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)

A five-year experience with the vasopressin analogue desmopressin acetate (DDAVP) for nocturnal enuresis is described in 59 children. The initial starting dose of 5 micrograms at bedtime is lower than that reported in other series. Eighty-one percent of patients required 10 micrograms or less to achieve improvement or resolution of bedwetting.
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PMID:Low-dose DDAVP in nocturnal enuresis. 158 97

An update of the pathogenesis and treatment of monosymptomatic bedwetting is presented. This frequently occurring entity seems to have a multifactorial pathogenesis incorporating arousal disturbances and disturbances to the circadian rhythm of diuresis modulating hormones. It has recently been substantiated that the bladder reservoir function in monosymptomatic bedwetting is normal. This is further underlined by the fact that treatment of instability of the bladder has proven futile. In a substantial part of the monosymptomatic bedwetters the changes in circadian rhythm of antidiuretic hormone can be counteracted by desmopressin diacetate (DDAVP), which abolishes the symptom in more than 2/3 of the patients. Monitoring circadian rhythms of arginine vasopressin (AVP) and treatment with DDAVP have led to increased understanding of the pathogenesis of monosymptomatic bedwetting and opened new fields of investigation.
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PMID:Monosymptomatic bedwetting. 160 54

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

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

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

Nocturnal enuresis is considered a benign condition partially explained by a defect circadian rhythm of vasopressin. An organic cause may be responsible for an abnormal pituitary function, when enuresis persists into adulthood. In the present study the pituitary gland and surroundings of 8 adults suffering from primary monosymptomatic nocturnal enuresis were studied by magnetic resonance imaging. The pituitary gland appeared normal in all, except from a Rathke's cleft cyst observed in one patient. This cleft cyst was not considered to be clinically important. It was concluded, that severe nocturnal enuresis persisting into adulthood is not likely to be combined with detectable pathology on magnetic resonance imaging of the pituitary gland.
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PMID:The pituitary gland in nocturnal enuresis: MR findings. 873 50

Nocturnal enuresis has several possible causes, including genetic inheritance, reduced bladder capacity, sleep disorders, abnormal secretion of antidiuretic hormone, psychologic abnormalities, neurologic dysfunction, bacteriuria, and diet. A through assessment of the patient's voiding history is of major importance in the management of nocturnal enuresis. Whether the patient has monosymptomatic or polysymptomatic nocturnal enuresis must be determined. Treatment options include pharmacotherapy, behavioral modification with an alarm system, or a combination of these modalities. In order for treatment to be successful, the physician, patient, and patient's parents must be involved in the decision-making process.
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PMID:Nocturnal enuresis: a guide to evaluation and treatment. 879 Feb 62

Body fluid homeostasis is maintained by the kidney. Such an accurate control in achieved via the secretion of antidiuretic hormone (ADH), the secretion of which is regulated by hypothalamic osmoreceptors. Both urine flow rate and the excretion of most electrolytes have a diurnal rhythm; they increase during daytime and decrease during nighttime. Such a rhythm seems to be absent in some subjects who suffer from bedwetting because of relative polyuria. In these cases, the polyuria is associated with a decreased nocturnal secretion of ADH and the subsequent excretion of dilated urine. A deficit in the nocturnal secretion of ADH thus appears to explain the response to desmopressin of children with a polyuric form of enuresis.
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PMID:[Endocrine theory of idiopathic nocturnal enuresis]. 918 Oct 1

After allergic disorders, nocturnal enuresis is the most common chronic childhood condition. Recent research has yielded abundant new knowledge about the condition, especially about its aetiology and pathophysiology, and the psychological consequences. A hereditary background has been substantiated by the identification in genetic linkage studies of areas in chromosomes 12 and 13 that are manifestly associated with bedwetting, though genotype expression in the phenotype appears to be complex and heterogeneous. Pathophysiologically, findings in current intensive research suggest three interactive factors to be involved: (i) relative nocturnal polyuria, due to insufficient antidiuretic hormone release during sleep in pre-teenagers, and due to renal tubular dysfunction in adolescents and adults; (ii) reduced nocturnal bladder capacity, especially in the 33 per cent of cases which do not respond to desmopressin treatment; and (iii) the patient's inability to waken in response to signals from a full bladder. Recent findings have also confirmed previous reports that with very few exceptions bedwetting is not caused by psychological factors. On the contrary, the condition causes psychological problems manifested in reduced self-esteem, shame and guilt, though self-esteem is restored by successful treatment. Active treatment should be started as soon as the child is ready to receive it, the main options being an enuresis alarm, desmopressin, or a combination of the two. If reduced bladder capacity is suspected, treatment with a detrusor relaxant should be included.
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PMID:[Nocturnal enuresis in children]. 946 1

Primary nocturnal enuresis is common and has considerable psychological ramifications for children as they get older. It is a familial condition with complex inheritance patterns. The pathophysiology of the condition appears to be related to poor arousal from sleep, nocturia due to deficient vasopressin release in sleep and possibly a decrease in functional bladder capacity especially at night. The mainstay of treatment is the bed-wetting alarm. In recent years, desmopressin nasal spray has found a clinical niche as a short-term solution for children attending school camps or sleeping over at friends' houses and as treatment in the medium term for those unresponsive to treatment with a bed-wetting alarm. It may also be used as an adjunct to the use of the alarm. Treatment with imipramine is increasingly in disfavour because the relapse rate is unacceptably high and fatal overdose is a real possibility.
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PMID:Nocturnal enuresis: what is happening? 1072 98


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