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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of primary nocturnal enuresis using DDAVP is based upon the hypothesis that antidiuretic hormone (ADH) secretion is insufficient at night. The known efficacy of the treatment on the one hand, and persisting doubts about its theoretical basis on the other, formed the background of the present study. Ten children (mean age 10.5 years) with primary nocturnal enuresis were compared with a corresponding control group of eight patients. Diurnal and nocturnal urine production, ADH secretion, and plasma osmolality were determined. No differences between the two groups were found for urine production, ADH levels during day and night, or plasma osmolality. However, in order to regulate plasma osmolality the enuretic children required a markedly greater output of ADH: 2.87 (95% confidence interval 0.091 to 40.35) pg/ml/mmol/kg v 0.56 (0.08 to 1.03) in the controls (p < 0.01). The results are consistent with the established fact that ADH secretion is a function of plasma osmolality, and they contradict the hypothesis that urine production is increased at night in enuretics because of lower ADH secretion. The findings do not solve the uncertainties in the pathogenesis of enuresis but they suggest there might be a difference between enuretic children and controls at the ADH receptor level.
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PMID:Antidiuretic hormone regulation in patients with primary nocturnal enuresis. 854 6

Although nocturnal enuresis was first described centuries ago, there is still a lot unknown about its pathophysiology. The functional bladder capacities, diurnal vasopressin levels, urine osmolalities and urine output of enuretic and normal children were compared. We have concluded that enuretics have normal bladder capacities insufficient for increased nocturnal urine volumes because of loss of diurnal variation in serum vasopressin levels and related decrease in urinary osmolalities.
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PMID:Enuresis nocturna: new concepts in pathophysiology. 858 17

Desmopressin is a commonly used, well-tolerated agent for the treatment of primary nocturnal enuresis and central diabetes insipidus. Intranasal desmopressin provides symptomatic relief with few serious complications. A 29-year-old woman with a long history of primary nocturnal enuresis began treatment with intranasal desmopressin. Although the enuresis ceased, she developed throbbing headaches, nausea, vomiting, paresthesia, lethargy, fatigue, and altered mental status over the next 7 days. When she came to the emergency room her sodium concentration was 127 mmol/L. The history of desmopressin use was not obtained at that time. She was treated with intravenous fluids and discharged. The symptoms returned and worsened over the next 4 days, and she returned to the emergency room stuporous. A repeat sodium was 124 mmol/L, and she was admitted. The history of desmopressin use was still not available. Medical evaluations included computerized tomography, lumbar puncture, complete blood counts, serum chemistries, and serologies. The next morning the woman was improved and informed clinicians of her desmopressin use. Without other causes for the hyponatremia, she was diagnosed with the syndrome of inappropriate antidiuretic hormone, presumably caused by desmopressin. Within 24 hours of fluid restriction and cessation of desmopressin, her symptoms and hyponatremia resolved. A review of the literature found 11 children and 2 adults in whom intranasal desmopressin was associated with hyponatremia, all of whom experienced seizures or altered mental status. Our patient illustrates the importance of early recognition and treatment of hyponatremia before the onset of seizures. When vague symptoms develop during desmopressin therapy, hyponatremia must be considered as part of the differential diagnosis. It may also be prudent to screen for electrolyte abnormalities in patients taking this agent to prevent serious iatrogenic complications.
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PMID:Intranasal desmopressin-induced hyponatremia. 888 98

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

Twenty-three patients (5 to 15 years of age) with primary nocturnal enuresis were treated with desmopressin (DDAVP) according to a four-step protocol with weekly reductions of daily doses (1 to 0.25 microgram/kg body weight) thus including aspects of behavior-oriented "bladder retention training". The rate of wet nights was significantly reduced while patients were on medication (p < 0.02), but the sample as a whole returned to baseline levels after medication was stopped. Six subjects (26%) were non-responders. A variety of psychological and psychosocial single factors did not significantly affect the outcome. However, a subgroup of seven patients assessed as "psychologically non-distressed" revealed better results both on medication (p < 0.02; reduction 73%) and off medication (p > or = 0.05; reduction 39%) compared to a "distressed" subgroup (N = 16). Both groups showed significant changes in wet nights over the treatment course (p < 0.02 and p > or = 0.002, respectively). There was no clear-cut relationship between laboratory data (urine volume, osmolality, vasopressin) and outcome in wet nights. Data did not suggest a subgroup of patients with particularly low nocturnal vasopressin (AVP) secretion and, thus, high rates of wet nights. Our results corroborated the finding that DDAVP is an effective substance in reducing wet nights in patients with primary nocturnal enuresis. However, with respect to major reductions and long-term results (off medication), these preliminary findings suggest that "psychological distress" seems to be a very important confounding outcome variable. Thus, careful consideration and assessment of psychological and psychosocial aspects of distress are recommended. Eventually, a combination of DDAVP treatment with counseling and/or psychotherapy may significantly improve results for the majority of patients and families.
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PMID:Primary nocturnal enuresis and desmopressin treatment: do psychosocial factors affect outcome? 881 16

Prospective controlled studies on the treatment of enuresis with desmopressin (DDAVP) indicate that cure rates (complete dryness) while on therapy are markedly lower than are response rates (decrease in wet nights). In an attempt to explain this discrepancy, we analyzed the etiological mechanisms for enuresis and found evidence that most children are not cured by DDAVP because their nocturnal wetting is not actually caused by the defect which DDAVP therapy aims to cure: low nocturnal vasopressin secretion with high nocturnal urinary output. Our study suggested that an arrest in the normal development of two separate areas of the central nervous system is necessary for enuresis to occur in many patients, yet cure of enuresis occurs if either developmental delay is eliminated. This hypothesis of a dual developmental delay helps to unify many diverse and often seemingly contradictory scientific observations about this condition and to explain why many patients react inconsistently to treatment aimed at a single etiology, yet eventually become dry.
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PMID:Cure of nocturnal enuresis: why isn't desmopressin very effective? 889 81

Water intoxication is a serious condition which may be caused by desmopressin overdose, with reversible or irreversible neurological complications. In the past, desmopressin was used in endocrinological centers for the treatment of antidiuretic hormone deficiency (central diabetes insipidus). Indications for hormone treatment have since widened, especially as an effective solution for nocturnal enuresis. It is now often prescribed in community clinics, and its use has been encouraged by extensive promotion. We describe a 15-year-old boy with primary nocturnal enuresis who started treatment with desmopressin 1 year prior to admission. He was allowed to use the drug without supervision, and drank excessively. The result was water intoxication which required admission for intensive care because of loss of consciousness and convulsions for 36 hours.
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PMID:[Water intoxication following desmopressin overdose]. 915 15

Interactions between the central nervous system, bladder and kidneys have been investigated for many years in animal studies and have shown that bladder distension, in animals, leads to decreased urine production. The objectives of the current study were to determine the effect of a full bladder on urinary output, vasopressin secretion and urine osmolality in humans. The study involved healthy volunteers. They were studied for a period of 48 hours. This period included two 24-hour studies, one involving regular and frequent voidings (to produce a minimal bladder filling) and the other voiding postponement (to produce maximal bladder distension). In contrast to enuresis studies a circadian rhythm of vasopressin secretion was observed in the males involved in this study, whereas no significant rhythm of vasopressin secretion could be detected in the female subjects. However, this study was unable to confirm that, in humans, a full bladder causes a decrease in urine production, an increase in vasopressin secretion or an increase in urine osmolality.
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PMID:The effect of the full bladder on vasopressin secretion in healthy young adults. 916 1

Aquaporins are proteins that mediate transmembrane water transport in a variety of tissues including the kidney. Vasopressin plays an important role in regulation of water metabolism, and under normal conditions the kidney collecting duct is extremely sensitive to vasopressin. Vasopressin stimulates the synthesis of aquaporin 2 (AQP2) in kidney collecting duct principal cells. Studies in Brattle Boro rats which are vasopressin deficient, revealed low levels of AQP2 in association with extreme polyuria. After vasopressin treatment for 5 days AQP2 levels increased threefold. Using rat models with nephrogenic diabetes insipidus (NDI) we have demonstrated that AQP2 expression is down regulated in association with polyuria, suggesting that reduced levels of AQP2 may be a general factor in acquired forms of NDI from a variety of reasons. The polyuria and urinary concentrating defects associated with an abnormal nightly-increase in AVP in patients with nocturnal enuresis may partly be due to a lack of vasopressin-mediated AQP2 expression since treatment with desmopressin in these patients have normalised their nocturnal urine production.
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PMID:Do aquaporins have a role in nocturnal enuresis? 916 2


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