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 57 year old woman presented with diffuse muscle spasms and delirium. Prior to presentation, she complained of progressive muscle pain, weakness and a weight loss of 10 kg over several months. Laboratory investigation showed hypopituitarism and a syndrome of inappropriate antidiuretic hormone secretion. Magnetic resonance imaging revealed an empty sella. The primary and secondary syndromes of empty sella are discussed.
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PMID:[Unexpected development during rehabilitation for suspected rheumatic disorder]. 1054 May 70

The Brown Norway (BN) rat is normotensive and has an extended lifespan but is extremely sensitive to hypertension-induced renal injury. Relative impairment of autoregulation has been implicated in the progression of renal failure whereas absence of myogenic autoregulation is associated with early renal failure. Therefore, we tested the hypothesis that there is conditional failure of renal autoregulation in BN rats. In isoflurane-anesthetized BN rats, the pressure-flow transfer function was normal when pressure fluctuated spontaneously. External forcing increased pressure fluctuation and exposed weakness of the myogenic component of autoregulation; the component mediated by tubuloglomerular feedback was less affected. In the presence of vasopressin to raise renal perfusion pressure, myogenic autoregulation was further impaired during forcing in BN rats but not in Wistar rats. Compensation by the myogenic system was rapidly restored on cessation of forcing, suggesting a functional limitation rather than a structural failure. Graded forcing in Wistar rats and in spontaneously hypertensive rats revealed that compensation due to the myogenic system was strong and independent of forcing amplitude. In contrast, graded forcing in BN rats showed that compensation was reduced when fluctuation of blood pressure was increased but that the reduction was independent of forcing amplitude. The results demonstrate conditional failure of myogenic autoregulation in BN rats. These acute studies provide a possible explanation for the observed sensitivity to hypertension-induced renal injury in BN rats.
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PMID:Impaired myogenic autoregulation in kidneys of Brown Norway rats. 1083 84

We report the case of a 62-year-old man who was administered sodium valproate (VPA) and who subsequently developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). He had been taking VPA for treatment of idiopathic generalized tonic-clonic convulsions since he was 56 years old. After substituting VPA with zonisamide, the serum sodium level returned to normal. We consider this episode of SIADH to be the result of a combination of factors including a weakness of the central nervous system and the long-term administration of VPA.
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PMID:Contribution of sodium valproate to the syndrome of inappropriate secretion of antidiuretic hormone. 1119 62

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

Hyponatremia can result from a wide range of causes. While hyponatremia is known to occur in patients with hypopituitarism, severe hyponatremia occurring as the presenting feature of hypopituitarism is very rare. We present two cases in which severe hyponatremia developed with weakness, light-headedness and seizure. The hyponatremia in these 2 cases mimicked the laboratory diagnostic criteria of a syndrome of inappropriate secretion of antidiuretic hormone (SIADH). However, the hormone studies displayed hypopituitarism. Hyponatremia was completely corrected after administering a supplement of prednisolone and L-thyroxine. Computerized tomography of the brain revealed an adenoma of the pituitary gland. These two cases illustrate that severe hyponatremia may be the presenting feature of clinically non-functional pituitary adenoma with hypopituitarism, which should be kept in mind in the differential diagnosis of hyponatremia mimicking SIADH.
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PMID:Severe hyponatremia as the presenting feature of clinically non-functional pituitary adenoma with hypopituitarism. 1183 7

Two major characteristics of space flight may be simulated to some degree by bed rest and by water immersion. These are inactivity and the lack of the hydrostatic stress on the systematic circulation. Studies prior to the advent of space flight led to the prediction of orthostatic intolerance, muscular weakness, and calcium loss. Prolonged space flight has heightened the interest in these simulations to provide information concerning the temporal cause of the "deconditioning" or disuse syndrome and the value of simulation for testing the effectiveness of remedial measures. This report will evaluate the extent to which the simulation appears valid. In its gross effects, orthostatic intolerance can be studied with respect to its temporal course, etiology and effectiveness of remedial measures. The intolerance develops more rapidly during water immersion with respect to cause as well as effect. The short term of immersion studies does not allow study of the secondary change in blood volume due to red cell mass changes, Remedial measures seem clearly defined in water immersion simulation and less clear in bed rest. Measures of venous pooling following water immersion appear different than those obtained following weightlessness. There also appear to be differences in the results of evaluation of protective devices and measures and in the time course of development and recovery of orthostatic intolerance. Correlates of the cardiovascular responses such as muscle tone, skeletal strength, and endocrine change (catecholamines, vasopressin and aldosterone) suggest a marked alteration in physiology during hypodynamic status. To date, work on exposure to increased G force has provided only extrapolated data concerning metabolic requirements.
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PMID:Cardiovascular studies during and following simulation and weightlessness. 1197 49

We report an autopsy-confirmed case of amyotrophic lateral sclerosis (ALS) accompanied by syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 67-year-old man was admitted to our hospital with muscle weakness, dysarthria and dysphagia. During hospitalization, respiratory insufficiency was ingravescent, and hyponatremia, hypo-osmolarity, elevated osmotic pressure of urine, and elevated urinary sodium excretion were noted. Based on these findings we diagnosed ALS with SIADH, and treatment with infusion of concentrated NaCl was started. However, the patient died of respiratory failure on day 50. We assumed that severely restrictive ventilatory impairment was the cause of SIADH in this case.
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PMID:An autopsy case of amyotrophic lateral sclerosis accompanied by syndrome of inappropriate secretion of antidiuretic hormone. 1205 91

We report on seven elderly patients with severe hyponatremia (plasma sodium < 125 meq/l). All were symptomatic for central nervous system disturbances, weakness, nausea/vomiting and met clinical and laboratory criteria for the diagnosis of inappropriate secretion of antidiuretic hormone (SIADH). Investigations performed to determine the etiology of the syndrome gave negative results, so that the form was considered to be idiopathic. TC scans or MNR showed brain atrophy and/or chronic ischemic lesions. According to the scant series found in the literature, we believe that aging itself may be a risk factor for SIADH. Lowering of the osmolal threshold and/or reduced receptors sensitivity to osmotic stimula, induced by ischemic changes in the hypothalamic region, can represent the underlying mechanisms.
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PMID:[Severe idiopathic hyponatremia caused by ADH inappropriate secretion in the elderly]. 1208 17

We describe an 18-year-old female who complained of general weakness, nausea, vomiting, headache, and lightheadedness. On physical examination, she was euvolemic without visual or neurological deficits. The striking biochemical abnormality was hyponatremia (125 mmol/l). This hyponatremia met the laboratory diagnostic criteria for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Two litres of normal saline were given per day for 4 days and this did not correct her hyponatremia. A spontaneous diuresis (6.6 l) developed in 1 day, causing a rise in her PNa of 26 mmol and a final PNa of 152 mmol/l. Magnetic resonance imaging revealed a dumbell-shaped intrasellar and suprasellar cyst. During transsphenoidal surgery, a Rathke's cleft cyst (RCC) lined with columnar epithelium containing mucoid material was resected. We speculate that the growing RCC may have produced critical compression over the stalk, thus contributing to the transition from SIADH with hyponatremia to transient central diabetes insipidus with hypernatremia.
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PMID:Rathke's cleft cyst presenting with hyponatremia and transient central diabetes insipidus. 1271 31

A 68-year-old man was admitted to our hospital because of muscle weakness. A complete medical examination led to a diagnosis of small cell lung carcinoma (SCLC) with Lambert-Eaton myasthenic syndrome (LEMS) and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Four courses of chemotherapy (carboplatin + etoposide) and one of radiotherapy with a total dose of 45 Gy to the mediastinum were performed and resulted in a partial response in the SCLC. After the second course of chemotherapy, the serum level of antivoltage-gated Ca2+ channel (VGCC) antibody decreased from 190 pg/ml to 120 pg/ml. Marked improvement of the muscle weakness was recognized only after 3 courses of chemotherapy. The patient, who had had difficulty in standing, recovered enough to be able to climb stairs after 4 courses of chemotherapy. Marked improvement of LEMS was achieved by treatment for small cell lung carcinoma.
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PMID:[Marked improvement of Lambert-Eaton myasthenic syndrome resulting from treatment for small cell lung carcinoma]. 1282 23


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