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 syndrome of inappropriate secretion of antidiuretic hormone is characterized by production of less than maximally dilute urine in the presence of hypotonic plasma. It may be secondary to malignant disease, central nervous system disorders, or pulmonary disease, among other conditions, or it may be idiopathic. Manifestations are those of water intoxication, eg, confusion, fatigue, nausea, headache, and neurologic signs. The pathogenesis is not completely understood. Restriction of fluid intake to obtain a negative water balance is effective treatment.
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PMID:Inappropriate secretion of antidiuretic hormone. An overview of the syndrome. 90 56

Four patients are presented, all having pathologic responses in plasma vasopressin concentration to changes in plasma osmolality. Clinically, three of them had the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The fourth had diabetes insipidus associated with an increased threshold for plasma osmolality. Two of the patients with SIADH had lowered thresholds for ADH secretion and one of these also had increased sensitivity to increments in osmolality. The latter patient, like another earlier reported similar case, had a defective blood-cerebrospinal fluid barrier. The third SIADH patient had no response at all to changes in osmolality from 230 to 305 mOsm/kg and had a small cell carcinoma of the lung. These examples illustrate that both the setting and the sensitivity of osmoreceptors and AVP-secreting neurons probably are under complex control from the CNS, and that CNS diseases can affect one or several of these pathways thereby affecting the setting of the osmoreceptor-vasopressin system.
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PMID:Defects in osmoregulation of vasopressin secretion. A report of four cases. 707 18

To clarify the characteristics of vasopressin (AVP) secretion in patients with the syndrome of inappropriate antidiuresis (SIAD) related to central nervous system disorders, we examined the response of AVP secretion to osmotic stimulus by hypertonic saline infusion and analyzed the possible causative factors in six patients with SIAD associated with head trauma or cerebral infarction. Hyponatremia developed after head trauma in four patients and cerebral infarction in two patients. In all patients the clinical state and laboratory findings fulfilled the criteria for SIAD, which was supported by either nonsuppressible plasma AVP levels or effectiveness of treatments with water restriction, demeclocycline, nonpeptide V2 AVP antagonist or diphenylhydantoin. Although patterns of plasma AVP response to the osmotic stimulus varied, plasma AVP concentrations neither increased nor decreased to undetectable levels with a rise in plasma osmolality. In one patient, plasma AVP levels responded to increasing plasma osmolality when plasma osmolality normalized; in which the threshold and the sensitivity of osmostat were normal. In two other patients, AVP secretion responded to plasma osmolality after the treatment. The changes in AVP secretion were not due to nonosmotic stimuli for AVP release. In conclusion, this study shows that patients with SIAD and central nervous system disorders may have persistent AVP secretion with a loss of hypotonic suppression such as found in patients with adrenal insufficiency or depletional hyponatremia in central nervous system disorders, indicating that careful evaluation is necessary to determine the relationship between persistent AVP secretion and the pathogenesis of hyponatremic disorders.
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PMID:Osmoregulation of vasopressin secretion in patients with the syndrome of inappropriate antidiuresis associated with central nervous system disorders. 1046 11

Hyponatraemia in patients with an acute central nervous system disease can be caused by two different mechanisms: (1) retention [corrected] of free water, i.e. the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and (2) excessive sodium retention [corrected], i.e., the cerebral salt wasting syndrome (CSW). Although the concept of CSW is well known in adult medicine, it is still not established in child neurology. We conducted a retrospective analysis of electrolyte disturbances in 195 children with various acute CNS diseases. In 20 children (10.3%) hyponatraemia with plasma sodium below 130 mmol/l was identified. On the basis of clinical and laboratory data 7 of these 20 children were diagnosed as having SIADH, and the other 9 children, as having CSW. Our data suggest that hyponatraemia attributable to CSW is at least as frequent in children as SIADH. Because of their different pathophysiological mechanisms, which require diametrically opposed therapeutic regimens, early differential diagnosis is mandatory if the correct treatment is to be given.
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PMID:Hyponatraemia in children with acute CNS disease: SIADH or cerebral salt wasting? 1121 25

The syndrome of inappropriate antidiuretic hormone (SIADH), the most common cause of euvolemic hyponatremia, is due to nonphysiologic release of arginine vasopressin from the posterior pituitary. Hyponatremia induced by SIADH can be caused by several conditions, such as central nervous system disorders, malignancies, various nonmalignant lung diseases, hypoadrenalism, and hypothyroidism. A 67-year-old man developed hyponatremia consistent with SIADH. Although common comorbid conditions associated with SIADH were excluded as possible causes, his medical history and drug regimen were extensive. However, he had been taking spironolactone, amiodarone, and simvastatin for less than 3 months. Amiodarone was discontinued based on a case report suggesting that this drug can cause SIADH-induced hyponatremia. The patient's serum sodium level began to rise within 3 days of discontinuation and returned to normal within 1 month. Although SIADH-induced hyponatremia occurs only rarely, it should be recognized as a possible adverse effect of amiodarone.
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PMID:Syndrome of inappropriate antidiuretic hormone-induced hyponatremia associated with amiodarone. 1201 66

Hyponatremia, the most common electrolyte disorder, occurs frequently in older people and in hospitalized patients. Physiological changes of aging that interact with diseases and drugs commonly present in older people put this population at greater risk for hyponatremia. It can accompany central nervous system disorders, pulmonary and renal disease, cancer, congestive heart failure, and liver cirrhosis, as well as many commonly used drugs. Delayed recognition can lead to symptomatic hyponatremia with consequent cerebral edema and possibly irreversible neurological damage. Symptoms and signs of hyponatremia may be subtle or not attributed to hyponatremia. Most cases are of the euvolemic type, in which extracellular fluid volume is normal and is often due to the syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia can also occur in association with hypervolemia or hypovolemia. Common to all of these circumstances is increased secretion of arginine vasopressin (AVP). Understanding of the pathophysiological basis of hyponatremia and of brain compensatory mechanisms is critical to safe treatment. Fluid restriction or infusion of hypertonic saline can improve symptoms and normalize serum sodium levels but does not address excess AVP, which in most cases is the underlying cause of the disorder. A major new approach to treatment of hyponatremia is the development of aquaretics: AVP-receptor antagonists that provide a targeted therapeutic approach to correcting the many kinds of hyponatremia caused by excess AVP levels.
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PMID:Hyponatremia and arginine vasopressin dysregulation: mechanisms, clinical consequences, and management. 1697 Jun 67

Hyponatremia, defined as a serum sodium concentration ([Na+]) less than 135 mEq/L, is commonly caused by elevated levels of the hormone arginine vasopressin (AVP), which causes water retention. The principal organ affected by disease-related morbidity is the brain. The neurologic complications associated with hyponatremia are attributable to cerebral edema and increased intracranial pressure, caused by the osmotically driven movement of water from the extracellular compartment into brain cells. Although neurologic symptoms induced by hyponatremia are limited by an adaptive brain mechanism known as "regulatory volume decrease," an overly rapid correction of serum [Na+] before the reversal of this adaptive response can also produce neurologic damage. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hyponatremia related to central nervous system disorders, neurosurgery, or the use of psychoactive drugs. Fluid restriction is the standard of care for patients with SIADH who are asymptomatic or who have only mild symptoms, but patients with severe or symptomatic hyponatremia require more aggressive therapy. Infusion of hypertonic saline is the usual approach to the treatment of symptomatic hyponatremia, but patients require frequent monitoring. Pharmacologic agents such as demeclocycline and lithium may be effective in some patients but are associated with undesirable adverse events. The AVPreceptor antagonists are a new therapeutic class for the treatment of hyponatremia. The first agent in this class approved for the treatment of euvolemic hyponatremia in hospitalized patients is conivaptan. Two other agents, tolvaptan and lixivaptan, are being evaluated in patients with euvolemic and hypervolemic hyponatremia. The AVP-receptor antagonists block the effects of elevated AVP and promote aquaresis, the electrolyte-sparing excretion of water, resulting in the correction of serum [Na+]. These agents may also have intrinsic neuroprotective effects.
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PMID:Cerebral correlates of hyponatremia. 1735 96

A 60-year-old female underwent right upper lobectomy of the lung and lymph node dissection under a diagnosis of cancer in the upper lobe of the right lung. Pathological examination showed stage IIIA adenocarcinoma with mediastinal lymph node metastasis. One month after the operation, adjuvant chemotherapy with carboplatin (CBDCA) and paclitaxel (PTX) was initiated. Four days after the chemotherapy, hyponatremia progressed, and central nervous system disorder developed. A diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was made. She recovered after fluid intake restriction and electrolyte correction. SIADH was considered to be due to the adverse effects of anticancer drugs. In postoperative adjuvant chemotherapy, attention should be paid to the serum Na level.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) following carboplatin-paclitaxel administration in a patient with lung cancer. 2202 33

Neurotrophic factors (NTFs) are endogenous polypeptides that regulate the growth, survival, differentiation, and functioning of neurons. The neuroprotective effects of NTFs in experimental animals give strong rationale for developing therapies for neurological disorders. However, when NTFs are applied in clinical trials, great expectation leads to equal disappointment. NTFs are large molecular-weighted and hydrophilic proteins, which limits their access to the central nervous system (CNS) after systemic administration, principally due to poor blood-brain barrier (BBB) permeability and unfavorable pharmacokinetic profiles. Although intracerebral infusion may transport NTFs into the CNS, the invasiveness limits its clinical application. Intranasal administration has been under research for decades and presents promising outcomes in preclinical studies for brain delivering of NTFs. After intranasal delivery, NTFs gain direct and quick access into the CNS at concentrations high enough to elicit their biological effects, bypassing the BBB and minimizing systemic exposure. Due to its invasiveness and convenience, intranasal delivery is feasible for NTFs administration. Although direct evidence of nose-to-brain pathway in human is lacking due to ethical problems, the existence of the nose-to-cerebral spinal fluid pathway has been verified in men. Furthermore, there is abundant indirect evidence for the nose-to-brain pathway as determined by the efficacy of intranasally administered neuroproteins, such as insulin, oxytocin, and vasopressin in clinical trials. Based on the solid preclinical research supporting the efficacy of intranasal NTFs, and the successful clinical application of neuroproteins (not NTFs), it is time to evaluate clinical application of NTFs in treating both acute and chronic CNS diseases.
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PMID:Intranasal administration: a potential solution for cross-BBB delivering neurotrophic factors. 2241 18

Euvolemic hyponatremia is most frequently caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Causes of SIADH-induced hyponatremia are myriad and include tumors, pulmonary diseases or central nervous system disorders. SIADH can also be induced by a broad spectrum of drugs such as antidepressants and antiepileptics. The unfavorable prognostic relevance of hyponatremia is often underestimated. SIADH therapy focuses on the treatment of the underlying disease. Thus, a thorough differential diagnostic assessment of the genesis of SIADH is crucial. Therapy options for euvolemic hyponatremia include fluid restriction, administration of hyperosmolar saline solution in case of severe symptoms, or therapy with tolvaptan. Tolvaptan is a selective, oral vasopressin-V2-receptor-antagonist that inhibits ADH-induced retention of electrolyte-free water in the connecting duct of the kidney. This inhibition results in an increased serum sodium level. Close monitoring of serum sodium levels and volume status is imperative, especially during the initial phase of therapy. Fluid restriction is unnecessary during tolvaptan therapy; a previously prescribed fluid re-striction should be stopped when therapy begins. Treatment with tolvaptan can often result in a rapid and controlled improvement of the symptoms. Different cases presented in this article illustrate the diversity of SIADH in clinical practice relating to its diagnosis and its therapy as well as difficulties in identifying the underlying cause in clinical practice.
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PMID:[Syndrome of inadequate ADH secretion: pitfalls in diagnosis and therapy]. 2573 77


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