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)

Neisseria meningitidis and Streptococcus pneumoniae are the most frequent causes of bacterial meningitis. The incidence of Haemophilus meningitis in the Netherlands is low due to successful Haemophilus influenzae type b vaccination. This implies that there is no need to take account into this microorganism in using initial empiric antimicrobial therapy for bacterial meningitis. Vomiting (especially children), headache, fever, and a stiff neck characterize acute bacterial meningitis. However, even without these signs a patient may still have acute bacterial meningitis. The characteristics in neonates are less specific. An emergency lumbar puncture should be performed in all patients with meningeal irritation or other signs of bacterial meningitis. Examination of the CSF is not indicated for convulsive children (between the ages of 6 months and 6 years) who do not exhibit other clinical signs. In patients who respond adequately to the treatment, it is not necessary to examine the CSF again. Papilloedema or focal neurological symptoms contraindicate a lumbar puncture in patients with bacterial meningitis, until CT results justify that it can be performed safely. Antibiotic treatment should not be delayed until after the CT. General practitioners should treat their patients with suspected meningococcus infection by admitting them to the hospital without first injecting antibiotics. In the Netherlands, patients with suspected pneumococcus meningitis may still be treated with benzylpenicillin. Patients with bacterial meningitis have no fluid restrictions; only in case of the syndrome of inadequate secretion of antidiuretic hormone is fluid reduction indicated. The physician is responsible for prescribing prophylaxis to family members. The Regional Health Services organize chemoprophylaxis for classmates. The latter is only indicated if at least 2 related cases occur in one month.
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PMID:[CBO-guideline 'Bacterial meningitis']. 1143 68

We present a case of subacute hyponatraemia which developed 3 days after a transurethral resection of the prostate. Symptoms consisted of nausea, vomiting and headache. Release of vasopressin due to excessive surgical bleeding, combined with liberal oral and intravenous administration of sodium-free fluids, was considered to be the cause.
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PMID:Subacute hyponatraemia after transurethral resection of the prostate. 1148 83

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

A 57-year-old man with amyotrophic lateral sclerosis (ALS) was admitted because of depressive state. Selective serotonin reuptake inhibitor (SSRI), an antidepressant, was started on the admission day. The throbbing headache in the right temporal region appeared on day 3, and an analgesic drug was not completely effective. Serum sodium value on admission was 131 mEq/l. After SSRI was started the hyponatremia rapidly progressed, and it became 112 mEq/l on day 4. SSRI was discontinued, and headache disappeared; serum sodium was improved to 129 mEq/l. It has been reported that syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may be associated with ALS. We consider that subclinical SIADH was manifested by SSRI in this case. SSRI seems to be a cause of headache, since headache disappeared completely by discontinuation of SSRI.
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PMID:[A case of amyotrophic lateral sclerosis with SIADH and throbbing headache induced by selective serotonin reuptake inhibitor]. 1235 54

We describe a 74-year-old man with rheumatoid arthritis (RA) who developed syndrome of inappropriate secretion of antidiuretic hormone (SIADH) 1.5 months after commencement of mizoribin prescription when his arthritis was improved. He noticed nausea and headache and serum Na fell as low as 118 mEq/l. Normal urinary Na excretion without hypotension or hemoconcentration negated the possibility of dehydration resulting from urinary Na loss. Serum antidiuretic hormone (ADH) remained elevated at 0.59 pg/ml in spite of a significant reduction in serum osmolality to 254 mosm/kg. He had no organic disease likely to cause SIADH. Despite infusion of hypertonic saline, his serum Na was not restored to normal. Shortly after mizoribin withdrawal, his serum Na increased significantly from 128 to 139 mEq/l and plasma osmolality from 265 to 287 mosm/kg. ADH hypersecretion in relation to plasma osmolality was reversed by mizoribin withdrawal, suggesting that bredinin might adversely induce SIADH. Additional predisposing factors were the patient's age and difficulty in urination due to benign prostatic hypertrophy. In summary, we report herein the first case of SIADH believed to be an adverse effect of mizoribin, which may therefore needed to be added to the list of drugs which can induce SIADH.
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PMID:A case of SIADH induced by mizoribin administration. 1239 45

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

Hyponatremia caused by an inappropriately high level of antidiuretic hormone secretion after spinal surgery is an uncommon and self-limiting phenomenon that resolves within 2 or 3 weeks. During the early postoperative period, the patient's urine output and serum level of sodium should be monitored closely to prevent possible serious complications of the syndrome of inappropriate secretion of antidiuretic hormone. Symptoms vary depending on the severity of the hyponatremia and can range from mild headache, muscle cramps, nausea, and vomiting to convulsions, coma, and death. Treatment options include fluid restriction, oral intake of salt, and hypertonic saline. It is important that spine surgeons recognize this phenomenon early and treat it appropriately and conservatively to prevent possible serious complications.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone and hyponatremia after spinal surgery. 1519 39

We enrolled six patients suffering from refractory chronic cluster headache in a pilot trial of neurostimulation of the ipsilateral ventroposterior hypothalamus using the stereotactic coordinates published previously. After the varying durations needed to determine optimal stimulation parameters and a mean follow-up of 14.5 months, the clinical outcome is excellent in three patients (two are pain-free; one has fewer than three attacks per month), but unsatisfactory in one patient, who only has had transient remissions. Mean voltage is 3.28 V, diplopia being the major factor limiting its increase. When the stimulator was switched off in one pain-free patient, attacks resumed after 3 months until it was turned on again. In one patient the implantation procedure had to be interrupted because of a panic attack with autonomic disturbances. Another patient died from an intracerebral haemorrhage that developed along the lead tract several hours after surgery; there were no other vascular changes on post-mortem examination. After 1 month, the hypothalamic stimulation induced resistance against the attack-triggering agent nitroglycerin and tended to increase pain thresholds at extracephalic, but not at cephalic, sites. It had no detectable effect on neurohypophyseal hormones or melatonin excretion. We conclude that hypothalamic stimulation has remarkable efficacy in most, but not all, patients with treatment-resistant chronic cluster headache. Its efficacy is not due to a simple analgesic effect or to hormonal changes. Intracerebral haemorrhage cannot be neglected in the risk evaluation of the procedure. Whether it might be more prevalent than in deep-brain stimulation for movement disorders remains to be determined.
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PMID:Hypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action. 1568 58

Levetiracetam (LEV) is increasingly used as adjunctive anticonvulsant therapy because of apparent low toxicity. Somnolence, asthenia, headache, dizziness, and nervousness are the most frequently reported side effects (1). We describe a patient, predisposed to the development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), in whom hyponatremia developed after two challenges of LEV.
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PMID:Hyponatremia associated with repeated use of levetiracetam. 1594 44

Escitalopram is the selective serotonin reuptake inhibitor (SSRI) most recently approved for use in the United States. It is structurally related to citalopram, but is felt to have a more tolerable side-effect profile than its parent compound. Side effects are not generally serious and include headache, diarrhea, and nausea. While hyponatremia and the syndrome of inappropriate antidiuretic hormone (SIADH) have been associated with treatment with other SSRIs, there has only been one case of escitalopram-induced SIADH reported in the literature to date. We now report another case of a patient who developed SIADH after being treated with escitalopram for 4 weeks. The patient's hyponatremia improved following the discontinuation of escitalopram. Clinicians should be aware of this uncommon but significant side effect of SSRIs and monitor high-risk patients for the development of SIADH.
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PMID:Syndrome of inappropriate antidiuretic hormone associated with escitalopram therapy. 1681 80


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