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 hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.
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PMID:Vasopressin: deficiency, excess and the syndrome of inappropriate antiduretic hormone secretion. 10 6

A 15 year old girl presented with excessive thirst and hypertension (170/110 mm Hg). Biochemical investigations revealed serum sodium 118 meq/liter, serum osmolality 238 mosmol/liter, urine sodium 90 meq/liter, urine osmolality 700 mosmol/liter, persistenly elevated serum antidiuretic hormone (ADH) levels (5.8 to 11.9 pg/ml) and no obvious cause for the hypertension. The hypertension is, at least in part, volume-related, diminishing with fluid restriction. Features of gross water intoxication (e.g., confusion, coma) have not occurred. The etiology of the inappropriate secretion of ADH is not obvious but is not thought to be due to "resetting of osmoreceptors" as evidenced by failure to maximally dilute urine following a water load test and persistently elevated serum ADH levels. A similar patient described by Epstein and associates in 1962 is presently well with persistent features of inappropriate secretion of ADH.
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PMID:Idiopathic, sustained, inappropriate secretion of ADH with associated hypertension and thirst. 47 98

Two patients with myxedema coma and extreme hyponatremia associated with the syndrome of inappropriate secretion of antidiuretic hormone are described. Both recovered following i.v. hypertonic saline, furosemide and thyroxine. A review of 22 cases from the literature suggests that this therapeutic approach could improve the poor prognosis in this condition.
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PMID:Hyponatremia in myxedema: a suggested therapeutic approach. 52 76

Eighty-eight patients with craniocerebral trauma were studied prospectively to assess the effects of the injury on sodium and water balance. Abnormalities of serum sodium and osmolality occurred in 11 of the 76 patients who were on the study more than 24 hours, and the incidence of these abnormalities was directly related to the severity of the craniocerebral injury. Hyponatremic hypo-osmolar states were as frequent as were hypernatremia and serum hyperosmolality. The major cause of the hyponatremia was inappropriate antidiuretic hormone secretion; hypernatremia was due to dehydration and occurred predominantly in comatose patients with increased insensible fluid losses associated with pyrexia. We recommend that the initial fluid intake after craniocerebral trauma be kept between 1500 and 1800 ml/24 hours and that further fluid management be dictated by repeated serum electrolyte determinations. The electrolyte balance should be monitored continuously after a significant head injury for up to 2 weeks, because hyponatremic states sometimes develop more than 1 week after injury. The serum alcohol was measured on admission, and the level of serum alcohol correlated well with the serum osmolality on admission; thus, the degree of elevation of serum osmolality was a very good guide to the serum alcohol level. However, there was no statistically significant correlation between alcohol intoxication or chronic alcoholism and the late development of serum sodium and osmolality disturbances.
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PMID:Metabolic disturbances after head injury: abnormalities of sodium and water balance with special reference to the effects of alcohol intoxication. 68 1

A case report is presented in which myxedema coma and inappropriate antidiuretic hormone secretion developed as a result of radiation therapy and surgery to the neck area in a patient with recurrent metastatic squamous cell carcinoma of the floor of the mouth. Laboratory findings of low thyroxine level and the findings of persistent hyponatremia and hypoosmolality of serum in spite of persistent sodium loss in the urine were helpful in diagnosing the problem. Treatment included thyroid hormone replacement and fluid restriction resulting in complete reversal of her condition. We believe that patients with head and neck cancer who have undergone a course of radiation to the neck, and particularly when thyroid function might have been altered by previous subtotal thyroidectomy as part of a curative resection, should be carefully followed with periodic thyroid function assays and serum electrolytes with particular attention to serum sodium values.
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PMID:Myxedema coma and inappropriate antidiuretic hormone secretion after deep neck irradiation: clinical implications and report of a case. 73 33

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.
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PMID:Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. 100 53

HFRS-related oliguria brings about hyperactivity of the system hypothalamus-hypophysis-adrenals and hyperfunction of the pancreas; glucose, urea and creatinine plasma levels are elevated. Prednisolone treatment leads to diminution of ACTH and cortisol levels, elevation of glucose, insulin and C-peptide concentrations in plasma compared to prednisolone-untreated patients, producing insignificant effect on plasma levels of STH, vasopressin, aldosterone, area and creatinine. Therefore, a course administration of glucocorticoids to HFRS patients is justified only in severe collapses and hypopituitary coma confirmed by the laboratory methods.
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PMID:[Effect of glucocorticoid hormones on the status of the hypothalamo-hypophyseal-adrenal system and endocrine function of the pancreas in patients with hemorrhagic fever with renal syndrome]. 197 53

Two cases of neurological deterioration and coma after the transsphenoidal decompression of a pituitary adenoma with marked suprasellar extension and invasion of the 3rd ventricle are presented. Emergency ventricular shunting led to prompt neurological improvement, which, supplemented by radiation therapy, allowed long-term amelioration of symptoms. Three possible explanations for this complication are offered: 1) traction of the attached 3rd ventricle into the decompression site, causing increased obstructive hydrocephalus, 2) vasopressin release by surgical manipulation of the pituitary stalk and circumventricular organs causing cerebral edema, and 3) edema in the residual tumor secondary to surgical manipulation causing further hydrocephalus. Subsequent patients with similar clinical and imaging criteria will have a planned perioperative ventricular shunting procedure performed.
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PMID:Progressive coma after the transsphenoidal decompression of a pituitary adenoma with marked suprasellar extension: report of two cases. 199 71

A 31-year-old woman with untreated chronic schizophrenia developed extreme polydipsia which rapidly led to coma and death due to cerebral edema. Hyponatremia (120 mEq/liter) and serum hypo-osmolality (260 mOsm/kg) were associated with marked polyuria (up to 1850 ml/hour) and appropriately low urinary osmolality (90 mOsm/kg) which responded to treatment. This case and few qualifying previous reports which are reviewed support the possibility that pure self-induced water intoxication with no major contribution of inadequate release of antidiuretic hormone may occur, and that extreme polydipsia can sometimes overwhelm normal renal diluting capacity in psychotic patients.
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PMID:Schizophrenia and fatal self-induced water intoxication with appropriately-diluted urine. 226 78

A retrospective study of 134 patients in a condition of prolonged unawareness state (that is, in coma for over 1 month) following brain trauma was conducted in order to identify prognostic factors. Eight easily evaluated parameters were found to be significant for predicting nonrecovery of consciousness. The following six features were present during the early posttraumatic phase (that is, during the 1st week after trauma): fever of central origin; diffuse body sweating; disturbances in antidiuretic hormone secretion; abnormal motor reactivity; respiratory disturbances; and diffuse nonneurological injuries. The first three features were manifestations of hypothalamic damage. Two factors, evident at a late phase following injury (after the 1st week posttrauma), namely late epilepsy and communicating hydrocephalus, were also significant in predicting nonrecovery.
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PMID:Outcome in 134 patients with prolonged posttraumatic unawareness. Part 1: Parameters determining late recovery of consciousness. 229 88


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