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)

A thirty-year-old male patient suffered subarachnoidal haemorrhage from an angioma positioned in the cranio-cervical transition. After rebleeding twice the patient developed a hydrocephalus internus malresorptivus and excessive natriuresis and polyuria, accompanied by depressed renin activity and extremely low aldosterone plasma levels. Neither fluid restriction and sodium substitution, nor administration of hydro-chlorothiazide/indomethacin affected natriuresis and polyuria. It was only after treatment with fludrocortisone-acetate/hydrocortisone that hyponatraemia and polyuria were resolved. At the same time a ventriculo-peritoneal shunt was applied. Differential diagnosis excluded the syndromes of inadequate antidiuretic hormone secretion, renal and cerebral diabetes insipidus, osmotic receptor hypofunction, chronic renal dysfunction and tubular necrosis. Natriuresis and polyuria developed under dexamethasone therapy. Since patient history, physical examination and laboratory criteria could not explain the electrolyte and fluid imbalance, this might be attributed to the hydrocephalus. Similar disturbances have been reported from other patients with intracranial disorders. Mechanical pressure exercised on the hypothalamus might cause the disturbance of fluid and sodium balance. Assuming a cerebral salt wasting syndrome, a putative natriuretic factor coming from the brain or an imbalance in the cerebral renin-angiotensin-system, as described in rats and dogs, must be discussed.
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PMID:[Massive natriuresis and polyuria after triple craniocervical subarachnoid hemorrhage: cerebral salt wasting syndrome?]. 148 43

An optic chiasm glioma may cause loss of vision, endocrine disturbances, hydrocephalus and cerebral ischemia due to its proximity to the pituitary, hypothalamus, III ventricle and internal carotids. A 3-month-old infant with optic chiasm glioma developed hypopituitarism and inappropriate secretion of antidiuretic hormone with plasma hypo-osmolality. The cerebrospinal fluid (CSF) protein concentration was markedly elevated. The impairment of fluid absorption via arachnoid villi and peritoneum by the high protein content, and reversed osmotic gradient between protein-rich CSF and hypo-osmolar plasma may have contributed to both nonobstructive hydrocephalus and recurrent ascites following ventriculoperitoneal shunting. Cerebral ischemia from carotid compression may have led to cerebral atrophy.
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PMID:Optic chiasm glioma associated with inappropriate secretion of antidiuretic hormone, cerebral ischemia, nonobstructive hydrocephalus and chronic ascites following ventriculoperitoneal shunting. 179 May 31

Two cases of neurological deterioration and coma after the transsphenoidal decompression of a pituitary adenoma with marked suprasellar extension and invasion of the 3rd ventricle are presented. Emergency ventricular shunting led to prompt neurological improvement, which, supplemented by radiation therapy, allowed long-term amelioration of symptoms. Three possible explanations for this complication are offered: 1) traction of the attached 3rd ventricle into the decompression site, causing increased obstructive hydrocephalus, 2) vasopressin release by surgical manipulation of the pituitary stalk and circumventricular organs causing cerebral edema, and 3) edema in the residual tumor secondary to surgical manipulation causing further hydrocephalus. Subsequent patients with similar clinical and imaging criteria will have a planned perioperative ventricular shunting procedure performed.
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PMID:Progressive coma after the transsphenoidal decompression of a pituitary adenoma with marked suprasellar extension: report of two cases. 199 71

A rare case of an abscess in the cavum septi pellucidi (CSP) is described and previously reported cases are reviewed. A 60-year-old male was admitted to the hospital because a diagnosis of cerebellar hemisphere infarction was made on CT scan. Seven years earlier, the patient had undergone a craniotomy for aneurysm clipping, and a ventriculo-peritoneal shunt was installed for normal pressure hydrocephalus 14 days after the aneurysmal rupture. On his second hospitalization CT scan also demonstrated CSP but this was not associated with ventriculomegaly. He was placed on a rehabilitation regimen and his hospital course was uneventful. Two months later, however, he developed hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. After analysis of CSF obtained from the shunting device, a diagnosis of meningitis was made and CSF culture revealed E. coli infection. A part of the peritoneal tubing was torn and missing when the tube was removed from the peritoneal cavity and converted to outer drainage. Being treated with intrathecal and intravenous antibiotics administration, the meningitis subsided. However, CT scan taken twelve days after the onset of the infection showed an abscess in CSP which showed ring enhancement after contrast media. Therefore, the patient continued to receive intravenous antibiotics to counter the mass effect due to the abscess. The abscess had disappeared on follow-up CT scan obtained ten days later. The patient, however, eventually expired after iatrogenic hypernatremia associated with acute renal failure. The patient was submitted to an autopsy. The authors speculate that the abscess developed through a retrograde cisternal route after infection which had originated from bowel perforation by the peritoneal shunt tube.
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PMID:[A case report: abscess of the cavum septi pellucidi]. 202 72

A retrospective study of 134 patients in a condition of prolonged unawareness state (that is, in coma for over 1 month) following brain trauma was conducted in order to identify prognostic factors. Eight easily evaluated parameters were found to be significant for predicting nonrecovery of consciousness. The following six features were present during the early posttraumatic phase (that is, during the 1st week after trauma): fever of central origin; diffuse body sweating; disturbances in antidiuretic hormone secretion; abnormal motor reactivity; respiratory disturbances; and diffuse nonneurological injuries. The first three features were manifestations of hypothalamic damage. Two factors, evident at a late phase following injury (after the 1st week posttrauma), namely late epilepsy and communicating hydrocephalus, were also significant in predicting nonrecovery.
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PMID:Outcome in 134 patients with prolonged posttraumatic unawareness. Part 1: Parameters determining late recovery of consciousness. 229 88

The authors report two cases of pseudotumor cerebri in patients taking lithium for treatment of bipolar disorder. Pseudotumor cerebri is a poorly understood syndrome characterized by chronic headaches, bilateral papilledema, and increased intracranial pressure without localized neurologic signs or symptoms, intracranial mass, or hydrocephalus. Ventriculography, computed tomography, and nuclear magnetic resonance imaging reveal normal or small ventricles. Multiple etiologies may include Vitamin A toxicity, obesity, head trauma, hypothyroidism or hyperthyroidism, prolonged steroid therapy or its withdrawal, Addison's disease, Cushing's disease, pituitary insufficiency, and lithium therapy. Patients treated with lithium whose antidiuretic hormone-cyclic adenosine monophosphate mechanism is disturbed are most likely to develop pseudotumor cerebri via disregulation of sodium balance, thyroid-stimulating hormone production, and glucose metabolism. The authors recommend careful medical monitoring to avoid iatrogenic effects of lithium, including pseudotumor cerebri.
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PMID:Pseudotumor cerebri associated with lithium therapy in two patients. 203 32

The concentration of arginine vasopressin (AVP) was measured in cerebrospinal fluid (CSF) by radioimmunoassay. Serial dilution curves and reversed-phase high-pressure liquid chromatography (HPLC) showed that the material measured behaved identically to authentic vasopressin. Levels of CSF AVP were reduced by 37% in Alzheimer's disease, but were normal in Huntington's disease, normal-pressure hydrocephalus, and several other neurologic disorders. On direct comparison, the CSF AVP concentration was significantly lower in Alzheimer's disease than in normal-pressure hydrocephalus. Low CSF levels of AVP may therefore assist in the identification of demented patients who are not likely to benefit from ventricular shunting.
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PMID:CSF vasopressin concentration is reduced in Alzheimer's disease. 373 84

The responses of plasma and ventricular cerebrospinal fluid (CSF) vasopressin concentration to dehydration, postural changes, and induction of nausea were studied in 21 patients with hydrocephalus of various etiology. The 24-h dehydration test evoked a significant increase in plasma osmolality and vasopressin concentration, whereas the concentration of vasopressin in CSF was unchanged. Head-up tilt to 50 degrees for 45 min with a tilt bed resulted in a modest increase of plasma vasopressin in patients who did not develop presyncopal symptoms, but no changes were seen in CSF vasopressin. Induction of nausea by subcutaneously injected apomorphine provoked a marked (20- to 50-fold) rise in plasma vasopressin concentration within 15 min, and the plasma concentration was significantly increased above base-line values for 60-120 min. Despite the prolonged period of high plasma vasopressin concentration CSF vasopressin was not influenced by the apomorphine injection. The findings suggest that the concentration of vasopressin in the CSF is controlled by mechanisms other than the well-known osmotic and nonosmotic stimuli of vasopressin release into the blood.
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PMID:Vasopressin in plasma and ventricular cerebrospinal fluid during dehydration, postural changes, and nausea. 397 Jan 88

Vasopressin was determined in CSF and plasma of 243 patients with different neurological and psychiatric disorders, including control patients. CSF vasopressin was significantly higher in patients with high pressure hydrocephalus, intracranial tumour, benign intracranial hypertension, intracranial haemorrhage, ischaemic stroke, and craniocerebral trauma. In patients with primary degenerative dementia, CSF vasopressin was lower than in control patients. Among patients with psychiatric disorders, CSF vasopressin was increased in manic patients, while in patients with depression CSF concentration of this hormone did not differ from that found in controls. However, an increase in CSF vasopressin level was found in patients recovering from a depression. The clinical significance of changes in CSF vasopressin concentrations in groups of patients with neurological and psychiatric disorders is still unknown.
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PMID:Cerebrospinal fluid vasopressin in neurological and psychiatric disorders. 397 21

The response of plasma and ventricular cerebrospinal fluid vasopressin concentration to short-time induced intracranial hypertension was studied in 8 patients with hydrocephalus, defined as ventricular enlargement on computerized tomography. In connection with measurement of conductance to cerebrospinal fluid outflow, the concentration of vasopressin in plasma and cerebrospinal fluid was measured during perfusion at a low (less than 10 mmHg) and at a high (greater than 20 mmHg) intraventricular pressure level. Mean plasma vasopressin concentration was increased from 2.4 +/- 0.4 pg/ml (SEM) during perfusion at the low pressure level to 4.2 +/- 0.8 pg/ml (p less than 0.01) at the high pressure level. The cerebrospinal fluid concentrations of vasopressin at the low and high intraventricular pressure were 1.2 +/- 0.1 pg/ml and 1.7 +/- 0.2 pg/ml (p less than 0.05), respectively. However, only half of the patients responded to the increase in intraventricular pressure with an increase in cerebrospinal fluid vasopressin concentration exceeding 50%. The results of the present study suggest that an increase in the intracranial pressure might be a stimulus for vasopressin release in both the blood and the cerebrospinal fluid.
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PMID:Cerebrospinal fluid and plasma vasopressin during short-time induced intracranial hypertension. 403 77


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