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)

Hyponatremia associated with high urine osmolality is usually caused by inappropriate secretion of antidiuretic hormone. However, secondary hypoadrenalism is also accompanied by hyponatremia and with features indistinguishable from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). As secondary hypoadrenalism requires a specific treatment, a high index of suspicion and appropriate hormonal testing are required to differentiate between these two entities. We retrospectively studied 10 patients with a previously undiagnosed hypothalamic-pituitary disease who presented with an acute symptomatic hyponatremia. Mean age (+/-SD) was 65.1+/-8.4 yr. Mean serum sodium was 120.7+/-2.9 nmol/l and urinary osmolality, 453.9+/-74 mosmol/kg. Serum creatinine, urea and uric acid were low. Mean serum morning cortisol was low, 104.0+/-55.2 nmol/l. High-dose ACTH test showed adequate increment of serum cortisol in 3 out of 7 patients tested. Two of these 3 patients did not respond adequately to the low-dose ACTH test. Endocrine evaluation disclosed partial or complete hypopituitarism in all 10 patients. Six patients had pituitary macroadenomas, one had a craniopharyngioma, one patient had a large aneurysm of the internal carotid with sellar destruction and two others had empty sella. Treatment by fluid restriction did not affect serum sodium levels significantly. In contrast, all patients achieved normal sodium when treated by glucocorticosteroid. Central hypoadrenalism should be considered in any patient presenting with hyponatremia with high urine osmolality. Low-dose ACTH test should be performed and followed by appropriate endocrine and imaging studies. Hyponatremia in these patients is promptly corrected by glucocorticosteroid replacement.
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PMID:Symptomatic hyponatremia as a presenting sign of hypothalamic-pituitary disease: a syndrome of inappropriate secretion of antidiuretic hormone (SIADH)-like glucocorticosteroid responsive condition. 1588 61

We report the case of an 81-year old woman with stupor, confusion, somnolence, vomiting, and reduced food intake for 5 days. Laboratory investigations revealed low serum concentrations of sodium and potassium with a serum osmolality of 225 mOsm/kg H (2)O in the face of an inappropriately concentrated urine with an osmolality in the normal range, suggesting the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in the absence of renal insufficiency, adrenal insufficiency, and hypothyroidism. Careful drug evaluation revealed amitriptyline and citalopram as possible inciters of antidiuretic hormone secretion. Subsequently, these drugs were withdrawn. Under continuous sodium substitution and fluid restriction serum sodium normalized and the patient's symptoms resolved. She was fully alert by day 15. We conclude that hyponatremia secondary to SIADH was the cause of the patient's neurologic symptoms. Clinicians should be aware of this possible side effect of central acting agents such as amitriptyline and citalopram, drugs that are often used to treat elderly patients suffering from depression or chronic pain.
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PMID:Citalopram therapy as a risk factor for symptomatic hyponatremia caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH): a case report. 1602 23

Steroid withdrawal syndrome (SWS) usually refers to relapse of the disease being treated after withdrawal of glucocorticoid therapy, or the symptoms of adrenal insufficiency which occur when glucocorticoids are rapidly reduced or stopped. A less well-recognised form of SWS is that which develops when patients experience a symptom complex similar to that of adrenal insufficiency despite acceptable cortisol levels. We describe three patients who presented with this form of SWS following surgical treatment for endogenous Cushing's syndrome. All responded well to a short-term increase in the dose of glucocorticoid replacement therapy, with the median duration of the syndrome being 10 months (range 6-10 months). Trough serum cortisol levels above 100 nmol/l, with peaks between 460 and 750 nmol/l were documented in the first two patients at presentation with SWS. It is thought that the syndrome may result from development of tolerance to glucocorticoids, and mediators considered to be important in its development include interleukin-6, corticotrophin-releasing hormone, vasopressin, and central noradrenergic and dopaminergic systems. The exact underlying mechanism for SWS remains unclear. However, with increasing recommendations for use of lower doses of replacement glucocorticoids, its incidence may increase. Physicians need to be aware of this condition, which is self-limiting and easily treated by a temporary increase in the dose of glucocorticoid replacement therapy. It is possible that a slower glucocorticoid tapering regimen than that used in the standard postoperative management of patients undergoing pituitary surgery may reduce the risk of development of SWS.
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PMID:Steroid withdrawal syndrome after successful treatment of Cushing's syndrome: a reminder. 1606 25

The syndrome of inappropriate antidiuresis (SIAD) is a disorder of sodium and water balance characterized by hypotonic hyponatremia and impaired water excretion in the absence of renal insufficiency, adrenal insufficiency, or any recognized stimulus for the antidiuretic hormone arginine vasopressin (AVP). Hyponatremia is primarily a result of excessive water retention caused by a combination of excessive intake and inappropriate antidiuresis. It is sometimes aggravated by a sodium deficiency caused by decreased intake and/or a secondary natriuresis triggered by and largely corrective of the increase in extracellular volume. Hence, there is neither edema nor signs of hypovolemia. Inappropriate antidiuresis is usually due to administration or endogenous production of AVP or another vasopressin receptor agonist such as desmopressin. Endogenous production can be either ectopic (from a tumor) or eutopic (from the neurohypophysis). The latter apparently is induced by a wide variety of diseases, drugs, or injuries and is divisible into 3 different types of abnormal AVP release during hypertonic saline infusion: high, erratic fluctuations unrelated to increases in plasma sodium (type A); a slow constant "leak" that is also unaffected by increases in plasma sodium (type B); and rapid progressive increases in plasma AVP that correlate closely with plasma sodium as it rises toward the normal range (type C or "reset osmostat"). In 5% to 10% of patients, there is no demonstrable abnormality in the osmoregulation of AVP (type D) and the cause of inappropriate antidiuresis is unclear. In some children it appears to be due to an activating mutation of the V2 receptor (V2R). In other patients, it may be due to abnormal control of aquaporin-2 water channels in renal collecting tubules or production of an antidiuretic principle other than AVP. These different types of osmoregulatory dysfunction underlying SIAD may result in marked differences in clinical presentation or response to therapy with fluid restriction, hypertonic saline infusion, or vasopressin antagonists.
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PMID:Regulation of arginine vasopressin in the syndrome of inappropriate antidiuresis. 1684 83

The transcription-intermediary-factor-2 (TIF-2) is a coactivator of the glucocorticoid receptor (GR), and its disruption would be expected to influence glucocorticoid-mediated control of the hypothalamo-pituitary-adrenal (HPA) axis. Here, we show that its targeted deletion in mice is associated with altered expression of several glucocorticoid-dependent components of HPA regulation (e.g., corticotropin-releasing hormone, vasopressin, ACTH, glucocorticoid receptors), suggestive of hyperactivity under basal conditions. At the same time, TIF-2(-/-) mice display significantly lower basal corticosterone levels and a sluggish and blunted initial secretory response to brief emotional and prolonged physical stress. Subsequent analysis revealed this discrepancy to result from pronounced aberrations in the structure and function of the adrenal gland, including the cytoarchitectural organization of the zona fasciculata and basal and stress-induced expression of key elements of steroid hormone synthesis, such as the steroidogenic acute regulatory (StAR) protein and 3beta-hydroxysteroid dehydrogenase (3beta-HSD). In addition, altered expression levels of two nuclear receptors, DAX-1 and steroidogenic factor 1 (SF-1), in the adrenal cortex strengthen the view that TIF-2 deletion disrupts adrenocortical development and steroid biosynthesis. Thus, hyperactivity of the hypothalamo-pituitary unit is ascribed to insidious adrenal insufficiency and impaired glucocorticoid feedback.
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PMID:Insidious adrenocortical insufficiency underlies neuroendocrine dysregulation in TIF-2 deficient mice. 1713 62

Cases of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with tuberculosis have been reported, however, in most of these cases, tuberculosis disease is miliary or severe. Here we report the first case of SIADH induced by ethionamide (TH). The case is a 76 year-old woman. She noticed cough in April 2004 and chest X-ray showed infiltrative shadows on the right upper lung field. Sputum examination revealed positive for TB-PCR, and she was referred to our hospital. Treatment was started with the combination of isoniazid (INH), rifampicin and ethambutol, however susceptibility test showed the bacilli were resistant to INH, then INH was replaced by TH on day 59. Loss of appetite developed 4 days later, the level of consciousness dropped to Japan Coma Scale II-20, and the Na concentration decreased to 113 mEq/l 6 days later. We made the diagnosis of SIADH based on the diagnostic criteria. She recovered from SIADH by the replacement of TH with SM, the restriction of water intake, and the loading of Na. Judging from the coincidence of the administration of TH and the onset of SIADH, no recurrence of SIADH after the cessation of TH, the mildness of tuberculosis, and the onset of SIADH in an already recovered case, we thought that SIADH in this case was causedly TH. Not only adrenal insufficiency but also SIADH should be considered when patients with tuberculosis show hyponatremia, and drugs on use should be reviewed as the possible cause of SIADH.
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PMID:[Case of SIADH caused by ethionamide in a patient with pulmonary tuberculosis]. 1724 Sep 18

Septic shock continues to be one of the leading causes of death in the intensive care unit today. The confluence of many factors contributes to the deterioration of patients' condition in septic shock. Increased levels of nitric oxide, in part, mediate the cardiovascular effects of septic shock. Nitric oxide is major mediator of vasodilation and hypotension as well as myocardial depression. It also contributes to decreased production and release of endogenous vasopressin. Vasopressin effects are actualized by stimulation of V1, V2, and V3 receptors located in various parts of the body. The response is dose dependent. Endogenous vasopressin and angiotensin II act synergistically to preserve and restore blood pressure levels. Decreased circulating vasopressin contributes to adrenal insufficiency via hypothalamic-pituitary-adrenal axis suppression and increased catecholamine resistance to vasopressors. Exogenous vasopressin supplementation in physiologic doses has been shown to improve blood pressure levels and decrease vasopressor needs in patients with septic shock.
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PMID:Effects of vasopressin in septic shock. 1867 Feb 3

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a disorder of sodium and water balance characterized by hypotonic hyponatremia and impaired water excretion in the absence of renal insufficiency , adrenal insufficiency or any recognized stimulus for the antidiuretic hormone (ADH). An inappropriate increase in ADH release of any cause produces hyponatremia by interfering with urinary dilution, thereby preventing the excretion of ingested water. Despite being the most common cause of hyponatremia in hospitalized patients, SIADH remains a diagnosis of exclusion. SIADH should be suspected in any patient with hyponatremia, hyposmolarity, urine osmolality above 100 mosmol/hgH2O, urine sodium concentration usually above 40 mEq/L, and clinical euvolemia. a number of modalities can be used to correct hyponatremia in SIADH, with water restriction and salt administration being the most important. The rate of correction is dependent upon the degree of hyponatremia and the presence or absence of symptoms. Patients with severe neurological symptoms require prompt correction; however, excessively rapid correction should be avoided because it can lead to the late onset of neurological complications from osmotic demyelination.
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PMID:[Hyponatremia secondary to inappropriate antidiuretic hormone secretion]. 1898 40

A 77-year-old man was admitted to our hospital complaining of general fatigue. Serum sodium was 116 mEq/l and serum antidiuretic hormone (ADH) was elevated. Radiologic examination revealed nodules in the brain as well as in both adrenal glands. Based on the findings of fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET), we had considered that the cause of the hyponatremia was syndrome of inappropriate secretion of antidiuretic hormone (SIADH) due to active extrapulmonary tuberculosis. Against our expectations, the patient's condition got worse just after he began antituberculous therapy; we finally diagnosed Addison's disease by additional hormonal tests. His condition recovered immediately with the administration of high-dose hydrocortisone, and the tuberculous lesions became smaller with antituberculous medications. Although tuberculous Addison's disease has been decreasing markedly in recent years, we have to consider the possibility of adrenal insufficiency when hyponatremia is observed in patients with active tuberculosis or those having a past history of tuberculosis.
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PMID:Addison's disease due to tuberculosis that required differentiation from SIADH. 1968 43

In the present paper, the authors reviews the endocrine and metabolic manifestations in tuberculosis. Disorders as adrenal insufficiency, the syndrome of inappropriate antidiuretic hormone secretion (SIADH), hypercalcemia, endocrine effects of antituberculous drugs, hypopituitarism, tuberculous involvement of the thyroid gland and pancreas and chest radiograph presentation in diabetes mellitus are discussed. In the literature, several reports support the presence of abnormal calcium metabolism in tuberculosis.
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PMID:[Endocrine and metabolic manifestations in tuberculosis]. 1977 92


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