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Keywords:

  • anticholinergic drug;
  • desmopressin;
  • diurnal pollakisuria;
  • lower urinary tract symptoms;
  • nocturia;
  • nocturnal polyuria;
  • polyuria

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Polyuria and nocturnal polyuria
  5. Bladder storage disorder
  6. References
  7. Appendix

Nocturia is a bothersome condition, defined as a complaint whereby the individual has to wake one or more times per night in order to void. Nocturia that occurs twice or more per night can have a substantial adverse effect on the patient's quality of life (QOL), and in many cases treatment may be required.

These guidelines provide a treatment algorithm for use by primary care physicians.

The initial assessment is conducted through a history taking interview. With a clear understanding of symptoms, patients can be classified into three broad categories: (1) nocturia only, (2) nocturia and diurnal pollakisuria without other lower urinary tract symptoms, and (3) nocturia and diurnal pollakisuria accompanying other lower urinary tract symptoms.

For treatment, the literature supporting each form of drug therapy was ranked and a recommendation grade was determined for each form of therapy. A grade of ‘F (pending)’ was applied to any drug not currently approved for use in Japan or for which the efficacy and safety in Japanese patients was unconfirmed at the time of evaluation.

We recommend instruction and guidance on water intake that will generally result in 24-h urine volume of 20 to 25 mL/kg. This corresponds to a daily water intake of 2.0% to 2.5% of body weight. In Japan, desmopressin is indicated for central diabetes insipidus and nocturnal enuresis, but not indicated for nocturia.

The therapeutic mechanism of the anticholinergic drugs for nocturia may depend on the action of the sensory nerve mediated by the muscarinic receptors.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Polyuria and nocturnal polyuria
  5. Bladder storage disorder
  6. References
  7. Appendix

An online keyword search of specific categories was carried out in the PubMed literature, primarily for the 12.5-year period from 1995 through to June 2007, and articles that were judged to be appropriate were used to create these guidelines. For treatment, the literature supporting each form of drug therapy was ranked and the recommendation grade was determined for each form of therapy as shown in Table 1. A grade of ‘F’ (pending) was applied to any drug not currently approved for use in Japan, or for which the efficacy and safety in Japanese patients was unconfirmed at the time of evaluation.

Table 1.  Basis for our ranking of articles and recommendations
  1. RCT, randomized controlled trial.

Level ranking of articles 
 ILarge-scale RCT with clear results
 IISmall-scale RCT with clear results
 IIINon-randomized study with simultaneous control
 IVNon-randomized study with historical control
 VCase series study (without control), with specialist opinion(s)
Recommendation ranking 
 ASupported by at least two clinical studies described in Level I articles
 BSupported by one Level I clinical study
 CSupported by Level II clinical studies
 DSupported by at least one Level III clinical study
 EOnly Level IV or Level V clinical studies available
 FPending (not yet approved in Japan, or not confirmed to be effective and/or safe in Japanese patients)

Nocturia is a bothersome condition, defined as a complaint whereby the individual has to wake one or more times per night in order to void.1,2 Nocturia that occurs twice or more per night can have a substantial adverse effect on the patient's quality of life (QOL), and in many cases treatment might be required. The condition can be caused by reduced bladder capacity and by increased nocturnal urine volume. Clinically, a variety of factors can contribute to nocturia, including polyuria, nocturnal polyuria, sleep disorder, bladder storage disorder (benign prostatic hyperplasia [BPH], overactive bladder [OAB], interstitial cystitis [IC], etc.) and advanced age.

These guidelines provide a treatment algorithm (Fig. 1) for use by primary care physicians, together with points to consider at each step when progressing through the algorithm.

image

Figure 1. Treatment algorithm for nocturia. FVC, Frequency volume chart.

Download figure to PowerPoint

  • 1
    The initial assessment is carried out through a history taking interview, in order to gain a clear understanding of the patient's symptoms. The patient should be evaluated for underlying disease and cardiovascular conditions, consumption of water, alcohol and caffeine should be determined, and urinalysis should be carried out.
    With a clear understanding of symptoms, patients can be classified into three broad categories:
    • 1
      nocturia only,
    • 2
      nocturia and diuria without other lower urinary tract symptoms, and
    • 3
      nocturia and diuria accompanying other lower urinary tract symptoms.
      Categories (1) and (2) are generally treated by primary-care physicians or internists. Category (3) occurs in response to a bladder storage disorder, and in many cases will require treatment by a urologist.
  • 2
    For patients with either (1) nocturia only or (2) nocturia and diuria not associated with other lower urinary tract symptoms, a voiding diary is kept in order to confirm the presence of polyuria or nocturnal polyuria. Ordinarily, the diary is kept for 3 days, and those records are evaluated. The voiding diary is a good source of information on parameters, including the number of voids, diurnal urine volume, nocturnal urine volume (nocturnal voiding volume including voiding on arising in the morning), 24-h urine volume and maximum single voided volume (functional bladder capacity).
    Polyuria is defined as a 24-h urine volume of 40 mL/kg bodyweight or above.3 Nocturnal polyuria is defined as a nocturnal polyuria index (nocturnal urine volume/24-h urine volume) of 0.33 or above in the elderly and 0.20 or above in youths.3 A template for the voiding diary can be downloaded from the home page of the Neurogenic Bladder Society (http://www.luts.gr.jp/).
  • 3
    There are three treatment approaches for bladder storage disorder, which can manifest as benign prostatic hyperplasia, overactive bladder and/or interstitial cystitis. Guidelines have been established for each of these conditions. See ‘Treatment guidelines for management of benign prostatic hyperplasia’4 and ‘Treatment guidelines for male lower urinary tract symptoms’5 for benign prostatic hyperplasia, ‘Treatment guidelines for overactive bladder’6 and ‘Treatment guidelines for overactive bladder, revised abridged edition’7 for cases of overactive bladder, and ‘Treatment guidelines for interstitial cystitis’8 for cases of interstitial cystitis. Early referral to a specialist is desirable in cases of interstitial cystitis.
  • 4
    In cases of refractory BPH and overactive bladder, the presence of polyuria or nocturnal polyuria must be confirmed through the use of a voiding diary. Data from the voiding diary can be used to calculate the nocturnal polyuria index, the predicted number of nocturnal voidings, and the nocturnal bladder capacity index. If the nocturnal bladder capacity index is 0 or above, the nocturnal functional bladder capacity is reduced.
    • • 
      Nocturnal polyuria index (NPi) = nocturnal urine volume/24-h urine volume
    • • 
      Nocturia index (Ni) = nocturnal urine volume/maximum single voided volume
    • • 
      Predicted number of nightly voids (PNV) =  nocturia index-1
    • • 
      Nocturnal bladder capacity index (NBCi) = actual number of nocturnal voids – predicted number of nocturnal voids

Polyuria and nocturnal polyuria

  1. Top of page
  2. Abstract
  3. Introduction
  4. Polyuria and nocturnal polyuria
  5. Bladder storage disorder
  6. References
  7. Appendix

(1) Lifestyle guidance and behavioral therapy

A keyword search for ‘nocturnal polyuria’ and ‘behavioral (therapy)’ on PubMed yielded 77 articles, but no original articles on nocturia in adults, so three review articles were referenced (Recommendation Grade E).9–11

All of these review articles recommended lifestyle guidance and behavioral therapy for the initial treatment of nocturnal polyuria.

Four articles were found that related to water intake.12–15

a. Instructions and guidance related to water intake

Because excessive nocturnal consumption of water, alcohol and caffeine are reported to be factors in nocturnal polyuria, patients should be instructed to avoid such consumption.11–13 In particular, excessive water intake makes it necessary for the body to regulate its water intake balance.11 It is necessary to obtain a clear understanding of water intake and urine volume, usually based on data from the voiding diary, in order to determine whether the patient experiences polyuria throughout the entire day, or only at night. Instructions about water intake restriction can lead to problems, however, because there might be a risk of the development or the exacerbation of dehydration-induced cerebral infarction. Particularly in the elderly, dehydration is reported to be a factor in the onset of cerebral infarction. However, there is no evidence that excessive water intake has any ‘blood-thinning’ preventative effect against cerebral infarction, and one report has shown no observable changes in blood viscosity after water intake (Level V).12

The standard for daily water intake is determined according to 24-h urine volume or bodyweight. Ordinarily in healthy adults the mean value for 24-h urine volume/bodyweight is 23 ± 2 mL/kg (Level III),13 and there is a reported risk of hyponatremia if that value exceeds 29 mL/kg (Level I).14 Another report states that values less than 20 mL/kg are associated with the risk of dehydration, whereas values of 30 mL/kg or above can be a factor in nocturnal polyuria (Level V).15 Based on these data, we recommend instruction and guidance on water intake that will generally result in a 24-h urine volume of 20–25 mL/kg. This corresponds to daily water intake of 2.0% to 2.5% of bodyweight. There are currently no reports available of randomized controlled trials (RCT) assessing the effects of water intake instructions on nocturnal polyuria, but one report stated that nocturnal polyuria was not improved simply by limiting water intake.10

b. Exercise therapy

Some researchers have reported the efficacy of exercise therapy (walking, exercising with weights and squats), carried out in the evening or at night. They postulate that the pumping action of the muscles returns accumulated interstitial fluid to the blood vessels and that some excess water is also removed as sweat.9–11 Exercise is also effective in relieving stress, which can be related to sleep disorders. However, these treatment methods have not yet been examined in the context of a RCT.

c. Other

Other techniques reported to be effective include a daytime nap of 30 min or less with the feet elevated, and the use of compression stockings.9,10 However, these treatment methods have not yet been examined in the context of a RCT.

(2) Drug therapy for nocturnal polyuria

Drug therapy for nocturnal polyuria is shown in Table 2, along with literature ranking and recommendation grade.

Table 2.  Drug therapy for nocturnal polyuria and nocturia
DrugsArticle rankGrade of recommendation
  • Indicated for nocturnal enuresis.

  • ‡Indicated for enuresis.

Nocturnal polyuria  
 • DesmopressinIF (pending) [special concern should be paid to the possibility of hyponatremia]
 • Diuretics  
  AzosemideIIC
  FurosemideIIC
  BumetanideIIC
 • Tricyclic antidepressants  
  ImipramineIIID
Nocturia accompanying overactive bladder  
 • Anticholinergic drugs  
  PropiverineIA
  OxybutyninIIC
  TolterodineIA
  SolifenacinIA
  ImidafenacinVE
 • Other drugs  
  FlavoxateIIID
  Capsaicin, resiniferatoxinIIF (pending) [not yet approved]
  Botulinum toxinIIIF (pending) [not yet approved]
Nocturia with benign prostatic hyperplasia  
 • α1 blocker monotherapy  
  TamsulosinIA
  NaftopidilIIC
  SilodosinNo articles evaluating use in nocturia
  PrazosinNo articles evaluating use in nocturia
  TerazosinIB
  UrapidilNo articles evaluating use in nocturia
  AlfusozineIF (pending) [not yet approved]
 • α1 Blocker + anticholinergic drug  
  TolterodineVF (pending)
  SolifenacinIIIF (pending)
 • 5α-Reductase inhibitors  
  FinasterideIF (pending) [not yet approved]
  DutasterideNo articles evaluating use in nocturia
 • Steroidal anti-androgenic agents  
  ChlormadinoneVE
  AllylestrenolNo articles evaluating use in nocturia
 • Amino acid preparations, plant-derived preparations  
  EviprostatIIC
  Cernitin pollen extractIIC
 • Kampo formulations  
  Sairei-toVE
  GoshajinkiganVE
 • Other drugs  
  LoxoprofenVF (pending) [not yet approved]
a. Desmopressin: Grade of recommendation: F, pending (Table 2)

The effects of desmopressin (DDAVP) on nocturia as a result of nocturnal polyuria, which have been studied in RCT, are based on age-related decreases in the secretion of arginine vasopressin (AVP) by the posterior lobe of the pituitary gland at night, resulting in increased nocturnal urine volume.16 The antidiuretic effects of desmopressin, which are 4000-fold greater than the drug's vasodilating action, are sustained for 6–22 h.17

Desmopressin's antidiuretic action increases water reabsorption in the renal collecting ducts and the ascending limb of Henle's loop, reducing urine volume and increasing urine osmolality.18 At the cellular level, this effect is manifested through V2 receptor-mediated elevation of intracellular adenylate cyclase.17,19 The antidiuretic effects are 3–10-fold greater than vasopressin.20 When given orally, the drug's bioavailability is reduced by the presence of a variety of enzymes to approximately 0.1% of that of subcutaneous injection.21

Currently desmopressin is given orally and pernasally. In Japan, the drug is available in three categories: (i) desmopressin nasal drops; (ii) nasal spray 2.5; and (iii) nasal spray 10. The first and second are indicated for central diabetes insipidus and are given at a dose of 5–10 µg per time. The spray 10 is indicated for nocturnal enuresis associated with decreased urine osmolality and/or decreased urine specific gravity, and is given at a dose of 10 µg (maximum 20 µg) once daily at bedtime. The drug is not indicated for nocturia, so caution is required.

(1) Therapeutic effects:  A PubMed search for the key words desmopressin and nocturia, limiting the search to articles describing RCT in subjects 45 years-of-age or older during the period between 1995 and 2007, yielded seven articles. Those articles have been used for reference in the following discussion of the therapeutic effects and adverse drug reactions (ADR) associated with this drug (Levels I and II).22–28

The mean age of subjects ranged from 57.1 to 74 years, and in most of the studies the subjects experienced two or more instances of nocturnal voiding per night and had a nocturnal urine volume/maximum bladder capacity in excess of 1. In nearly all of the studies cited, patients were excluded from participation if they were receiving concomitant drug therapy for cardiovascular disease, kidney disease, liver disease, hyponatremia or treatment-refractory hypertension with orally administered drugs (diuretics, antidepressants) that would affect desmopressin action.

The treatment period ranged from 3 days to 3 weeks. Six articles described oral administration of the drug, and one article described pernasal administration. The dose used was 0.1–0.4 mg for oral administration, and 20 or 40 µg for pernasal administration. In most of the studies reported, the RCT was preceded by an optimal dose-finding period. The optimal dose was defined as the dose required to reduce the number of nocturnal voidings to 0, or the dose level that provided maximum effectiveness with tolerable ADR.

For therapeutic effects, the primary end-point in most studies was a significant percentage of reduction from treatment baseline in the number of nocturnal voidings in comparison with the placebo group. That percentage was 33–46% in the desmopressin groups, in comparison with 3–11% in the placebo groups, a statistically significant difference. The number of nocturnal voidings was reduced by 0.8–1.3 times per night, and time to first voiding after going to sleep was increased by 1.5–2.2 h. Evaluations related to quality of life also showed significant improvement from baseline in the desmopressin groups. Therapeutic effects were not greatly affected by factors such as drug dose, drug concentration in blood, age or sex. There are no studies discussing the therapeutic effects of various drug formulations, so no firm judgment can be reached, but it seems likely that these various formulations do not differ in therapeutic effectiveness (Levels I and II).22–28

No RCT have been carried out for long-term administration, and only one report describing long-term administration was found in the literature (Level III).29 That was a large-scale multicenter study to evaluate the effectiveness of desmopressin for nocturia over a treatment period of 12 months and 1 month after drug withdrawal in 249 patients (mean age 60.8 years, 132 men and 117 women). The therapeutic effects were sustained throughout the treatment period, and the level and severity of ADR were similar to those seen in short-term studies. Clinical effects reportedly returned to baseline 1 month after the discontinuation of desmopressin treatment.

(2) Adverse drug reactions:  ADR characteristically appeared early in treatment and were seen predominantly in patients 65 years-of-age and older.24,29 Some researchers found a correlation between ADR and desmopressin dosage,26 but other researchers reported no dose dependence.29 In most cases, ADR were mild or moderate in severity and were resolved with discontinuation of drug treatment or by limiting water intake.23–29 The most common ADR were headache, lower-extremity edema, nausea, dizziness and hyponatremia. Of these, hyponatremia has been reported as a grade V ADR (Level V),30 and requires particular attention.

A systematic review of desmopressin-induced hyponatremia showed one report of hyponatremia developing in 7.6% of cases, including asymptomatic cases (Level I),14 a clear warning that the occurrence of hyponatremia might be higher than anticipated in an actual clinical setting. Hyponatremia-induced symptoms are frequently complicated by general symptoms, such as lower extremity spasm and generalized spasm, so if hyponatremia is observed the drug should be immediately discontinued and appropriate measures should be taken, such as restriction of water intake and the use of diuretics as needed. In order to reduce the occurrence of ADR, on discontinuation of drug administration the patient's water intake should be strictly controlled (for example, limiting water intake to 1 L daily)30 (Level V). It is important to re-examine the patient within 3 days after discontinuation of treatment, carrying out both an overall evaluation (headache, edema, bodyweight increase etc.) and an electrolyte assessment. The same procedures should also be followed when increasing the therapeutic dose (Level III).29

b. Diuretics: Grade of recommendation: C (Table 2)

A PubMed keyword search for ‘nocturnal polyuria’ and ‘diuresis’ yielded 14 articles in the literature. These included two original articles regarding RCT in adults with nocturia. These were referenced, along with one important article.31–33

The daytime use of diuretics is effective against nocturnal polyuria. In particular, cases of elevated human atrial natriuretic peptide (hANP) can be considered as latent heart failure, and azosemide (60 mg) has been reported to be significantly more effective in such patients than in those with normal hANP levels (P = 0.0026; Level II).31

Of the articles regarding the use of diuretics for nocturia or nocturnal polyuria, two discussed placebo-controlled RCT. Reynard et al. described 43 male patients 50 years-of-age or older who were randomly allocated into groups treated with 40 mg furosemide or placebo 6 h before bedtime. Results showed significant reductions in the furosemide group compared with the placebo group, both in the number of nocturnal voidings (reduction of 0.5 times vs 0 times) and nocturnal urine volume (−18% vs 0%). Within the furosemide group, the number of nocturnal voidings was reduced by one or more in seven out of 19 patients. This level of reduction was experienced by only one out of 20 patients in the placebo group (Level II).32 Pedersen et al. reported a double-blind crossover study enrolling 28 patients (13 women and 15 men), in which patients were treated with bumetanide or placebo for two treatment periods of 2 weeks duration. During the period of placebo administration, patients experienced 13.8 nocturnal voidings per week. This figure was reduced by 3.8 times per week during bumetanide administration. Bumetanide had no effect in 10 patients with BPH, but in the remaining 18 patients nocturnal pollakiuria was reduced by four voidings per week in comparison with the placebo period. Of those 18 patients, three reported that they preferred the placebo, 11 preferred bumetanide and four expressed no preference33 (Level II).

c. Tricyclic antidepressants: Grade of recommendation: E (Table 2)

A PubMed keyword search for ‘nocturia’‘nocturnal polyuria’ yielded seven articles, and a search for ‘antidepressants’‘imipramine’ yielded five articles. However, there were no original articles on RCT in adults with nocturia.

Imipramine and the other tricyclic antidepressants, in addition to their relatively mild central and peripheral anticholinergic activity, also inhibit the reuptake of serotonin and noradrenaline, and provided antidiuretic action. These drugs also inhibit peripheral catecholamine reuptake, resulting in a sympathomimetic effect. As antidepressants, these drugs act as central nervous system (thymoleptic) agents, and also show anticholinergic action and direct inhibitory action on smooth muscle.

In research on the antidiuretic effects of imipramine in nocturnal polyuria, Hunsballe et al. worked with 15 patients 15–37 years-of-age who suffered from uncomplicated primary nocturnal emesis and eight control subjects 25–32 years-of-age. Subjects took imipramine (1 mg/kg bodyweight) at 8:00 pm, and nocturnal urine volume, urine osmolality, creatinine clearance, osmotic clearance, free water clearance, solute excretion, sodium excretion rate, and potassium (K) and plasma vasopressin excretion rates were compared for treated and untreated periods. Imipramine administration provided antidiuretic effects in six youths suffering from nocturnal enuresis with severe nocturnal polyuria. This imipramine-induced reduction in urinary excretion was accompanied by reduced osmotic clearance. In conclusion, imipramine provides anti-diuretic effects independent of antidiuretic hormone (ADH). Effects are reported to be due primarily to alpha-adrenergic receptor (alpha-AR) stimulating action in the proximal tubules, and secondarily to increased distal tubular urea and water reabsorption (Level III).34

No RCT were included in the articles that discuss the use of tricyclic antidepressants or imipramine in the treatment of nocturia or nocturnal polyuria. Although these drugs appear to be effective in nocturia, at present they are indicated only for enuresis and nocturnal enuresis, and there is no evidence of their efficacy in the treatment of nocturia or nocturnal polyuria. ADR include cardiovascular effects (arrhythmia etc.), drowsiness, and reductions in attention span, concentration and capability for reflex movement. There have been reports of serious events, including cardiac arrest, so caution is required when prescribing these drugs. (Tomonori Yamanishi and Akihide Hirayama).

Bladder storage disorder

  1. Top of page
  2. Abstract
  3. Introduction
  4. Polyuria and nocturnal polyuria
  5. Bladder storage disorder
  6. References
  7. Appendix

(1) Nocturia accompanying overactive bladder

The literature reviewed in this section was selected through PubMed searches in the time period from 1995 through to 2007. A keyword search for ‘nocturia’ in conjunction with ‘overactive bladder’ (OAB), ‘antimuscarinic drugs’, ‘anticholinergic drugs’, ‘pharmacological treatment’, or ‘detrusor overactivity’ yielded 270 articles, from which 40 articles were selected that clearly documented findings for nocturia. To this, two recent articles in the literature were added and one article on muscarinic receptors.

Overactive bladder is defined as a syndrome with the principal symptom of urinary urgency associated with pollakiuria and urge urinary incontinence,1,2 and is considered to be a typical bladder storage disorder. Drug therapy is the fundamental treatment for OAB.35 Efficacy and safety have been widely investigated for the anticholinergic drugs, which are the drugs most widely used for the treatment of OAB at present, although a number of other drugs are also now available. When using the anticholinergic drugs, it is important to give careful consideration to ADR that might result from the blocking of systemic muscarinic receptors. Epidemiological surveys in Japan show that, of all lower urinary tract symptoms (LUTS), nocturia has the greatest adverse effect on quality of life,36 and recent studies indicate that nocturia might also affect quality of sleep.37

Drug therapy for nocturia is shown in Table 2, along with literature ranking and recommendation grade.

a. Anticholinergic drugs

There are almost no reports in the literature of investigations of the mechanism through which anticholinergic drugs produce improvement in nocturia, but one suggested mechanism for nocturia relates to involuntary contraction of the detrusor muscles during the night, with a resulting reduction in bladder capacity.38 Hirayama et al. carried out an ice-water test in 114 male patients 50 years-of-age or older with LUTS. Their results showed significantly smaller bladder capacity and a significantly higher number of nocturnal voidings in patients with detrusor overactivity and a positive response to the ice-water test than in patients with detrusor overactivity who showed a negative response to that test (Level II).39 In addition, because the ratio of detrusor overactivity patients who were ice-water-test-positive was significantly higher in the nocturia group, these findings also suggested that, in addition to nocturnal polyuria, C fiber sensory nerve activation might also contribute to nocturia. Recently, some researchers have suggested that the mechanism of action of the anticholinergic drugs might involve sensory nerve action mediated by the muscarinic receptors (Level III),40 and that this might suggest a role for anticholinergic drugs in the therapeutic mechanism of action against nocturia.

A wide range of anticholinergic drugs are currently available for the treatment of OAB in Japan, including some new OAB drugs that have been recently approved. These drugs provide a significant improvement in the number of voidings and in urge urinary incontinence, and their safety has been confirmed in numerous RCT (Level I).41–49 However, only a few RCT have focused on nocturia. The effects of the various types of anticholinergic drugs on nocturia will be discussed below.

(1) Propiverine: Grade of recommendation: A (Table 2):   This drug provides both antimuscarinic action and calcium antagonist action. Its pharmacokinetic effects and action of metabolites remain incompletely elucidated. Propiverine is the drug most frequently used in Japan for the treatment of pollakiuria and urinary incontinence, and its safety has been confirmed. The dose is 20 mg/day (in one dose or two partial doses). Several reports are available on studies of the efficacy of this drug in patients with nocturia.

The clinical effectiveness of propiverine in cases of pollakiuria and urinary incontinence has been studied in comparison with placebo tablets. Results showed that propiverine provided a significantly greater improvement in nocturia symptoms than the placebo control (Level I).50 In a study of the efficacy and safety of concomitant administration of propiverine and tamsulosin in comparison with tamsulosin monotherapy in patients with BPH complicated by pollakiuria and/or urinary incontinence, findings for the number of nocturnal voidings confirmed that improvement was significantly greater in the tamsulosin + propiverine combined therapy group than in the tamsulosin monotherapy group (Level I).51 We found no articles on overseas RCT of propiverin that met our literature search criteria. In some cases, this was because the overseas study used dosage levels different from those utilized in Japan, whereas in other cases the article did not discuss nocturia. However, there were a number of articles from within Japan on the efficacy and safety of this drug in nocturia.

(2) Oxybutynin: Grade of recommendation: C (Table 2):   In addition to its antimuscarinic effects, oxybutynin also acts directly as a smooth muscle relaxant and paralytic. The usual daily dose in Japan is 6–9 mg, in 2–3 partial doses. There have been no RCT regarding the effects against nocturia of the immediate-release tablets used in Japan, but a number of reports are available from overseas studies.

Johnson et al. studied 131 patients with nocturia from within a group of 197 women with confirmed urge urinary incontinence or urge-predominant mixed urinary incontinence. The researchers carried out a comparative study of behavioral therapy (pelvic floor exercises with biofeedback), anticholinergic drugs (oxybutynin 2.5–5 mg, three times daily) and placebo. Patients kept a voiding diary and data from that diary was used to evaluate effectiveness against nocturia. The researchers reported that behavioral therapy reduced the number of nocturnal voidings by 0.5 times per night, but that oxybutynin also provided significantly greater reduction (0.3 times/night, P = 0.02) than the placebo (0 times/night, P < 0.01) (Level II).52

A large-scale clinical trial of an oxybutynin patch (the MATRIX study) was carried out in 2878 patients, of whom 97.5% had confirmed nocturia. In this study, 41% of patients experienced improvement and just 10.2% experienced a worsening of their condition (Level V).53,54 In a comparative study of oxybutynin sustained-release tablets, electrical stimulation therapy and placebo for treatment of wet OAB, electrical stimulation therapy was the most effective. Oxybutynin provided a significant reduction in the number of nocturnal voidings, but the difference between oxybutynin and placebo was not statistically significant (Level II).55

(3) Tolterodine: Grade of recommendation: A (Table 2):   Tolterodine is a muscarinic receptor antagonist that was developed for the treatment of urinary urgency and urge urinary incontinence. Studies in animals and humans have shown that this product does not have muscarinic receptor subtype selectivity, and that it shows greater selectivity for the urinary bladder than for the salivary glands. This drug is relatively insoluble in lipids, which means that it has only limited potential for crossing the blood–brain barrier and is thus expected to have little effect on cognition. Tolterodine is the most widely used anticholinergic drug in Europe and the USA. It was first marketed in Japan in 2006. Its effectiveness against nocturia has been widely investigated.

In an open study enrolling 3824 patients having symptoms of OAB, administration of tolterodine sustained-release tablets was associated with significant improvement in nocturia (Level II).56,57 The level of improvement was similar to that seen in patients with urge urinary incontinence and mixed urinary incontinence (−33% vs−50%) (Level I).58 In addition, findings from a 139-patient study comparing bladder training, tolterodine monotherapy and combined therapy, the tolterodine monotherapy group showed a −65.4% change in the number of nocturnal voidings, similar to the results obtained in the bladder training group and the combined therapy group (Level II).59 In a RCT enrolling 513 patients with OAB and nocturia, but without urinary incontinence, urinary urgency was evaluated on a 5-point scale to assess OAB severity. Among those patients judged to have severe OAB, the number of nocturnal voidings was significantly reduced in the tolterodine group in comparison with the placebo group (Level I).60 Investigations have also been carried out regarding night-time administration of tolterodine and associated ADR. Night-time administration was associated with a reduction in the number of both diurnal and nocturnal voidings. In OAB patients diagnosed with urinary urgency of grade 3 or above on a 5-point scale, tolterodine provided a significantly greater improvement than the placebo in the treatment of nocturia. Additionally, findings showed that the incidence of adverse events might be lower with evening administration than with administration after breakfast (Level I).61

(4) Solifenacin: Grade of recommendation: A (Table 2):   Solifenacin is a long-acting anticholinergic drug. The drug's pharmacokinetics, characterized by Tmax values of 5–6 h and a long plasma elimination half-life of approximately 50 h, contribute to its sustained effectiveness and low incidence of ADR. In addition, solifenacin, which first reached the market in 2006, is a drug that permits flexible dosage and is now coming into wide use. Its effectiveness against nocturia has been widely investigated.

The VOLT study enrolled 2205 patients. In cases where the 5-mg dose was insufficiently effective, the dose was increased from 5 mg to 10 mg after 4 weeks. A significant improvement was seen in all OAB symptoms, including nocturia, and improvement was also noted in QOL scores related to those symptoms (Level I, Level II).62,63 Meta-analysis of four phase III clinical trials of solifenacin was reviewed with regard to various patient characteristics in OAB patients, and results were reported. For all patients, solifenacin at doses of 5 mg or 10 mg provided significant improvement in nocturia (Level I).64 Meta-analysis of elderly patients (65 years-of-age and above) showed similar results (Level I).65 Efficacy assessment in dry OAB patients showed that solifenacin 10 mg provided a significantly greater improvement in nocturia than the placebo (Level I).66 Researchers also investigated the extent to which the presence of nocturnal polyuria influenced solifenacin's effect in improving nocturia, and reported that solifenacin significantly improved nocturia in patients without nocturnal polyuria (Level I).67 In a phase III study carried out in Japan, administration of solifenacin 10 mg was associated with a significantly greater improvement than the placebo in the number of nocturnal voidings (Level I).45

(5) Imidafenacin: Grade of recommendation: E (Table 2):   Imidafenacin is characterized by its selective affinity for muscarinic receptor subtypes, with relatively high selectivity for M1 and M3 receptors. This drug is thought to act by blocking the M1 receptors on the cholinergic nerve terminals, thus reducing the amount of acetylcholine released and inhibiting bladder activity. This anticholinergic drug reached the market in 2007, and its efficacy and safety in the treatment of OAB-induced pollakiuria, urinary urgency and urge urinary incontinence were confirmed in a phase III clinical trial.68

The effectiveness of imidafenacin in nocturia was investigated in a multicenter study carried out in 37 Japanese medical facilities and enrolling 121 OAB patients who experienced two or more nocturnal voidings per night. Results showed that imidafenacin 0.2 mg twice daily for 8 weeks provided a significant improvement in nocturia, from 2.5 to 1.8 voidings per night (Level V).69 Findings also showed a correlation between the number of nocturnal voidings and quality of sleep, with imidafenacin therapy associated with a significant improvement as measured by the Pittsburg Sleep Quality Index and the Epworth Sleepiness Scale. This is the first report to clearly show that imidafenacin improves nocturia and might significantly reduce sleep disorders in OAB patients with nocturia.

b. Other drugs

(1) Flavoxate: Grade of recommendation: D (Table 2):   Flavoxate's mechanism of action on urinary bladder smooth muscles has yet to be elucidated. This drug does not have anti-muscarinic action, but provides moderate calcium antagonism and phosphodiesterase inhibition along with local smooth muscle paralytic effects. Flavoxate (200 mg/time, 3 times daily) is prescribed relatively frequently in Japan for patients with storage symptoms. Experience with the drug has confirmed that it produces almost no ADR. However, almost no research has been carried out on the effectiveness of flavoxate in patients with nocturia.

In a study of 1800 patients with urge urinary incontinence as a result of unstable bladder, reported findings showed a 53% decrease in the number of nocturnal voidings during 2-week administration of flavoxate 600–800 mg (Level III).70

(2) Capsaicin and resiniferatoxin: Grade of recommendation: F (Table 2):  Resiniferatoxin (RTX) is a neurotoxin extracted from the cactus-like plant Euphorbia resinifera. The drug provides action similar to that of capsaicin. Capsaicin and RTX, which are members of the vanilloid receptor family, selectively stimulate the unmyelinated sensory nerves (C fibers) that transmit thermal nociceptive information. At high concentrations, these substances produce a sustained and prolonged absence of response to stimulus through desensitization. Effects on nocturia have been investigated in patients with painful bladder syndrome and in patients with interstitial cystitis.

In 36 patients with severe bladder pain, injection of capsaicin 10 µm directly into the bladder provided significant improvement in nocturia in comparison with the placebo-injected group71 (Level II). There are also a number of reports available on the injection of RTX. In a small study of 18 patients complaining of bladder hypersensitivity, the RTX group showed a significant improvement in comparison with the placebo group (Level II).72 In contrast, a report from a large-scale RCT in patients with interstitial cystitis, using a single injection of RTX and with the primary end-point of global subjective improvement, showed no improvement in a variety of parameters including nocturia (Level II).73

(3) Botulinum toxin: Grade of recommendation: F (Table 2):  Botulinum toxin is thought to inhibit bladder contractions, primarily through chemical denervation that blocks the release of acetylcholine from the cholinergic nerves. The compound has also been found to inhibit the release of noradrenaline in some tissue types, and recent research suggests that botulinum toxin might also act on the centripetal nerves to inhibit the release of neurotransmitter substance. Effectiveness has also been noted against nocturia.

In 100 cases of idiopathic OAB treated by injection into the bladder of Botox A, the number of nocturnal voidings was reportedly reduced by an amount ranging from 1.5 to 4 times per night (Level III).74 An investigation of neurogenic OAB as a result of multiple sclerosis showed nocturia improvement of 33–72% over a period of 3–6 months (Level V).75

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Polyuria and nocturnal polyuria
  5. Bladder storage disorder
  6. References
  7. Appendix
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Appendix

  1. Top of page
  2. Abstract
  3. Introduction
  4. Polyuria and nocturnal polyuria
  5. Bladder storage disorder
  6. References
  7. Appendix

Appendix I

The Clinical Guidelines for Nocturia of the Neurogenic Bladder Society Committee

Committee Chairman

Osamu Nishizawa

Department of Urology

Shinshu University School of Medicine

Committee

Isao Araki

Department of Urology

University of Yamanashi, Faculty of Medicine

Osamu Ishizuka

Department of Urology

Shinshu University, School of Medicine

Naohisa Uchimura

Department of Neuropsychiatry

Kurume University, School of Medicine

Hitoshi Oh-oka

Department of Urology

National Hospital Organization, Kobe Medical Center

Seiichiro Ozono

Department of Urology

Hamamatsu University School of Medicine

Hidehiro Kakizaki

Department of Urology

Asahikawa Medical College School of Medicine

Masato Kasahara

Department of Medicine and Clinical Science

Kyoto University Graduate School of Medicine

Momokazu Gotoh

Department of Urology

Nagoya University School of Medicine

Ryuji Sakakibara

Neurology Division, Department of Internal Medicine

Toho University Sakura Medical Center

Hitoshi Shinbo

Department of Urology

JA Shizuoka Kohseiren Enshu Hospital

Kimio Sugaya

Division of Urology, Department of Organ-oriented Medicine

University of the Ryukyu Faculty of Medicine,

Yasuyuki Suzuki

Department of Urology

Jikei University School of Medicine

Atsushi Sone

Department of Urology

Kosei General Hospital

Mineo Takei

Department of Urology

Harasanshin Hospital

Masayuki Takeda

Department of Urology

University of Yamanashi, Faculty of Medicine

Akihide Hirayama

Department of Urology

Nara Medical University

Yukio Homma

Department of Urology

The University of Tokyo, Faculty of Medicine and Graduate School of Medicine

Osamu Yamaguchi

Department of Urology

Fukushima Medical University

Tomonori Yamanishi

Department of Urology

Dokkyo University School of Medicine

Osamu Yokoyama

Department of Urology

University of Fukui, Faculty of Medical Science

Masaki Yoshida

Department of Urology

Kumamoto University, Faculty of Medical and Pharmaceutical Sciences