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)

Vasopressin is a naturally available neuropeptide that subserves important vasomotor, antinociceptive, behavior control, fluid and electrolyte balance, platelet aggregation and blood coagulation functions. This review focuses on the clinical phenomena of migraine that are likely to influence vasopressin bioavailability or efficacy as well as the modulating influence of vasopressin itself. As part of a complex homeostatic adjustment to stress and pain, the intricacies of vasopressin metabolism may have particular relevance to the pathophysiology of migraine.
Cephalalgia 1997 Aug
PMID:A clinical review of the adaptive role of vasopressin in migraine. 925 70

The majority of cases of central diabetes insipidus are still pathogenetically unclear (idiopathic). Atherosclerotic cholesterol emboli might be partly responsible for some of these idiopathic cases. A 54-year-old woman with known aortic valve stenosis and a history of a transitory ischemic attack presented with sudden-onset polyuria and polydipsia of up to eight l/d, which had started acutely with headaches. She had been treated with lithium for 3 years because of cyclothymic depression. Plasma sodium was in the upper normal range (142-148 mmol/l). Hypertonic saline infusion during lithium therapy revealed a normal threshold of thirst and resetting of vasopressin secretion (osmotic threshold > 300 mosmol/l), whereas vasopressin reserve was normal. Lithium withdrawal led to an even greater delay of vasopressin release upon hypertonic saline infusion (> 310 mosmol/l). Pituitary function tests revealed a normal anterior pituitary function. MR imaging of the hypothalamo-hypophyseal region showed a normal hypothalamic region and a highly intensive neurohypophyseal signal in the T1-weighted image. The patient responded well to desmopressin. We suggest that in this rare case clinical symptoms as well as biochemical findings like impairment of AVP release might be related to a minor structural hypothalamic damage by a vascular lesion, caused, for example, by an atheromatous (cholesterol) embolism in the hypothalamic region responsible for integration of osmoreceptor function and AVP-secretion. The patient's atherosclerosis and aortic stenosis might be responsible for this event.
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PMID:Atherosclerosis, aortic stenosis and sudden onset central diabetes insipidus. 928 11

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is characterized by hyponatraemia due to water retention resulting from the persistent release of antidiuretic hormone (vasopressin). It may occur in a variety of malignant and non-malignant conditions, in particular in association with oat cell carcinoma, pulmonary and cerebral diseases. We report the case of a male patient affected by melanoma of the right temporal region with brain metastasis who developed acute headache, drowsiness, nausea, vomiting and pathological reflexes. Clinical and laboratory investigations led us to the diagnosis of SIADH. Restriction of fluid intake obtained a good clinical improvement with normalization of laboratory alterations; after 2 months the patient experienced a new episode of SIADH which was promptly treated. As melanoma has been occasionally observed in association with SIADH it should be included in the list of tumours that can cause this particular syndrome.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in a patient affected by metastatic melanoma. 976 13

We describe a patient who had metastatic carcinoma of the stomach and severe headaches, weakness, and diplopia. The patient had meningeal carcinomatosis that was confirmed by examination of the cerebrospinal fluid after computed tomography of the brain was normal. Weakness was explained by the finding of hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). We believe this is the first reported case of meningeal carcinomatosis in which stomach carcinoma caused SIADH. The differentiation between SIADH and cerebral salt wasting due to malignant tumors is emphasized.
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PMID:Meningeal carcinomatosis and syndrome of inappropriate antidiuretic hormone in a patient with metastatic carcinoma of the stomach. 982 97

Motion sickness provides a unique setting for the study of nausea. Studies of illusory self-motion have linked nausea and objective measures of gastric dysrhythmias and the stress hormones vasopressin and epinephrine. Electrogastrographic methods utilize Ag-AgCl electrodes placed on the abdominal surface in the epigastric region to record electrogastrograms (EGGs), a noninvasive measure of gastric myoelectrical activity. The EGG frequencies of interest are the normal range (2.4-3.6 cpm), tachygastrias (3.6-9.9 cpm), and bradygastrias (1.0-2.4 cpm), and duodenal respiratory frequencies (10.0-15.0 cpm). Illusory self-motion or vection is produced with a rotating drum. Minutes before vection-induced nausea is reported, the baseline EGG signal shifts into tachygastrias or mixed tachygastrias and bradygastrias. Quantitative analyses show that the percentage of power in the tachygastria range correlates with the intensity of nausea. Plasma vasopressin levels correlate positively with intensity of nausea. Asian subjects have higher intensity nausea and higher vasopressin levels compared with Caucasian subjects, indicating a potential genetic susceptibility to vection-induced motion sickness and nausea. Vection-induced motion sickness represents an experimental model of acute-onset nausea with accompanying symptoms such as headache, drowsiness, cold sweating, and fatigue. Illusory self-motion is a purely central nervous system (visual-vestibular) stimulation that evokes dramatic shifts in gastric electrical activity and significant release of the posterior pituitary hormone vasopressin. Central nervous systems pathways that evoke gastric dysrhythmias and release vasopressin may also have a pathophysiologic role in the cyclic vomiting syndrome.
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PMID:Illusory self-motion and motion sickness: a model for brain-gut interactions and nausea. 1049 40

The causes of pituitary apoplexy are unclear. We report a case of pituitary apoplexy presenting with headache and nausea. On June 17th, 1997 a 74-year-old woman had complained of retro-orbital headache, fever and vomiting. A cold was diagnosed for which she recurred medication. In addition to the previous symptoms she was getting to lose appetite. She was admitted to our hospital for further examination and treatment on June 21. On admission neurological examination showed left pupil mydriasis, the left eye had no light reflex and the right eye had only a slight response to the light. She could hardly move both eyeballs up. Laboratory data showed a normal white blood cell count and the CRP was 16.2 mg/dl. Lumbar puncture showed 97 mg/dl total protein and 82 cells per microliter, most of which were lymphocytes. We diagnosed viral infection based on the evidence of clinical symptoms and lumbar puncture data. The patient was treated with gamma-globulin and improved. From the 16th day of sickness we recognized symptoms of oculomotor paralysis and the syndrome of inappropriate antidiuretic hormone. On the 23rd day of sickness we strongly suspected pituitary apoplexy based on transaxial MR images. After absorption of intra-tumor hemorrhage, the oculomotor symptoms recurred. We finally reached a diagnosis of pituitary apoplexy based on pathological material, MR images, symptoms and laboratory data. We must think of pituitary apoplexy when we see an aged out-patient with severe headache, nausea, vomiting and oculomotor paralysis. It was difficult to diagnose this disease in the early time course of the disease.
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PMID:[A case of pituitary apoplexy approving as severe headache and nausea]. 1065 40

Pituicytoma is a rare, poorly characterized tumor of the sella and suprasellar region that is distinct morphologically from other local tumors and is thought to be derived from neurohypophyseal pituicytes. Clinical data, neuroimaging studies, and microsections were reviewed from nine such low-grade gliomas. Immunostains for glial, neuronal, and proliferation markers were performed on all nine tumors and six control neurohypophyses. Three tumors were studied ultrastructurally. Six men and three women, age 30 to 83 years (mean, 48 years), presented with visual symptoms, headache, or hypopituitarism. Magnetic resonance images showed solid, discrete, contrast-enhancing masses, four within the sella and five in the suprasellar space. The tumors consisted of sheets and/or fascicles of plump spindle cells with slightly fibrillar cytoplasm and slightly pleomorphic, oval-to-elongate nuclei with pinpoint nucleoli. Extracellular mucin was prominent in one tumor. Rosenthal fibers, granular bodies, and Herring bodies (granular axonal dilatations characteristic of the normal neurohypophysis) were lacking. Mitoses were rare or absent. MIB-1 labeling indices were low (0.5-2%). Tumor cells were strongly reactive for vimentin and S-100 protein, variably positive for glial fibrillary acidic protein, and nonreactive for synaptophysin and neurofilament protein. Cytoplasm varied in electron density and contained intermediate filaments. Neither meningothelial nor ependymal features were noted. Two tumors recurred at 20 and 26 months after subtotal resection, but none of the six completely resected tumors have done so. Pituicytomas are discrete, largely noninfiltrative low-grade gliomas of the sellar region that occur in adults. Their histologic appearance is distinct from pilocytic and ordinary, infiltrative astrocytomas. The distinction between pituicytoma and normal neurohypophysis is aided by the latter's content of axons, Herring bodies, and perivascular anucleate zones rich in axonal terminations. Although curable by total excision, subtotal resection can be associated with recurrence.
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PMID:Pituicytoma: a distinctive low-grade glioma of the neurohypophysis. 1071 49

A 73-year-old man with acute adult T-cell leukemia (ATL) in remission was re-admitted to our hospital due to drowsiness, headache, and bilateral knee joint pain on May 17, 1998. On admission, examinations revealed decreased serum sodium concentration (112 mEq/l), low plasma osmotic pressure (259 mOsm/l), and elevated antidiuretic hormone(5.6 pg/ml). Cerebrospinal fluid examination showed an increased number of abnormal flower-like lymphocyte (951/microliter). Brain computed tomography and magnetic resonance imaging found no abnormality in the hypothalamus or pituitary gland. These findings yielded a diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Though ATL patients typically exhibit a variety of clinical symptoms, SIADH is rarely one of the complications. Further investigation showed that IL-1 beta and IL-6 concentrations were increased in spinal fluid but not in serum. Recently, it has been reported that exogeneous IL-6 is an inducer of ADH secretion, and that primary ATL cells and HTLV-I infected cell lines can produce IL-6. In this case, we speculated that IL-6 produced by ATL cells that infiltrated a cerebral lesion may have played an important role in the development of SIADH.
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PMID:[Syndrome of inappropriate antidiuretic hormone secretion associated with meningeal infiltration of tumor cells and elevated interleukin-1 beta and interleukin-6 in cerebrospinal fluid of a patient with adult T-cell leukemia]. 1072 44

Sinonasal teratocarcinosarcoma (SNTC) is a rare, aggressive, histologically heterogeneous neoplasm of the paranasal sinuses and nasopharnyx of adults that is composed of variably benign or malignant neuroepithelial, epithelial, and mesenchymal elements. Occasional cases show intracranial extension and may be operated on by neurosurgeons and encountered by neuropathologists who may not be familiar with the entity. STNCs have not previously been associated with functional hypersecretory status. We report a 59-year-old male who presented with headache and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and was subsequently found to have a bulky tumor of the frontal and ethmoid sinuses with focal dural invasion. The tumor was predominantly composed of olfactory neuroblastoma areas (90% of tumor) admixed with unusually well-developed craniopharyngioma-like mature squamous epithelium and ghost cells ( 10% of tumor). Scattered neuroblastoma tumor cells showed strong immunoreactivity with antibodies to arginine vasopressin, supporting ectopic hormone secretion by the tumor. While the coexistence of neuroectodermal and oral ectodermal-like differentiation in SNTCs is characteristic, in our case it was developed to an extreme functional and morphologic degree and was unassociated with other mesenchymal or epithelial elements often found in these complex tumors. SNTCs with limited differentiation have prompted controversy in classification.
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PMID:Sinonasal teratocarcinosarcoma ("mixed olfactory neuroblastoma-craniopharyngioma") presenting with syndrome of inappropriate secretion of antidiuretic hormone. 1074 86

We report a case of a seventy-year-old woman with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by Rathke's cleft cyst. She experienced nausea, vomiting, diarrhea, and headache and disturbance of consciousness induced by hyponatremia at a serum sodium level of 100 mEq/l. In spite of severe hyponatremia, urinary sodium excretion was not suppressed and serum osmolality (270 mOsm/kg) was lower than urine osmolality (304 mOsm/kg), and arginine vasopressin (AVP) remained within normal range. SIADH was diagnosed because she was free from other diseases known to cause hyponatremia such as dehydration, cardiac dysfunction, liver dysfunction, renal dysfunction, hypothyroidism, and adrenal insufficiency. Cranial computed tomographic (CT) scan and cranial magnetic resonance (MR) imaging showed a cystic lesion of approximately 2 cm in diameter in the pituitary gland. These images suggested that the cystic lesion was a Rathke's cleft cyst, which was the cause of SIADH. Water restriction therapy normalized her serum sodium concentration and improved her symptoms. After one year, she suffered from general fatigue, appetite loss, fever, and body weight loss (5 kg/2 months). She had neither hypotension nor hypoglycemia, but her serum sodium level was low and serum cortisol, ACTH, and urine free cortisol were very low. Therefore, secondary adrenal insufficiency was suspected and diagnosed by stimulation tests. After start of hydrocortisone replacement therapy (10 mg/day), her symptoms disappeared. In conclusion, Rathke's cleft cyst should be kept in mind as a potential cause in a patient with SIADH, hypopituitarism, and/or adrenal insufficiency.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by rathke's cleft cyst: a case report. 1107 19


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