Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diurnal antidiuretic hormone levels were studied in eleven enuretics and related to urine production and functional bladder capacity. A fluid deprivation test monitoring antidiuretic hormone levels was undertaken in four patients. The study suggests that the normal increase in nighttime antidiuretic hormone levels is absent in enuretics, who show a stable hormone level both day and night. Consequently the volume of night urine production approximates day urine production per hour. The functional bladder capacity was clearly exceeded at night in eight of eleven patients. The fluid deprivation test showed a normal response to fluid deprivation. In conclusion, the study adds further evidence that bladder capacity is a major factor in enuresis. Urine volumes that exceed bladder capacity at night may be caused by a lack of diurnal rhythmicity in antidiuretic hormone levels.
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PMID:Diurnal anti-diuretic-hormone levels in enuretics. 405 64

Various treatment modalities have been used in Primary Nocturnal Enuresis (PNE) and pharmacotherapy is widely accepted. Prostaglandins increase detrusor pressure, decrease urethral pressure and lead to sodium excretion. They also antagonize hydro-osmotic effect of vasopressin by competing with this hormone. According to these functions of prostaglandins it is suggested that inhibition of prostaglandin synthesis may have value in the management of PNE. We evaluated the efficacy or oral diclofenac sodium treatment in 78 patients. We conclude that diclofenac sodium, an inhibitor of prostaglandin synthesis, is a good alternative agent for nocturnal enuresis particularly as a supplementary treatment combined to Imipramine, with 60% complete response and 13.3% recurrence rate.
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PMID:A prostaglandin synthesis inhibitor, diclofenac sodium in the treatment of primary nocturnal enuresis. 748 20

Chronic cervical spinal cord injury is characterized by defects in sodium and water homeostasis and defects of adaptive hormonal responses. The plasma osmolality is maintained in a relatively narrow range, the lower limit of which is determined by osmotic threshold for vasopressin release and the upper limit by the third threshold. Antidiuretic hormone as an important mediator of fluid and electrolyte balance was well investigated in able bodied children comparing children with normal voiding pattern and children with enuresis. The normal subjects were found to have higher plasma ADH at night, not detected in the group with enuresis. The findings were similar in elderly patients with increased diuresis at night, suggesting an important role of ADH in nocturnal decrease of urine output. Investigators studied the effect of rapid tilt on plasma ADH in tetraplegic compared with normal subjects, but there are no data available in the literature regarding ADH and its effects on water and electrolyte balance in healthy tetraplegic subjects with a normal lifestyle. We decided to undertake a pilot study to attempt to establish baseline ADH levels in this subject group, to better understand and manage tetraplegic patients with water and electrolyte dysregulation. Our preliminary data suggest that these individuals lack the normal diurnal variation of ADH, a phenomenon similar to that demonstrated in enuretic children and elderly, and furthermore appear to have generally depressed ADH levels.
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PMID:Antidiuretic hormone levels and polyuria in spinal cord injury. A preliminary report. 775 75

The purpose of this study is to determine the efficacy of desmopressin (DDAVP), a synthetic analogue of antidiuretic hormone, as an alternative therapy in the management of spinal cord injured (SCI) patients with neurogenic bladder dysfunction unresponsive to conventional therapy. Seven SCI patients (three men and four women) were treated with DDAVP after urodynamic evaluation. Despite treatment with anticholinergic agents, urodynamic evaluation demonstrated uninhibited detrusor contractions exceeding 30 cm H2O pressure at less than 300 ml cystometric capacity in all seven patients. Three patients had been managed with intermittent self-catheterization, but had socially unacceptable short intervals between catheterizations. Two women with incomplete injury were afflicted with significant nocturia (> 3 episodes/night). The remaining two patients managed with intermittent self-catheterization were troubled with nocturnal enuresis. The patients received 10 micrograms intranasal DDAVP once every 24 hours. Prior to DDAVP administration, the four patients who used DDAVP nightly experienced a median of four episodes of nocturia. After one month of DDAVP treatment, two patients had only one episode of nocturia per night and in the other two patients, nocturnal enuresis was completely eliminated. Three patients used daytime DDAVP administration at work to avoid frequent catheterization. The median period between bladder catheterizations increased from 2.5 hours before DDAVP to 6 hours while using DDAVP. Symptomatic improvement persisted during the follow-up period of 6-20 months (mean = 12). Side effects were infrequent; only one patient complained of transient headaches. Neither hyponatremia nor serum electrolyte abnormalities occurred. Our preliminary results suggest that DDAVP is safe and effective in the symptomatic management of complicated neurogenic bladder dysfunction in selected SCI patients.
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PMID:DDAVP in the urological management of the difficult neurogenic bladder in spinal cord injury: preliminary report. 786 58

Plasma and urinary levels of vasopressin were measured by radioimmunoassay in 18 children with primary nocturnal enuresis and 20 age and sex matched controls. All subjects followed a protocol whereby all urine were collected and divided up into daytime (8 a.m.-8 pm) and night-time (8 p.m. - 8 a.m.) samples. Urine osmolality and urinary vasopressin levels were measured and, following an overnight observation period, the following morning (8 a.m.) plasma vasopressin was measured. Plasma vasopressin was significantly lower in the enuretic group (2.86 +/- 0.44 pg/ml) compared to the control group (3.64 +/- 1.35 pg/ml) (p = 0.011). Total urinary vasopressin excretion over 24 hours was lower in the enuretic group but the difference was not significant. These results support the hypothesis that one of the factors responsible for nocturnal enuresis in children may be due to a reduced nocturnal secretion of vasopressin. This may explain why the vasopressin substitution therapy is able to successfully abolish nocturnal enuresis symptoms.
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PMID:Plasma and urinary levels of vasopressin in enuretic and non-enuretic children. 793 60

A 4-year-old boy was treated with oxybutinine and desmopressine because of bladder instability associated with secondary enuresis. He was admitted with obnubilation, vomiting and experienced two seizure episodes concomitantly with hyponatremia and hypoosmolality. The child healed promptly under water restriction and intravenous administration of sodium chloride. This case report suggests that desmopressine may be responsible for severe side-effects. This drug should not be widely used and its indications should be restricted to patients with proven antidiuretic hormone secretion abnormalities.
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PMID:[Desmopressin and water intoxication. Apropos of a case treated for enuresis]. 801 69

Desmopressin is a potent antidiuretic for nocturnal enuresis with few and mostly insignificant adverse reactions. Almost 80 years ago, the antidiuretic effects of extracts of the posterior pituitary were first reported. The molecular structure of the peptide vasopressin arginine vasopressin (AVP) became known in 1956, and by 1967, a synthesized modification of AVP, known as DDAVP, or desmopressin, was introduced. Toxicity studies performed on experimental animals support the conclusion that desmopressin is considerably more potent as an antidiuretic than AVP and has an exceptional safety margin. Further, clinical experience reveals that from 1974 to June 1992 only 21 patients using desmopressin had serious adverse reactions (water intoxication), and no fatalities occurred. Seven of 10 children with nocturnal enuresis who receive desmopressin stop their bedwetting completely or reduce it significantly, with best results noted in children over 10 years of age. Given these results, the preferred treatment in Europe for children with nocturnal enuresis is the sequential combination of desmopressin and the enuresis alarm.
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PMID:Efficacy, safety, and dosing of desmopressin for nocturnal enuresis in Europe. 803 34

Conclusive evidence of a polyuric etiology from a failure of vasopressin elevation led to a new pharmacologic approach to the treatment of childhood nocturnal enuresis. Desmopressin acetate, a vasopressin analogue, has been used successfully since 1978 to treat this condition. Desmopressin's efficacy at doses of 5 to 40 micrograms has been demonstrated in Europe and the United States. Similarly, its safety has been established, and it is a first-line choice for physicians worldwide.
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PMID:The American experience with desmopressin. 803 36

Bedwetting is the most common urologic complaint among children. Wetting frequency at age 7 years varies from 5% to 15%. Treatment has been multimodal: drugs to depress bladder activity, increase urethral resistance, or modulate sleep; electrophysiologic treatment; and, recently, urine production modulation. All of these approaches reflect a lack of sufficient knowledge of the underlying pathophysiology of nocturnal enuresis. Over the last 13 years, enuresis studies at the Institute of Experimental Clinical Research, the University of Aarhus, Denmark, have focused on sleep disturbances, bladder reservoir function, urine output, and a combination of the three. Sleep studies indicate that: enuretic patients are normal sleepers; the voiding characteristics of an enuretic episode are similar to those of voluntary voiding during the day; and enuresis can take place during any stage of sleep, but generally occurs when the bladder is filled to the equivalent of maximal daytime functional capacity. Bladder reservoir capacity appears to be normal and bladder instability an unimportant factor in the pathology of nocturnal enuresis. However, enuretic patients have been shown to lack the normal nocturnal increase in antidiuretic hormone levels and had nocturnal urine production up to four times the volume of functional bladder capacity, which explains the need for bladder emptying. These findings open new avenues to the approach to treatment based on antidiuretic therapy.
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PMID:The pathophysiology of enuresis in children and young adults. 803 40

The lack of circadian rhythmicity of plasma arginine vasopressin (AVP) in primary nocturnal enuresis (PNE) in some children is known. The original test protocol is time-consuming and needs excellent compliance by children and parents. The goals of the presented study are the introduction of a simple screening test and the evaluation of the response of treatment using intranasal synthetic vasopressin. Fifty-five children (aged 8.2 +/- 3.1 years) with PNE and 15 children (aged 7.9 +/- 2.4 years) of a control group were investigated. Using a standardized protocol, AVP levels were measured by radioimmunoassay (RIA) under controlled water intake 3 times per day over a period of 72 h. Fourteen of 55 tested children (25.5%) with PNE had a significant decrease in nocturnal AVP when compared to the control group. We measured also an increased nocturnal urine volume and a lower urine osmolality in this enuretic group. Eight of 14 patients (57.1%) with plasma AVP deficiency (AVPD) also had bladder instability. Nine of 14 patients (64.3%) with AVPD with or without concomitant bladder instability were totally dry during desmopressin treatment, but only 2 (14.3%) remained dry after discontinuation of treatment. Our data suggest that nocturnal urine osmolality measurement may reflect AVPD and predict a positive treatment outcome.
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PMID:Vasopressin deficiency in primary nocturnal enuresis. Results of a controlled prospective study. 826 4


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