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)

Psychotropic drugs, as well as some psychiatric disorders, can produce neurotoxic and life-threatening abnormalities of water and electrolyte balance that require prompt and appropriate medical intervention. Compulsive fluid intake by psychotic patients (primary polydipsia) can produce delirium due to water intoxication with hyponatremia. Several psychotropic drugs cause water retention by decreasing renal clearance, as in the syndrome of inappropriate antidiuretic hormone secretion. Lithium and other agents interfere with renal resorption of water to cause nephrogenic diabetes insipidus. Clinical signs in these disorders range from lethargy and confusion to stupor, seizures, coma, and death. This overview provides a conceptual framework for differentiating among and safely managing these relatively common disorders.
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PMID:Primary and drug-induced disorders of water homeostasis in psychiatric patients: principles of diagnosis and management. 1037 Apr 44

Rathke's cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernig's sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. Magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.
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PMID:Hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report. 1046 7

To analyze the physiological functions of CLC-K1 in vivo, we generated mice lacking CLC-K1 by targeted gene disruption. Homozygous mutant Clcnk1-/- mice produced approximately 5 times more urine than Clcnk1+/- and Clcnk1+/+ mice. After 24-hour water deprivation, Clcnk1-/- mice became severely dehydrated and lethargic. Intraperitoneal injection of the V2 agonist, deamino-Cys(1), D-Arg(8) vasopressin, induced an increase in urine osmolarity in Clcnk1+/- and Clcnk1+/+ mice from approximately 1,000 to approximately 3,000 mosm/kg H(2)O, whereas the increase in Clcnk1-/- mice was only from approximately 600 to approximately 840 mosm/kg H(2)O, indicating nephrogenic diabetes insipidus in Clcnk1-/- mice. These results clearly established that CLC-K1 plays a major role in the urinary-concentrating mechanisms.
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PMID:Severely impaired urine-concentrating ability in mice lacking the CLC-K1 chloride channel. 1101 33

We present the case of a 6-week-old male infant who had a convulsion due to pertussis pneumonia. He was admitted to our emergency department because of lethargy and hypothermia. He developed a generalized tonic-clonic convulsion, requiring various treatments, including artificial ventilation. A chest CT showed bilateral pneumonia and laboratory data revealed hyponatremia with other features of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although SIADH has been recognized as a cause of hyponatremia in association with pneumonia, there is little in the literature regarding SIADH caused by pertussis. Hyponatremia caused by SIADH must be considered as a differential diagnosis of seizures in pertussis infection of infants.
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PMID:Pertussis pneumonia complicated by a hyponatremic seizure. 1297 26

Traumatic hypopituitarism was diagnosed in an 11-month-old male neutered cat. The presenting complaints were polydipsia, polyuria and lethargy of three months' duration. Craniocerebral trauma, as a result of a road traffic accident, had preceded the onset of clinical signs by six weeks. Neurological examination revealed right-sided mydriasis, reduced visual and tactile left forelimb placing reflexes and decreased proprioception in both the left fore- and hindlimb. Initial laboratory findings included hypernatraemia, hyperchloraemia, mild azotaemia, eosinophilia and isosthenuria. Low basal cortisol, thyroxine, thyroid-stimulating hormone and insulin growth factor-1 were noted. Subsequent to treatment with prednisolone, a water deprivation test confirmed the presence of central diabetes insipidus and therapy with synthetic antidiuretic hormone successfully ameliorated the polydipsia.
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PMID:Traumatic partial hypopituitarism in a cat. 1535 10

A previously healthy 30-day-old girl presented with seizures, irritability and inability to sleep for three days. Vitamin K was not given just after birth. She was lethargic. A multifocal clonic seizure was evident during examination. Anisocoria was diagnosed on eye examination. Brain magnetic resonance imaging showed intracerebral hemorrhage, ventricular dilatation, and hematoma in the left temporofrontal region extending to the hypothalamus. Central diabetes insipidus was diagnosed by water deprivation due to dehydration and hypernatremia, and then desmopressin was added to phenobarbital. The possible mechanism of central diabetes insipidus in our patient is damage of vasopressin pathway resulting from compression of hemorrhage. An operation of ventriculoperitoneal shunt was also performed due to hydrocephalus. While she was symptom-free except for neurological sequel during routine control examinations after discharging from hospital, the parents said that she died, most probably from bronchopneumonia, at the age of 7.5 months. In conclusion, we emphasize that prophylactic vitamin K should be administrated to all babies just after birth, and infants with intracranial hemorrhage should carefully be monitored for central diabetes insipidus.
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PMID:Central diabetes insipidus following intracranial hemorrhage due to vitamin K deficiency in a neonate. 1630 78

The syndrome of inadequate secretion of the antidiuretic hormone (SIADH) is a very rare complication after carotid endarterectomy, characterized by hyponatremia, decrease of serum osmolarity as well as an increase in urinary osmolarity. We report the case of an 80-year-old woman who developed, 24 hours after the surgery, a picture of drowsiness and lethargy without neurological focality. The diagnosis of SIADH was suspected. We conclude that is important to have in mind this clinical entity in the differential diagnosis of non-focal neurological deficit after carotid endarterectomy.
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PMID:Inappropriate secretion of antidiuretic hormone: a rare complication after carotid endarterectomy. 1686 Oct 16

Hyponatremia is often associated with arginine vasopressin (AVP) dysregulation that is regulated by the hypothalamo-neurohypophyseal tract in response to changes in plasma osmolality, commonly in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Potentially lethal complications of hyponatremia most frequently involve the central nervous system and include anorexia, fatigue, lethargy, delirium, seizures, hypothermia and coma, and require prompt treatment. Chronic hyponatremia also complicates patient care and is associated with increased morbidity and mortality, particularly among patients with congestive heart failure. Conventional treatments for hyponatremia (e.g. fluid restriction, diuretic treatment, and sodium replacement) may not be effective in all patients and can lead to significant adverse events. Preclinical and clinical trial results have shown that AVP receptor antagonism is a promising approach to the treatment of hyponatremia that directly addresses the effects of increased AVP and consequent decreased aquaresis, the electrolyte-sparing excretion of free water. Agents that antagonize V(2) receptors promote aquaresis and can lead to increased serum sodium. Dual-receptor antagonism, in which both V(2) and V(1A) receptors are blocked, may provide additional benefits in patients with hyponatremia.
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PMID:Hyponatremia, arginine vasopressin dysregulation, and vasopressin receptor antagonism. 1717 May 24

Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is a common occurrence in inpatients with psychiatric disorders. The underlying pathophysiology of this syndrome is unclear, and multiple factors have been implicated, including a hypothalamic defect and adverse medication effects. Hyponatremia in PPD can progress to water intoxication and is characterized by symptoms of confusion, lethargy, and psychosis, and seizures or death. Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities.
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PMID:Psychogenic polydipsia review: etiology, differential, and treatment. 1752 21

The use of psychotropic drugs has been frequently associated with hyponatremia, which is defined as a serum sodium level of less than 136 mEq/l. The main cause in the psychiatric population is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Age, female sex and polypharmacy are risk factors for hyponatremia. In psychiatric patients, the symptomatology caused by hyponatremia may be confused with the mental illness itself, delaying its diagnosis. Early symptoms are nausea, vomits, anorexia, headaches, weakness, irritability, agitation, lethargy, confusion and cramps. The risk of hyponatremia increases with the use of several psychiatric drugs associated with SIADH. This complication is more often diagnosed at the first weeks of treatment. The first step of treatment is to determine the real level of hypoosmolality by measuring plasmatic osmolality. A urinary osmolality equal to or higher than 100 mOsm/kg combined with an elevated concentration of urinary sodium may lead to the diagnosis of SIADH. The main treatment for drug-caused hyponatremia is medication monitoring and normalization of extracellular liquid volume. In most cases this is achieved by discontinuing medication and restricting fluid intake.
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PMID:[Hyponatremia associated with psychotropic drugs: a side effect to consider]. 1942 19


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