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)

We report an unusual case of inappropriate antidiuresis with undetectable vasopressin in an elderly man presenting with confusion due to severe hyponatremia. Further investigations led to the diagnosis of non-functional pituitary macroadenoma. The patient had normal thyroid and adrenal function. The abnormal water balance resolved promptly after transsphenoidal removal of the tumor, confirmed by a repeat water loading test. We conclude that inappropriate antidiuresis in the absence of excess vasopressin secretion may implicate mass effect from an underlying pituitary tumor.
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PMID:Inappropriate antidiuresis associated with pituitary adenoma--mechanisms not involving inappropriate secretion of vasopressin. 1096 94

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

We present a 79-year-old woman with severe hyponatremia secondary to resumption of treatment with paroxetine, a selective serotonin-reuptake inhibitor antidepressant. Confusion and fatigue followed re-initiation of paroxetine after a 3-month hiatus. Hyponatremia, serum hypoosmolality, and urine hyperosmolality strongly suggested the syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia was quickly resolved after discontinuation of paroxetine and initiation of intravenous normal saline infusion together with oral fluid restriction. This case underscores the importance of monitoring serum sodium in elderly patients taking paroxetine, whether this represents a new prescription or reintroduction of the drug.
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PMID:Hyponatremia upon resumption of paroxetine therapy. 1580 1

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

Diuretics are an integral part of the management of symptomatic heart failure. Although they have been used for several decades, there is still some ambiguity and confusion regarding the outcome and the optimal way of using these common agents. There are no large-scale randomized controlled trials that have evaluated the effect of diuretics on mortality and long-term morbidity in diastolic and systolic dysfunction. Nonetheless, in short-term studies furosemide has demonstrated to reduce symptomatic congestive heart failure and hospitalization, and to improve exercise capacity in the setting of systolic dysfunction. In this review, the classes, sites of action and renal effect of diuretics are reviewed and the various indications, optimal doses and recommendations on effective use and disuse are discussed. Namely, this review addresses the effects of emerging diuretic agents such as eplerenone--a selective mineral corticoid receptor antagonist, nesiritide--a brain natriuretic peptide-recombinant, and conivaptan--a vasopressin antagonist, in attempt to provide an update on current knowledge, even though adequate clinic data are not available for all agents.
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PMID:[Use of diuretics in congestive heart failure: renal effects]. 1663 94

Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is a common occurrence in inpatients with psychiatric disorders. The underlying pathophysiology of this syndrome is unclear, and multiple factors have been implicated, including a hypothalamic defect and adverse medication effects. Hyponatremia in PPD can progress to water intoxication and is characterized by symptoms of confusion, lethargy, and psychosis, and seizures or death. Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities.
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PMID:Psychogenic polydipsia review: etiology, differential, and treatment. 1752 21

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a common consequence of neurologic and pulmonary infections as well as drug intake and many other clinical situations. This report describes SIADH that developed in an elderly woman with single dermatomal herpes varicella zoster ophthalmicus without evidence of varicella zoster encephalitis or dissemination. A 76-year-old woman was admitted to our department for evaluation of left facial pain, confusion and disorientation. Further investigation revealed hyponatremia 112 mEq/L, low serum osmolality, high urine osmolality, normal renal function, normal adrenal and thyroid hormones, and high plasma vasopressin 40 pg/mL. These results indicate that the hyponatremia in this case was due to SIADH and that SIADH was caused by an increased release of vasopressin probably because of the antiviral drug (acyclovir) or infection of varicella zoster virus (VZV) in a single dermatome.
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PMID:Herpes zoster ophthalmicus and syndrome of inappropriate antidiuretic hormone secretion. 1831 Sep 84

We report an 82-year old man prescribed paroxetine who had hyponatremia and in whom the syndrome of inappropriate secretion of antidiuretic hormone was diagnosed. He had taken sulpiride for depressed mental status. However, he showed parkinsonism, which was an adverse effect from the treatment of sulpiride. Therefore sulpiride was changed to selective serotonin reuptake inhibitor, paroxetine 10mg daily. His depressed mental status deteriorated after paroxetine treatment started. His depression had not lessened after 12 days, and the dosage was increased to 20mg daily. On the 15th day after starting paroxetine, routine laboratory tests showed that his serum sodium level was 126 mEq/l. We recognized that his confusion and loss of appetite were symptoms of hyponatremia, rather than of worsening depression. Laboratory data revealed hyponatremia, low serum osmolarity (242 mOsm/kg) with a relatively high level of serum antidiuretic hormone, and concentrated urine (439 mOsm/kg). We diagnosed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), associated with paroxetine. The dosage of paroxetine was reduced gradually and the serum sodium level returned to normal on day 2 after medication ceased completely. Paroxetine produces fewer adverse effects than other types of antidepressants. However, its use can be associated with inappropriate secretion of antidiuretic hormone in the body and may lead to SIADH, which is characterized by hyponatremia, a potentially fatal condition that is typically asymptomatic until it becomes severe. SIADH is more likely in some populations, including the elderly. Serum sodium levels should be monitored closely, especially in elderly patients.
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PMID:[Paroxetine-induced hyponatremia in an elderly man due to the syndrome of inappropriate secretion of antidiuretic hormone]. 1833 78

Exercise-associated hyponatremia (EAH) is a potentially fatal fluid imbalance largely resulting from sustained fluid intake beyond the capacity for fluid excretion during endurance exercise. Common symptoms include vomiting, confusion, altered mental status, and seizures; however, these symptoms can also be seen with hypernatremic encephalopathy, making measurement of plasma sodium concentration imperative when athletes present with these symptoms. Recent evidence supports the inappropriate secretion of the antidiuretic hormone, arginine vasopressin (AVP), as the primary pathophysiological mechanism underlying the development of dilutional EAH. It appears that AVP is stimulated normally during prolonged endurance running by non-osmotic factors such as an exercise-induced plasma volume decrease; therefore, any excess fluid intake will likely be retained, and sodium will likely be excreted. The capacity for a small concentrated bolus of a hypertonic saline solution to rapidly reverse cerebral edema and remove any decreased plasma volume stimulus to AVP secretion is the most efficacious treatment for acute EAH encephalopathy to date. The prompt administration of an intravenous (IV) bolus of hypertonic saline in the field or hospital setting can be lifesaving once EAH is documented. Conversely, oral sodium supplementation will not prevent the development of EAH encephalopathy if exuberant fluid intake combined with non-osmotic secretion of AVP occurs during prolonged physical activity. As a result, the seemingly paradoxical use of sodium supplementation as the most effective practical management therapy (IV bolus) and ineffective preventive strategy can be reconciled through a more complete understanding of the pathophysiological mechanisms underlying EAH.
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PMID:Practical management of exercise-associated hyponatremic encephalopathy: the sodium paradox of non-osmotic vasopressin secretion. 1861 87

The use of psychotropic drugs has been frequently associated with hyponatremia, which is defined as a serum sodium level of less than 136 mEq/l. The main cause in the psychiatric population is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Age, female sex and polypharmacy are risk factors for hyponatremia. In psychiatric patients, the symptomatology caused by hyponatremia may be confused with the mental illness itself, delaying its diagnosis. Early symptoms are nausea, vomits, anorexia, headaches, weakness, irritability, agitation, lethargy, confusion and cramps. The risk of hyponatremia increases with the use of several psychiatric drugs associated with SIADH. This complication is more often diagnosed at the first weeks of treatment. The first step of treatment is to determine the real level of hypoosmolality by measuring plasmatic osmolality. A urinary osmolality equal to or higher than 100 mOsm/kg combined with an elevated concentration of urinary sodium may lead to the diagnosis of SIADH. The main treatment for drug-caused hyponatremia is medication monitoring and normalization of extracellular liquid volume. In most cases this is achieved by discontinuing medication and restricting fluid intake.
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PMID:[Hyponatremia associated with psychotropic drugs: a side effect to consider]. 1942 19


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