded to the treatment allocation scored the diaries.

Data Analysis

Participants in the two treatment groups were compared on demographic and health characteristics using chi-squared and t-tests where appropriate. The two groups were compared with respect to frequency of baseline nocturia, as well as at specific time points during and after intervention (up until post-treatment) using t-tests. When post-treatment values were missing, the last value was carried forward. Mean and median changes in the frequency of nocturia between the baseline and post-treatment time points were calculated and compared within the treatment groups using paired t- and Wilcoxon signed rank tests, respectively. Between-treatment-group differences were compared using t- and Wilcoxon rank sum tests. Finally, a mixed statistical model was used to compare the change in nocturia frequency across all study visits.

The main analyses used all participants with ≥1 episode of nocturia per night at baseline. To allow comparisons with other nocturia clinical trials [20], additional analyses were conducted, limiting the analysis to those with ≥2 episodes per night, to compare treatment groups on the proportion of participants who achieved a mean reduction of ≥1 nocturia episode per night and to compare groups on proportion who achieved ≥50% reduction from baseline.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

Participants

Details of the participants included in this current analysis and the relationship to the parent trial are shown in the CONSORT diagram (Fig. 1). Of the 143 participants randomized in the parent study [18], only the 127 with a mean ≥1 episode of nocturia/night (or the 76 with ≥2 episodes) after 4 weeks of α-blocker therapy were considered in the present study.

Participants with ≥1 Episode of Nocturia

Characteristics of the 127 men with ≥1 episode nightly nocturia are shown in Table 1. Participants ranged from 42 to 88 years of age. Before treatment, the two groups were comparable on all key parameters. Also, the 16 men with ≤1 episode of nocturia were not significantly different from the 127 men with nocturia. Several conditions associated with nocturia such as diabetes, lower extremity oedema and nocturnal polyuria were common, while congestive heart failure was less common. None of these conditions was found to be unequally distributed between the two treatment groups (Table 1).

Table 1. Characteristics of participants.
Variable

Behavioural treatment

N = 64

Drug treatment

N = 63

P
  1. *As a percentage of 24-h total volume; Defined as nocturnal urine volume ≥33% of 24-h urine volume [1].

Demographic variables   
Mean (sd) age, years64.3 (10.2)66.0 (9.0)0.30
Race, %  0.23
African-American39.728.6 
Non-Hispanic White58.771.4 
Hispanic1.60.0 
Income <$30 000, %54.054.70.94
Conditions contributing to nocturia   
Diabetes, %19.424.20.51
Congestive heart failure, %3.18.10.3
Lower extremity oedema, %68.669.80.9
Mean (sd) nocturnal urine volume*, %38.3 ± 0.137.9 ± 0.10.9
Nocturnal polyuria, %64.862.10.8

There were 64 participants randomized to behavioural treatment and 63 to drug therapy. Dropouts for each allocation and final drug dosages are shown in Fig. 1. A pill count showed a mean of 96% adherence to the prescribed drug. For behavioural treatment, the self-rated adherence to prescribed pelvic floor muscle exercises was 63%.

Behavioural treatment resulted in a median reduction of 0.86 voids per night compared with 0.57 voids per night in the drug therapy group (Table 2). While both allocations reduced nocturia significantly when added to α-blocker therapy, behavioural treatment was more effective than drug therapy (P = 0.03). We performed a sensitivity analysis including only those 43 participants allocated to drug treatment who took oxybutynin XL for at least 8 weeks (i.e. excluding dropouts and those titrated to 0 mg). Restricting the sample did not change the results meaningfully: the difference between behavioural and oxybutynin (a median reduction of 0.86 and 0.57, respectively) remained significant.

Table 2. Changes in nocturia with behavioural and drug therapy among men with ≥1 episode per night.
 

Behavioural treatment

N = 64

Drug treatment

N = 63

P*
  1. *Between-group differences compared using t- and Wilcoxon rank sum tests; mean pre-post changes in frequency of nocturia calculated using paired t-tests; median pre-post changes in frequency of nocturia calculated using Wilcoxon signed rank tests.

Mean (sd) no. of episodes of nocturia per night   
Baseline2.50 (1.47)2.31 (0.94)0.40
2 weeks1.85 (1.66)1.97 (1.33)0.67
4 weeks1.81 (1.17)1.76 (1.28)0.82
6 weeks1.77 (1.32)1.80 (1.93)0.92
8 weeks1.52 (1.34)1.75 (1.19)0.32
P<0.0010.0010.12
Change in nocturia   
Mean change−0.97−0.56 
P<0.001<0.0010.01
Median change−0.86−0.57 
P<0.001<0.0010.03
Min., Max.−6.00, 0.83−2.57, 1.71 

Participants with ≥2 Episodes of Nocturia

Of the 143 participants randomized, 16 had a mean of <1 episode of nocturia per night and 51 individuals had a mean in the range of 1.00–1.99 episodes of nocturia. The remaining 76 individuals with ≥2 nightly episodes of nocturia did not differ significantly from the 51 with a mean of 1.00–1.99 episodes of nocturia with respect to the participant characteristics listed in Table 1. Of these 76 participants, 38 were randomized to each arm (Fig. 1). The frequency of nocturia before treatment did not differ significantly between the two groups (Table 3; P = 0.21) nor were there differences in the baseline characteristics from Table 1. Of those continuing medication, the estimated adherence to medications via pill counts was 96%. Of those allocated to behavioural treatment, the self-rated adherence to exercise was 64% of total prescribed exercises.

Table 3. Changes in nocturia with behavioural and drug therapy among men with ≥2 episodes per night.
 

Behavioural Treatment

N = 38

Drug treatment

N = 38

P*
  1. *Between-group differences compared using t- and Wilcoxon rank sum tests; mean pre-post changes in frequency of nocturia calculated using paired t-tests; median pre-post changes in frequency of nocturia calculated using Wilcoxon signed rank tests.

Mean (sd) no. of episodes of nocturia per night   
Baseline3.23 (1.50)2.89 (0.76)0.21
2 weeks2.37 (1.91)2.37 (1.14)0.99
4 weeks2.21 (1.28)2.31 (1.22)0.75
6 weeks2.16 (1.51)2.53 (2.14)0.38
8 weeks1.97 (1.54)2.28 (1.15)0.32
P<0.0010.060.02
Change in nocturia   
Mean change−1.26−0.610.008
P><0.0001<0.0001 
Median change−1.21−0.640.01
P><0.001<0.001 
Min., Max.−6.0,0.83−2.57,1.71 

For those individuals with ≥2 nocturia episodes at baseline, behavioural treatment resulted in a median reduction of 1.21 voids per night and drug therapy resulted in a median 0.64 reduction. While both treatments were effective in terms of achieving significant reductions of nocturia, behavioural treatment resulted in statistically greater reductions (P = 0.01). Again, we performed a sensitivity analysis in which only those taking oxybutynin (by 8 weeks, n = 29) were compared with those on behavioural treatment. In this analysis, behavioural treatment showed a reduction of 1.26 and oxybutynin a reduction of 0.58 episodes per night (P = 0.01).

For those who had ≥2 episodes at baseline, the percentage having a reduction in nocturia of ≥50% from baseline was 29.0% for behavioural treatment vs 21.1% for drug therapy (P = 0.43). The percentage of men reducing their mean nocturia by ≥1 episode was 55.3% for those with behavioural treatment and 36.8% for those with drug therapy (P = 0.11).

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

The MOTIVE trial compared adding behavioural treatment with adding antimuscarinic therapy in men whose urinary frequency persisted >8 episodes/24 h) despite 4 weeks of α-blocker therapy [18]. While behavioural treatment and drug therapy reduced urinary frequency significantly and to an equal degree, drug therapy reduced urgency more and behavioural treatment reduced nocturia more. While behavioural therapy is a well-established treatment for urinary incontinence, this finding showing efficacy for this approach for nocturia in men is novel.

In these analyses, we included only those men who had nocturia ≥1 nightly episode) and those with clinically meaningful nocturia ≥2 nightly episodes). For those with ≥1 episode, the mean reduction was 0.97 episodes for adding behavioural treatment and 0.56 episodes for adding drug therapy. The advantage of behavioural treatment over drug therapy persisted when the sample was restricted to those with ≥2 baseline nocturia episodes, with mean reductions of 1.26 episodes for behavioural treatment and 0.61 for drug therapy.

The effect size of behavioural treatment in the present trial may be explained in part by its multiple components. It is possible that the pelvic floor muscle training, urge suppression strategies and fluid restriction after 6 pm addressed more than one causal factor or used more than one therapeutic mechanism; however, the study design does not allow us to assess the relative contributions of the individual components.

Although less effective, there are sound reasons for using antimuscarinic therapy for nocturia. Urinary urgency, the prime symptom of overactive bladder, has been shown to be a strong risk factor for nocturia in men (odds ratio 7.4, 95% CI 4.5–12) [21]. Others have proposed that urinary urgency is the primary driver of all overactive bladder symptoms, including nocturia [22]. Interestingly, in the parent MOTIVE trial, drug therapy reduced urgency to a greater extent than behavioural treatment, but was not superior for nocturia [18]. While epidemiological data show urgency to be a strong risk factor for nocturia, clinical trials of antimuscarinics have been inconsistent for nocturia reduction, with some having positive results [23] and others showing no benefit [13, 24]. In 850 male and female participants (49% men) in a 12-week randomized trial, tolterodine (median reduction of 19%) did not significantly reduce the total number of nocturnal micturitions when compared with placebo (median reduction of 23%) [24]. In 907 treated participants (20% male), solifenacin 10 mg (−0.71 episodes), but not 5 mg (−0.52 episodes), significantly decreased episodes of nocturia vs placebo [23]. Combining antimuscarinics with other therapies (α-blockers, in particular) has also been shown to be a useful approach for nocturia [13].

Questions about the clinical meaningfulness of the reductions achieved with behavioural treatment might remain. The nocturia reductions here (−1.26 episodes for behavioural treatment; −0.61 for titrated oxybutynin) compare favourably with those of other interventions. Titrated oral desmopressin showed a mean difference of −1.3 nocturia episodes, compared with −0.5 episodes for placebo [20]. Also, in a multi-dosage, randomized, controlled trial of orally dissolving desmopressin, changes in nocturia for men were −0.54, −0.83, −1.13, −1.38 episodes for 10, 25, 50, and 100 μg, respectively vs −0.84 episodes for placebo [25]. In a 12-week study in men, nighttime frequency was significantly reduced (−0.6 episodes) with combined tamsulosin and tolterodine compared with placebo (−0.3 episodes), while either treatment individually was not statistically different from placebo [26]. It is difficult to assess the impact of prostate surgery on nocturia, owing to the relative lack of randomized, controlled trials of procedures vs medical therapy and the absence of metrics specifically assessing nocturia as an individual outcome, yet the net change in nocturia from TURP is believed to range from −0.8 to −1.6 [27]. One recent randomized, controlled clinical trial in men (mean age 68 years), who were previously untreated, compared TURP with tamsulosin 0.4 mg daily for nocturia. Participants receiving TURP or tamsulosin had reductions of 0.9 vs 0.5 episodes at 6 months and 1.0 vs 0.6 at one year, respectively [28]. While the authors of that study judged TURP to be superior, the interpretation of the results should consider the likelihood (P = 0.056) that nocturia was different at baseline in the two groups (2.4 episodes for the TURP group and 2.0 episodes for the tamsulosin group).

Other trials have examined nocturia reductions differently, including calculating the percentage of participants starting from a baseline of ≥2 episodes of nocturia for whom nocturia was reduced by ≥50%. In a secondary analysis of data from a BPH trial, nocturia reduction of ≥50% occurred in 39% of men treated with terazosin, compared with 22% of men treated with placebo [12]. Antidiuretic therapy trials have typically shown large nocturia reductions: in the largest randomized, placebo-controlled trial of oral desmopressin in men (n = 151) to date, desmopressin given at an individually titrated, optimized dosage offered 34% of participants a 50% reduction in nocturia from baseline, vs 2% of the placebo group [20]. The proportion of men who were at least 50% improved in the current analysis was somewhat lower, 29% for behavioural treatment and 21% for drug therapy. Behavioural treatment would, however, seem to have fewer safety concerns than antidiuretic therapy, particularly in treating an older population [29].

The present analysis has many strengths. The parent study was a controlled clinical trial with random allocation to treatment arms. Seven-day bladder dairies were used for the main outcome measure, and scored by staff blinded to treatment assignment. Medication adherence was measured by pill counts. The data analysis was conservative, with an intention-to-treat framework. Compliance with the interventions was assessed. Additional sensitivity analyses were performed including only those men who continued on oxybutynin XL, showing that even when only those taking pills were included, behavioural treatment was still superior. An evaluation of comorbid conditions often associated with nocturia revealed a high prevalence of diabetes, lower extremity oedema and nocturnal polyuria. Because the overall sample size was too small to perform multiple subset analyses, we could not reliably assess whether certain comorbid conditions influenced response to treatment; however, the statistically significant response to either therapy in the presence of these conditions suggests that these treatments are likely to be meaningful in patients with a variety of causes of nocturia, and warrants further evaluation of the mechanism leading to reduction of nocturia using behavioural therapy or antimuscarinic drug therapy. In addition, the present analysis includes a sizable proportion of African-American participants. Past studies have shown African-Americans to be at a higher risk of having nocturia [5, 30, 31]. Also, the total net nocturia reductions from study entry (counting both the effect of the α-blocker run-in and either the behavioural treatment or oxybutynin drug therapy) may be greater than the reductions shown here (as they were calculated from a baseline that occurred after α-blocker run-in) [26].

There are also some limitations to the current study. Participants had four visits to titrate the medication dosage or to adjust behavioural treatment. This maximized efficacy, but it probably does not represent usual clinical practice. We know that individuals had fewer nighttime episodes of nocturia, but we cannot ascertain if their sleep was meaningfully changed. We were not able to collect specific information about participants' sleep, either by polysomnography or wrist-actigraphy. As the present trial contained no true placebo arm, the net benefit of treatment cannot be estimated. Given that the primary outcome measure of MOTIVE was 24-h urinary frequency, individuals who may have had nocturia after the α-blocker run-in, but had ≤8 daily voids were ineligible. This may make generalization to all male populations with nocturia difficult [32]. There are other possible combinations of drug therapy with α-blockers (i.e. 5-α-reductase inhibitors [12, 15], phosphodiesterase 5 enzyme inhibitors) that were not tested, so we cannot say that behavioural treatment is superior to all other drug therapies. Although the present trial was limited by the absence of specific quality-of-life measures for nocturia, having ≥2 episodes of nocturia has been shown to be strongly associated with increased bother and worse quality of life when compared with having 0 or 1 episodes [2].

In conclusion, behavioural treatment was more effective than antimuscarinic drug therapy for improving nocturia episodes among men who had persistent LUTS, including ≥1 or a ≥2 nightly episodes of nocturia, after 4 weeks of α-blocker therapy.

Acknowledgements

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

The research reported here was supported by a Merit Review grant from the Department of Veterans Affairs, Veterans Health Administration, Rehabilitation Research and Development Service.

The authors thank Lee Hammontree, MD, for contributions to design and conception of the trial, Terri Renea Lane, MSN, CRNP, Donna Lewis, MSN, GNP, Nicole Davis, MSN, CRNP, and R. Jeannine McCormick, MSN, CRNP for implementing interventions; April Snow, BA, Susan Barnacastle, BA and Zobair Nagamia, MD, for project management, and Derry Crawford, MSHA for data management, Jean Marie White, BA, for project coordination and data entry, Tyler Smith, BA, for project coordination, Janice Taylor, MSN, for subject recruitment, and Sabrina W. Bradley, MPH, Sean Halpin, MA, and Rachel Wolf, MPH, for research assistance.

ClinicalTrials.gov: NCT01187498.

Conflict of Interest

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

Gerald McGwin, David T. Redden, Alayne D. Markland, Janet L. Colli: none; Theodore M. Johnson II: Pfizer research, Ferring, Pfizer consultant; Joseph G. Ouslander: Pfizer, Astellas consultant; Patricia S. Goode: Pfizer research, Astellas consultant; Kathryn L. Burgio: Pfizer research; Astellas, J&J, Pfizer consultant; Camille P. Vaughan: Astellas research.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information

Supporting Information

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Conflict of Interest
  9. References
  10. Supporting Information
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Appendix S1 Instructions given to participants on urge suppression strategies specific for nocturia.

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