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)

To elucidate the role of antidiuretic hormone (ADH) on water and electrolyte balance in patients with asthmatic attacks, urinary arginine vasopressin (AVP) was assayed in 28 asthmatic patients. In a 3-year-old girl with status asthmaticus who developed a grand mal seizure in association with hyponatremia, urinary AVP levels remained high and fluctuated before convulsion; the cause of the convulsion was considered to be water intoxication due to inappropriate ADH secretion. In 19 of 28 patients with moderately severe asthmatic attacks, increases in urinary AVP levels occurred before treatment (300 +/- 80 pg/ml vs. 40 +/- 24 pg/ml (normal controls), p less than 0.01); elevated AVP levels tended to fall in response to intravenous fluid therapy (appropriate ADH secretion) in 2 of 6 patients, but did not fall (inappropriate ADH secretion) in the remaining patients. It is concluded that inappropriate ADH secretion may occur in asthmatic attacks, and that in such a condition there seems to be a potential risk of water intoxication during fluid therapy, as demonstrated in the present patient.
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PMID:Urinary arginine vasopressin in asthma: consideration of fluid therapy. 211 72

A patient with small cell carcinoma of the lung developed asymptomatic autonomic neuropathy, inappropriate antidiuretic hormone (ADH) secretion and Lambert Eaton myasthenic syndrome. The autonomic neuropathy and inappropriate ADH secretion were present at the time of diagnosis of the tumour. Following chemotherapy these resolved, but 5 months later the patient developed Lambert Eaton syndrome which responded to 3,4-diaminopyridine. This sequence of changes appears to be unique.
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PMID:Lambert Eaton syndrome: autonomic neuropathy and inappropriate antidiuretic hormone secretion in a patient with small cell carcinoma of the lung. 217 71

A patient with encephalopathy developed triphasic changes in the clinical course, starting with diabetes insipidus (DI), then the syndrome of inappropriate ADH secretion (SIADH), and followed by the final phase of DI. The clinical course of encephalopathy was very rapid. The patient lost consciousness completely within only one day after the onset. During the early phase, he lapsed into a condition of "brain death". We could not identify the etiology of the encephalopathy. The triphasic change referred to above is similar to previous reports of cats model after stereotactic destruction of the supraopticohypophyseal tract. We speculate that our case may have been associated with neurohypophyseal dysfunction caused by supraopticohypophyseal tract damage.
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PMID:Triphasic AVP secretion in encephalopathy. 222 36

The effect of therapy for hyponatremia with central origin (cerebrovascular disease and head injury) was investigated in order to examine contributing factors. Out of a total of 58 subjects admitted to the hospital during the previous three years with cerebrovascular disease (49 cases), and head injuries (9 cases), hyponatremia with central origin occurred within 2 weeks. Special treatment for hyponatremia was not given in 30 of the 58 cases (control group). The group (28 cases) which underwent therapy was optionally selected in terms of the following-SIADH, natriuretic polypeptide involvement and sick cells resulting from Na-K pump disorder. These 28 cases were classified into subgroups: water restricted (7 cases), hypertonic NaCl load (9 cases), glucose/insulin/potassium (GIK) therapy (4 cases), phenytoin administration (8 cases). In all of the 58 patients, the serum sodium, potassium and osmolarity and urinary sodium and potassium were measured daily. The balance of water, sodium and potassium were calculated on hyponatremic phase. Plasma levels of such hormones as antidiuretic hormone, aldosterone and cortisol were measured on hyponatremic phase. For each group, onset day and duration of hyponatremia and lowest sodium value were investigated for the sake of comparison. No significant difference for onset day and lowest sodium value was found between each group. Duration was as follows: control group 9.4 +/- 3.3 days, water restricted 7.4 +/- 2.1 days, hypertonic NaCl load 3.3 +/- 1.4 days, GIK therapy 7.3 +/- 2.9 days and phenytoin administration 8.9 +/- 3.7 days. Hypertonic NaCl load indicated a significantly shorter duration compared with the other groups. Hypertonic NaCl load was found to be most effective for hyponatremia with central origin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanism and therapy of hyponatremia with central origin]. 269 88

Red blood cell indices in four adolescent and preadolescent patients with documented inappropriate antidiuretic hormone secretion (SIADH) following spinal fusion were examined for evidence of dilution. The blood indices in these preoperative patients demonstrated evidence of dilution on both the intracellular and extracellular levels. The major factors causing these dilutional effects were elevated ADH, intravenous fluid overloading, and mobilization of "third space" fluids. It appears that extracellular dilution secondary to these factors results in spuriously low blood indices (namely, hemoglobin, hematocrit, and red blood cells) during the postoperative period. These findings suggest that an awareness of SIADH and avoiding intravenous fluid overloads by accurately managing intraoperative and postoperative fluids will decrease the dilutional effects observed on blood indices and perhaps save patients from unwarranted transfusions.
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PMID:The syndrome of inappropriate antidiuretic hormone secretion and its effect on blood indices following spinal fusion. 277 22

An inappropriate antidiuretic hormone secretion (SIADH) has been recognized as the cause of hypotonic hyponatremia, and the occurrence of this syndrome, accompanied by an ADH-producing adenocarcinoma in the nasal cavity, is reported. In February, 1987, a 50-year-old male, showing sights of delirium, disorientation, and irritability was admitted to the hospital. The patient was observed to be healthy, except for a neck lymphnode metastasis that was present up to the time of his hospitalization. The hyponatremia was incidentally found, although dehydration or intravascular volume depletion were not noted. These neuropsychiatric symptoms were considered to be associated with hyponatremia due to SIADH. He had had a partial maxillectomy, a neck dissection, and irradiation to the nose and nasal cavity 32 months earlier, and then underwent a surgical resection of the neck metastasis; he had a total of 10 other operations before the onset of the symptoms. Upon initial inspection, since neither an intracranial invasion nor a brain metastasis was found, we diagnosed that his symptoms were due to an autonomic disturbance caused by surgical and mental "stress". When he died of cardiac failure due to a mediastinal invasion 8 months after the onset of SIADH, tumor tissues was extirpated in an autopsy and was then cultured. In this manner, it was proved that the tumor cells had been producing ADH. This procedure clarified that the syndrome had resulted from an ADH-producing tumor of the nasal cavity.
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PMID:[A case of adenocarcinoma of the nasal cavity associated with syndrome of inappropriate secretion of antidiuretic hormone(SIADH)]. 277 60

A 52-year-old man, known to be alcohol dependent, was admitted to hospital because of intense drowsiness. He had previously drunk over 100 g alcohol daily, but for the last 2 days "not a drop". Serum sodium concentration was 103 mmol/l, serum osmolarity was low (216 mosmol/l) and urine osmolarity remarkably high (373 mosmol/l). These abnormalities, taken in conjunction with his normal water balance (absence of obvious edema or dehydration), suggested the diagnosis of inappropriate secretion of antidiuretic hormone (ADH), and this was confirmed by a water loading test. Exclusion of the recognized causes of inappropriate ADH secretion left alcohol withdrawal as the only tenable explanation. The reabsorption of water which it induced was the cause of the patient's hyponatraemia and drowsiness. Restriction of fluid intake to 500 ml daily with continued total abstinence from alcohol led to rapid recovery. The discovery of hyponatraemia in an alcoholic in a state of normal water balance should rouse suspicion of inappropriate ADH secretion.
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PMID:[Inappropriate ADH secretion caused by alcohol withdrawal: a rare cause of hyponatremia]. 280 92

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyponatremia with high plasma ANP level--report of two cases with emphasis on the pathophysiology of cerebral salt wasting]. 296 7

Disorders of thirst and vasopressin secretion present clinically in one of three ways: as hypotonic polyuria (DI), as hypodipsic hyponatremia, and as hyponatremia. In evaluating a patient with DI, the major challenge is to differentiate between primary polydipsia and neurogenic and nephrogenic DI. This is best accomplished through a series of steps that start with simple clinical observation, and progress, as necessary, to more complicated diagnostic procedures (Fig. 1). If the diagnosis is not clear from the clinical setting and the patient's history, the first step is to measure plasma osmolality and sodium under conditions of ad libitum fluid intake. If the results are clearly above the upper limit of normal range, primary polydipsia is excluded and the work-up can proceed directly to administration of vasopressin or DDAVP and/or a measurement of plasma vasopressin levels to differentiate between neurogenic and nephrogenic DI. If basal plasma osmolality and sodium fall within normal range, the standard dehydration test should be performed. If urine osmolality does not increase above that of plasma despite evident dehydration, primary polydipsia is excluded and the effect of vasopressin or DDAVP on urine osmolality should be examined to differentiate between neurogenic and nephrogenic DI. If administration of antidiuretic hormone increases urine osmolality by more than 50 per cent, the patient has severe neurogenic DI. If the increase in urine osmolality is less than 50 per cent, the patient has nephrogenic DI. In patients who do not concentrate urine above that of plasma in response to dehydration, the best approach is to measure plasma vasopressin, osmolality, and sodium after the latter have been increased above normal range by dehydration and/or infusion of hypertonic saline. When these results are plotted on a suitable nomogram (Fig. 2), neurogenic DI can be clearly diagnosed from the relative deficiency of vasopressin. In patients with normal vasopressin levels, primary polydipsia can be differentiated from nephrogenic DI by examining the relationship of urine osmolality to plasma vasopressin (Fig. 3), obtained during dehydration and/or graded vasopressin infusion. In evaluating a patient with sustained hypernatremia, it is only necessary to assess thirst, which can be done by a simple bedside observation. In a patient without obvious neurologic or cognitive impairment, absence of thirst in the face of plasma osmolality above 305 mosm/kg (plasma sodium above 150 mEq/L) is diagnostic for hypodipsic hypernatremia. In a patient who presents with hyponatremia, the main objective is to differentiate between hyper-, hypo-, and euvolemic (SIADH) types
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PMID:Disorders of antidiuretic hormone. 304 88

Nine cases with hyponatremia were precisely examined during the past 2 years. Seven of them showed normal plasma volume, serum aldosterone and pituitary function, although ADH was detected. Therefore, those seven cases were diagnosed without dilutional hyponatremia due to SIADH (a syndrome of inappropriate secretion of antidiuretic hormone). The mechanism of hyponatremia of such a type has not been yet explained definitely, but it may be referring to excess natriuresis. Only each one case of hyponatremia due to hypopituitarism and dilutional hyponatremia due to SIADH was verified in this series. SIADH showing high plasma volume value was thought to be rare. Differential diagnosis between SIADH and hyponatremia due to excess natriuresis is essential and simple. Non-invasive plasma volume measurement using RISA is significantly useful for it. For the hyponatremia due to excess natriuresis, water restriction is not necessary, but digestive supply of NaCl is needed.
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PMID:[Hyponatremia due to excess natriuresis]. 341 57


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