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)

An 83-year-old Japanese woman was admitted to our hospital with severe hyponatremia (sodium, 108 mEq/L [108 mmol/L]), hypokalemia, hypochloridemia, hypocalcemia, hypophosphatemia, and hypouricemia. Despite low plasma osmolarity (232 mOsm/kg [232 mmol/kg]), urine osmolarity (320 mOsm/kg) was greater than that of plasma, and she had increased urinary sodium excretion (88 mEq/L [88 mmol/L]) and an unsuppressed high plasma level of antidiuretic hormone (ADH; 5.5 pg/mL [5.1 pmol/L]). These findings indicated that she had syndrome of inappropriate ADH secretion (SIADH). In addition, she had a generalized reabsorption defect of the proximal tubules, including decreased tubular reabsorption of phosphate, increased fractional excretion of uric acid, glycosuria despite a normal blood glucose level, and panaminoaciduria. Thus, combined SIADH and Fanconi syndrome was diagnosed. The cause was thought to be the antidepressant paroxetine, which is a selective serotonin reuptake inhibitor (SSRI). Several of the abnormal values resolved within 1 week after discontinuation of this drug. Although the precise mechanism responsible was not elucidated, we report an extremely rare case of combined SIADH and Fanconi syndrome, probably caused by short-term SSRI therapy.
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PMID:A rare case of combined syndrome of inappropriate antidiuretic hormone secretion and Fanconi syndrome in an elderly woman. 1679 99

Pharmacologic treatment may lead to diverse disturbances of water and electrolyte metabolism as adverse drug events. Diuretics are particularly likely to cause these complications typically including volume depletion, metabolic alkalosis, hyponatremia, and hypokalemia. Salt and water retention with edema formation is most frequently elicited by antihypertensives, steroid hormones, and nonsteroidal anti-inflammatory drugs. Drug-induced disorders of Na+ concentration may usually be attributed to altered antidiuretic hormone (ADH) effects, either as diabetes insipidus or as the syndrome of inappropriate ADH secretion. With hyper- and hypokalemia, redistribution between intra- and extracellular fluid as well as renal excretion play a role. Strategies to prevent these adverse drug reactions include careful consideration of risk factors and clinical and laboratory controls in the course of treatment.
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PMID:[Drug-related disorders of water and electrolyte metabolism]. 1698 2

Two children with complete congenital anterior hypopituitarism developed hyponatremia; inappropriate secretion of antidiuretic hormone was documented despite adequate hormonal replacement therapy. These cases show that congenital hypopituitarism can be associated with SIADH in children later than the neonatal period, despite adequate replacement therapy.
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PMID:Complete congenital anterior pituitary insufficiency and syndrome of inapropriate antidiuretic hormone secretion: a rare association in children. 1725 98

Unlike the more commonly used diuretics, aquaretic agents can induce an increase in urinary volume without incurring a loss of electrolytes. These molecules belong to a family of vasopressin receptor antagonists, V2 in particular, that regulate optional renal water re-absorption via the synthesis and expression of aquaporin-2. In view of their properties, they have become the agent of choice in the treatment of hyponatremic states with water retention, and different studies have demonstrated that they are more effective and practical to use than other traditional approaches in the treatment of diseases such as cirrhosis-related ascites, SIADH and, above all, heart failure. However, the future probably holds the promise of new and unexpected applications for this type of drug in the treatment of several conditions, including polycystic kidney and glomerular disease, glaucoma and Meniere's syndrome.
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PMID:Aquaretic agents: what's beyond the treatment of hyponatremia? 1743 Jan 86

Syndrome of inappropriate secretion of antidiuretic hormone and diabetes insipidus occurring in very short order in the same patient is rare. We report a 9 month-old male infant suffering form holoprosencephaly developed syndrome of inappropriate secretion of antidiuretic hormone followed by diabetes insipidus within a relative short time postoperatively after his third operation. Inability to suppress as well as to stimulate arginine vasopressin secretion and anesthetic and surgical stresses, were thought to be the possible causes of this event.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion and diabetes insipidus in an infant following surgery. 1769 89

Aquaretic drugs, by definition, can induce an increase in urinary volume and urinary free water associated with a decreased urinary osmolarity with a consequent increase in plasma sodium. This enhanced diuresis is not accompanied by an increased loss of electrolytes, whereas traditional diuretics have the opposite, so-called saluretic effect. Aquaretics belong to a family of vasopressin receptor antagonists, V2 in particular, that regulate tubular water reabsorption. Several studies have confirmed their utility in the treatment of hyponatremic states associated with water retention such as heart failure, cirrhosis related ascites and SIADH. Furthermore, new applications may include the treatment of arterial hypertension, polycystic kidney disease, glaucoma and Meniere's syndrome.
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PMID:[Therapy with vasopressin receptor antagonists: the aquaretics]. 1788 7

Acute hyponatremia, following neurosurgery, results from inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW). CSW is due to abnormally high atrial or brain natriuretic peptides (ANP, BNP), which block all stimulators of zona glomerulosa steroidogenesis, resulting in mineralocorticoid deficiency. A 3 year-old girl presented CSW at day 4, after resection of craniopharyngioma and hypophysectomy. Hyponatremia, hyperkalemia and high natriuresis occurred on day 8, with low renin and aldosterone and elevated BNP 120.3 ng/ml (undetectable before surgery). Fludrocortisone 100 microg/day controlled natriuresis and restored electrolytes within 24 hours. A 5 year-old boy presented CSW at day 6 after partial resection of optic glioma. Fludocortisone 100 microg/day restored electrolytes within 8 hours. ANP was elevated, 60.6 ng/l, aldosterone and renin were low. Fludrocortisone supplementation should be considered in CSW, as excessive natriuresis is controlled, and electrolytes are easily restored, avoiding life-threatening complications of this complex disorder.
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PMID:Mineralocorticoid deficiency in post-operative cerebral salt wasting. 1805 34

Primary laryngeal small cell neuroendocrine carcinoma (SCNC) is an unusual malignancy accounting for <0.5% of laryngeal carcinomas. To date, approximately 200 cases of primary and 5 of secondary SCNC of the larynx have been reported. This tumor most often presents in the sixth and seventh decades in men who are heavy cigarette smokers. The lesion may be associated with different paraneoplastic syndromes (ectopic adrenocorticotropic hormone syndrome, Schwartz-Bartter syndrome or syndrome of inappropriate secretion of antidiuretic hormone, and Eaton-Lambert myasthenic syndrome) or with ectopic hormone production. The diagnosis is based essentially on the histologic appearance of the tumor, confirmed by immunocytochemical investigations. Concurrent chemoradiotherapy regimens offer potential for long-term survival. This tumor is biologically aggressive, and the extent of the disease is the most significant independent prognostic factor of survival. The survival rate is similar to that with pulmonary SCNC.
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PMID:Primary and secondary small cell neuroendocrine carcinoma of the larynx: a review. 1830 54

Etiopathogenesis, diagnostics and therapy of hyponatremias are summarized for clinicians. Hyponatremia is the most common electrolyte abnormality. Mild to moderate hyponatremia and severe hyponatremia are found in 15-30% and 1-4% of hospitalized patients, respectively. Pathophysiologically, hyponatremias are classified into two groups: hyponatremia due to non-osmotic hypersecretion of vasopressin (hypovolemic, hypervolemic, euvolemic) and hyponatremia of non-hypervasopressinemic origin (pseudohyponatremia, water intoxication, cerebral salt wasting syndrome). Patients with mild hyponatremia are almost always asymptomatic. Severe hyponatremia is usually associated with central nervous system symptoms and can be life-threatening. Diagnostic evaluation of patients with hyponatremia is directed toward identifying the extracellular fluid volume status, the neurological symptoms and signs, the severity and duration of hyponatremia, the rate at which hyponatremia developed. The first step to determine the probable cause of hyponatremia is the differentiation of the hypervasopressinemic and non-hypervasopressinemic hyponatremias with measurement of plasma osmolality, glucose, lipids and proteins. For further differential diagnosis of hyponatremia, the determination of urine osmolality, the clinical assessment of extracellular fluid volume status and the measurement of urine sodium concentration provide important information. The most important representative of euvolemic hyponatremias is SIADH. The diagnosis of SIADH is based on the exclusion of other hyponatremic conditions; low plasma osmolality (<275 mosmol/kg) and inappropriate urine concentration (urine osmolality >100 mosmol/kg) are of pathognomic value. Acute (<48 hrs) severe hyponatremia (<120 mmol/l) necessitates emergency care with rapid restoration of normal osmotic milieu (1 mmol/l/hr increase rate of serum sodium). Patients with chronic symptomatic hyponatremia have a high risk of osmotic demyelination syndrome in brain if rapid correction of the plasma sodium occurs (maximal rate of correction of serum sodium should be 0.5 mmol/l/hr or less). The conventional treatments for chronic asymptomatic hyponatremia (except hypovolemic patients) include water restriction and/or the use of demeclocycline or lithium or furosemide and salt supplementation. Vasopressin receptor antagonists have opened a new forthcoming therapeutic era. V2 receptor antagonists, such as lixivaptan, tolvaptan, satavaptan and the V2+V1A receptor antagonist conivaptan promote the electrolyte-sparing excretion of free water and lead to increased serum sodium.
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PMID:[Etiology, diagnostics and therapy of hyponatremias]. 1861 66

The most frequent electrolytic disorders associating with tumors are hypercalcemia and hyponatremia, which should often be dealt with on an emergency basis. Hypercalcemia is observed in around 10% of metastatic solid tumors including lung, breast, head and neck and renal cancers. In hematological malignancies, hypercalcemia is observed with a relatively high incidence in malignant lymphoma. Hypercalcemia is caused by bone metastasis or PTH-rP secreted from tumors. In other cases, it is induced by calcitriol produced from tumor. Hypercalcemia sometimes results in a fatal outcome, and should be carefully monitored. Hyponatremia presented as SIADH is sometimes caused by arginine vasopressin derived from tumors. In other cases, SIADH is induced with chemotherapeutic drugs such as cyclophosphamide and cisplatin. Neither hypercalcemia nor hyponatremia has any specific symptoms. Delayed treatment often results in severe condition, such as unconsciousness or even death. Therapy for hypercalcemia is started by infusion of normal saline, and a patient with severe hypercalcemia should be treated with bisphosphonates. Zoledronic acid is the best bisphosphonate among them at this present. Treatment of SIADH is started by water restriction. In an emergency, treatment with hypertonic saline(3-5%)should be considered together with loop diuretics. Demethyl chlorotetracycline is considerable in poor response cases, and mozavaptan hydrochloride is applicable in case of vasopressin-producing tumors. In any case, inappropriate rapid correction of hyponatremia could induce severe brain damage called CPM without careful management.
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PMID:[Treatment for the electrolytic disorders in cancer patients]. 1909


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