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)

Exercise-induced hyponatremia is commonly believed to be associated only with extraordinary physical efforts, or particularly strenuous exercise. Hyponatremia complicating moderate exercise has not been described previously. The authors describe the characteristics of seven patients with life-threatening hyponatremia associated with mild to moderate exercise. All patients suffered from nausea, vomiting, agitation, and confusion, appearing during or after moderate physical activity. Grand mal convulsions occurred in five of the patients. In laboratory results, hyponatremia was as low as 115 mEq/L, with a relatively high sodium concentration in the urine. High serum creatine kinase activity levels were found in most of the patients. All patients were discharged in good condition, without neurologic sequela. The authors conclude that hyponatremia is a possible complication of moderate exercise, and not only of endurance sports, and that exercise-induced hyponatremia can produce severe neurologic manifestations. The mechanism of the hyponatremia is unclear, but may be due to a hemodynamically inappropriate stimulus for antidiuretic hormone secretion.
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PMID:Case series: hyponatremia associated with moderate exercise. 861 81

Six patients are with inappropriate secretion of antidiuretic hormone syndrome are reported (two with bacterial acute meningitis, two with bacterial pneumonia, one with oat cell lung carcinoma, other with mediterranean fever boutonneuse) and the clinical manifestations were: mind changes (four cases) nausea-vomiting (two cases) and inappetence (six cases). All patients presented hyponatremia criteria, serum decreased osmolarity, urinary sodium and osmolarity increased, without edemas, renal disease endocrine (hypophysis, thyroids, adrenal) without diuretic treatment. Treatment was, effective water restriction in three patients and hydrochloride of demeclocycline in other three patients.
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PMID:[Inappropriate ADH secretion syndrome]. 867 42

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

The general goals of treatment of cyclic vomiting syndrome (CVS) are: interruption of established episodes, amelioration of symptoms in patients whose episodes cannot be interrupted, aborting episodes during prodromal symptoms, prophylaxis to abolish or lessen the frequency of episodes, and recovery. Complications of cyclic vomiting episodes include esophagitis, hematemesis, depletion of intracellular electrolytes, hypertension, and secretion of inappropriate antidiuretic hormone.
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PMID:Management of cyclic vomiting syndrome. 870 70

A case of malignant thymoma with pure red cell aplasia (PRCA) complicated by syndrome of inappropriate secretion of antidiuretic hormone (SIADH) following intrathoracic cisdichlorodiammine platinum (CDDP) administration is reported. A 59-year-old Japanese woman who presented with severe general fatigue was diagnosed with PRCA associated with a thymoma, based on the findings of a bone marrow biopsy, computed tomography of the chest, and the existence of anti-acetylcholine receptor antibodies. She underwent a thymectomy after frequent blood transfusions. This was followed by intrathoracic CDDP administration, because of pleural dissemination. Nine days following chemotherapy, her serum sodium concentration was found to be 104mM, while her consciousness was drowsy with severe fatigue and vomiting. This hyponatremic state was diagnosed as SIADH induced by CDDP infusion into the thoracic space, based on the hypo-osmolality of her serum, the hyper-osmolality of her urine, and an inappropriate level of plasma vasopressin.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone following intra-thoracic cisplatin. 873 84

In this prospective study, a series of 1812 consecutive mild head injured adult patients who visited the hospital emergency department were assessed. Twenty-eight patients (1.5%) deteriorated after head injury; 23 of these (1.3% of the series) required surgical intervention. Five patients (0.3%) deteriorated due to non-surgical causes [post-traumatic seizure 2, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) 3]. Most of the deterioration occurred within the first 24 hours (57%). Post-traumatic headache was found in 280 patients (15.5%) and 84 patients (4.6%) suffered post-traumatic vomiting. The relative risk is calculated. Age over 60, presence of drowsiness, focal motor weakness, post-traumatic headache and vomiting has increased risk of deterioration (p < 0.001). This study suggests that post-traumatic headache and vomiting deserve more clinical attention rather than being considered as post-traumatic syndrome only.
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PMID:Relative risk of deterioration after mild closed head injury. 874 3

A 15-year-old boy with sequelae of perinatal asphyxia experienced intractable startle-induced epileptic seizures, which were transiently suppressed with episodic vomiting. His vomiting was associated with adrenocorticotropin and antidiuretic hormone discharge, and the alteration of urinary catecholamine excretion, which might modulate epileptic seizures. Because startle-induced epileptic seizures are resistant to conventional antiepileptic therapy, this case is informative for the treatment of startle epilepsy.
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PMID:Vomiting attack with ACTH and ADH discharge improves startle epilepsy. 880 77

The use of diuretics leads to a negative sodium and fluid balance without primary effects on serum sodium concentration. This parameter is regulated by the activity of the antidiuretic hormone (ADH) system. Secondary changes in other electrolyte systems and in acid base homeostasis also are induced by diuretic therapy. Especially diuretic induced hypokalemia is important as it is responsible for the excess mortality observed in patients with diuretic treated essential hypertension and cardiac abnormalities. All adverse metabolic effects of diuretic therapy are, in contrast to the antihypertensive action, dose dependent. Changes in fluid and electrolyte metabolism induced by diuretics occur within the first 2 or 3 weeks after initiation of medication. Counterregulatory mechanisms are activated and a new steady state is established. Serial laboratory determinations after this period are not necessary as long as this steady state is not affected by additional events (like a change in therapy or diet as well as the occurrence of vomiting or diarrhea).
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PMID:[Effects of diuretic therapy on electrolyte and acid-base homeostasis]. 903 78

The aim of the present study was to investigate the effects of a serotonin subtype 3 receptor antagonist, ondansetron, on arginine vasopressin secretion in humans. Plasma vasopressin concentrations were determined in 24 breast cancer patients undergoing adjuvant chemotherapy, before and after ondansetron intravenous (i.v.) administration. Ondansetron (8 mg i.v. at time 0 and 8 mg po at time 240 min) was administered alone in 12 patients and afterwards in combination with chemotherapy in all patients. No changes in hormone levels were found after ondansetron alone and in 17 patients who did not claim nausea and/or emesis after chemotherapy. In seven patients who experienced nausea and /or emesis, vasopressin levels significantly (P < 0.01) increased (from 6.3 +/- 0.9 ng/L in basal conditions to 15.1 +/- 3.3 ng/L at 10 h; P < 0.05 vs baseline). The results suggest the possibility that in humans, serotoninergic mechanisms, which modulate vasopressin secretion, may involve the activation of the serotonin receptors recognised by ondansetron.
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PMID:Effect of the 5-HT3 receptor antagonist ondansetron on plasma AVP secretion: a study in cancer patients. 909 Oct 68

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is characterized by hyponatraemia due to water retention resulting from the persistent release of antidiuretic hormone (vasopressin). It may occur in a variety of malignant and non-malignant conditions, in particular in association with oat cell carcinoma, pulmonary and cerebral diseases. We report the case of a male patient affected by melanoma of the right temporal region with brain metastasis who developed acute headache, drowsiness, nausea, vomiting and pathological reflexes. Clinical and laboratory investigations led us to the diagnosis of SIADH. Restriction of fluid intake obtained a good clinical improvement with normalization of laboratory alterations; after 2 months the patient experienced a new episode of SIADH which was promptly treated. As melanoma has been occasionally observed in association with SIADH it should be included in the list of tumours that can cause this particular syndrome.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in a patient affected by metastatic melanoma. 976 13


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