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 syndrome of inadequate secretion of antidiuretic hormone (SIADH) following treatment with a tricyclic antidepressant is demonstrated using the example of a 70 year-old man admitted for weakness and cognitive disturbances. Because of incontinence he had been periodically treated since 1989 with imipramine (Tofranil) by his family doctor. On admission he was seriously hyponatriemic and had low plasmatic osmolality, significantly lower than urinary osmolality. Creatinine, urea and uric acid in serum were also below normal values. Like other drugs tricyclic antidepressants can rarely induce an increased release of ADH by direct hypothalamic stimuli. In this patient imipramine was terminated and within a few days of reduced fluid intake and substitution of sodium a sustained clinical improvement and normalisation of laboratory parameters was noted. The patient was discharged to his home after three weeks.
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PMID:[Clinical-pharmacological case report: drug-induced inappropriate ADH secretion]. 144 36

We report a 52-year-old male patient with Shy-Drager syndrome (SDS) complicated by an occurrence of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The patient first developed impotence at the age of 48, accompanied by urinary incontinence, and episodes of dizziness while standing. The following year, the patient had developed a staggering gait and speech became monotonous. At age 52, the patient was admitted to the hospital after experiencing frequent episodes of syncope associated with complete loss of consciousness. Upon examination, blood pressure was 100/70 in a recumbent position, and 80/60 when standing. The pulse rate varied from 60 per minute to 62. The patient was alert. The alternating Horner sign was observed, and a paucity of facial movements was visible. His speech was slow and monotonous. Muscle tone was increased bilaterally. There was incoordination. A laboratory examination revealed reduced serum sodium levels of 127 mEq/L and increased sodium excretion with plasma hypoosmolality (262 mOsm/kg/H), urine hyperosmolality and low serum renin activity (0.2 ng/ml/h). Renal functions were normal and the levels of adrenocortical and thyroid hormones were normal. There were no abnormalities observed in the chest roentgenogram taken. The level of antidiuretic hormone (ADH) was unreasonably high (5.74 pg/ml). A water-load test demonstrated failure of both water diuresis and inhibition of ADH secretion. These data suggested that hyponatremia in this case was caused by SIADH. The correlation between plasma osmolality and the concentration of ADH suggested that osmolality that initiates ADH release appeared to have been reset to around 230 mOsm/kg lower than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Shy-Drager syndrome and the syndrome of inappropriate secretion of antidiuretic hormone]. 161 76

Thirteen patients with advanced multiple sclerosis and urge urinary incontinence were treated with desmopressin--a synthetic analogue of antidiuretic hormone--in a double-blind cross-over study. The micturition frequency decreased significantly (p less than 0.05). Less leakage was considered valuable for daily life. Peroral medication was favourable in these patients with muscular dysfunction. Side-effects were few.
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PMID:Desmopressin: a new principle for symptomatic treatment of urgency and incontinence in patients with multiple sclerosis. 219 44

Although nursing homes are potentially important sites for geriatric research, previous reports have identified impediments to subject recruitment in this setting. We are conducting five simultaneous clinical studies in a 725-bed nursing home. Utilizing a systematic subject recruitment methodology designed to minimize patient and staff burden, we have recruited over 100 subjects. The average recruitment rate over two years from nursing home residents meeting study entry criteria was 43%. The rate was highest (81%) for a study of urinary incontinence offering direct benefit to participants, and lowest (28% and 14% respectively) for physiologic studies of vasopressin regulation and dermal vitamin D production, offering no direct benefit. Studies of syncope and dementia which benefitted groups affected by these problems but not controls, had intermediate recruitment rates (46 and 44%, respectively, P less than .002 compared to incontinence). Thus, clinically relevant projects, sensitive to the needs of the patient and institution, can recruit subjects from the nursing home.
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PMID:Biomedical research in the nursing home: methodological issues and subject recruitment results. 358 66

Primary NE is probably a condition rooted in biologic problems. There is a strong hereditary component. Altered nervous system function may lead to disorganization of how bladder function is controlled and how vasopressin is released. In extreme cases, this disorganization may also be reflected in psychologic issues, such as attention-deficit disorder. Primary NE should not be viewed as laziness of the child, but as an obstacle the child needs professional help to hurdle. The practitioner should collaborate with a pediatrician, urologist, and psychologist in managing children who wet. Routine office evaluation should exclude incontinence as a cause of wetting. When a screening ultrasonogram is normal, this helps the practitioner determine that striking birth defects are unlikely. Follow-up of management by interview with interested staff is necessary. Wetting is reliably correctable and probably best addressed by combination treatment structured as an ETP. Specific treatments vary according to personal preferences. The treatment with strongest scientific research, desmopressin, may be the least effective for cure. The most effective treatment for cure, alarm with behavior reinforcement, is the least often prescribed. A miscellany of adjunctive treatments should be suggested when there are abnormalities in functional bladder capacity, defecation, urethritis, vulvitis, diet sensitivity, upper-airway obstruction, and other areas.
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PMID:Diagnosis and treatment for children who cannot control urination. 828 78

Central autonomic dysfunctions can be due to primary (degenerative) or secondary disorders. Autonomic failure (AF) may be a major manifestation of multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD). In both MSA and IPD, AF is almost invariably associated with neuronal loss in the intermediolateral cell columns. Dysautonomia in MSA is early, severe, and progressive, including marked orthostatic hypotension and urinary incontinence and is complicated by respiratory disturbances, such as laryngeal stridor and sleep apnea. MSA/AF can be differentiated from primary (or pure) autonomic failure (PAF) without central nervous system involvement. PAF is mainly a disorder of the postganglionic neurons. In contrast to PAF, MSA/AF has preserved basal sympathetic activity, decreased cerebrospinal fluid (CSF) neurotransmitter markers, impaired vasopressin response to hypotension, and impaired adrenocorticotrophic hormone/beta endorphin response to hypoglycemia. AF in IPD is generally less severe than in MSA. Poor response to L-Dopa, abnormal urethral sphincter electromyography, and CSF markers may distinguish MSA from IPD. Secondary autonomic disorders may result from traumatic, vascular, inflammatory, demyelinating, or neoplastic lesions involving corticolimbic, hypothalamic, brainstem, or spinal autonomic network. These disorders can cause AF or autonomic hyperactivity, such as arrhythmia, hypertension, and hyperthermia. However, many disorders may only produce subclinical abnormalities.
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PMID:Central autonomic disorders. 845 95

Autonomic dysfunction is responsible for much of the morbidity associated with frequently encountered neurological disorders, such as Parkinson's disease, multiple sclerosis, cerebrovascular disease, and peripheral neuropathies, as well as with the rarer primary autonomic nervous system degenerations. We review the treatment of those aspects of autonomic dysfunction that often present to the neurologist, including orthostatic hypotension, urinary incontinence and retention, and bowel dysmotility syndromes. Pathophysiology is discussed in each instance as it relates to a rational approach to therapy. For management of orthostatic hypotension, we review the use of mineralocorticoids, direct and indirect sympathomimetic agents, other pressors, dopamine-blocking agents, vasopressin receptor agonists, and others. Treatment of urinary incontinence and retention is addressed, with attention to drugs that modulate bladder contractility and bladder outlet resistance. Therapies for bowel dysmotility syndromes (such as gastroparesis, diarrhea, and fecal incontinence) are described, including bulk agents, laxatives, prokinetic agents, and antidiarrheal drugs.
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PMID:The treatment of autonomic dysfunction. 845 96

Bladder dysfunction with increased voiding frequency and incontinence is a common problem in patients with multiple sclerosis (MS). In the present study, the effect of the synthetic vasopressin analogue, desmopressin, was evaluated on the voiding frequency in 26 patients with MS suffering from socially handicapping voidings and incontinence problems during daytime. A two-week run-in observation period to establish normal voiding patterns was followed by a double-blind, placebo-controlled cross-over study with 20 micrograms intranasal desmopressin during daily activities. There was a significant decrease in the number of voidings during the 6-h period after intranasal intake of desmopressin. Side effects were well tolerated and there was no hyponatremia or hypertension registered. Intranasal desmopressin is an efficient and well-tolerated treatment of voiding problems in patients with MS during daily activities.
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PMID:Nasal spray desmopressin treatment of bladder dysfunction in patients with multiple sclerosis. 887 90

A 79-year-old woman suffering from urinary incontinence and unsteady gait was diagnosed as having idiopathic normal pressure hydrocephalus (NPH) with hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The concentration of antidiuretic hormone was high while the plasma osmolality was low in the presence of concentrated urine during the episodes of hyponatremia. Magnetic resonance imaging (MRI) of the head showed enlargement of the third and lateral ventricles. After ventriculoperitoneal shunt surgery, the symptoms of NPH and hyponatremia improved. It may be possibly explained that mechanical pressure on the hypothalamus from the third ventricle is responsible for hyponatremia.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone associated with idiopathic normal pressure hydrocephalus. 1033 45

Excess intake of water by schizophrenic patients is referred to as psychiatric polydipsia. This symptom causes incontinence, vomiting and hyponatremia, and may sometimes lead to death. We have no effective therapeutic methods other than administrating sodium chloride solution and diuretics, or restricting the intake itself. A case was reported stating that demeclocycline, used in case where there is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), was effective for the treatment of psychiatric polydipsia. We administered demeclocycline to 8 schizophrenic patients with psychiatric polydipsia, and noticed improvement in incontinence, vomiting and hyponatremia. There was also a decrease of polydipsic behavior. Demeclocycline inhibits the antidiuretic effect of vasopressin on the distal renal tubule. Considering the function of demeclocycline and the relevance of vasopressin to the central nervous system, it has been suggested that demeclocycline has effects on the central nerve through vasopressin or cyclic AMP.
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PMID:[Effects of demeclocycline on psychiatric polydipsia in schizophrenic patients]. 1037 40


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