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)

Central diabetes insipidus (DI) can be the outcome of a number of diseases that affect the hypothalamic-neurohypophyseal axis. The causes of the condition can be classified as traumatic, inflammatory, or neoplastic. Traumatic causes include postoperative sella or transection of the pituitary stalk, while infectious or inflammatory causes include meningitis, lymphocytic hypophysitis, and granulomatous inflammations such as sarcoidosis and Wegener's granulomatosis. Various neoplastic conditions such as germinoma, Langerhans cell histiocytosis, metastasis, leukemic infiltration, lymphoma, teratoma, pituitary adenoma, craniopharyngioma, Rathke cleft cyst, hypothalamic glioma, and meningioma are also causes of central DI. In affected patients, careful analysis of these MR imaging features and correlation with the clinical manifestations can allow a more specific diagnosis, which is essential for treatment.
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PMID:MR imaging of central diabetes insipidus: a pictorial essay. 1175 30

Diabetes insipidus is a disorder of the water retaining ability of the organism. It is a polydipsic-polyuric syndrome caused by partial or complete vasopressin deficiency (central diabetes insipidus) or vasopressin resistance of the kidney tubules (nephrogenic diabetes insipidus) or increased water intake due to oversensitivity of the thirst centre (dipsogenic diabetes insipidus = primary polydipsia). The pathogenetic factors may affect the osmoreceptors, the vasopressinergic magnocellular nuclei of the hypothalamus, the median eminence, the pituitary stalk, the vasopressin release from the neurohypophysis, the vasopressin inactivating mechanisms and the renal structures mediating the antidiuretic effect of vasopressin. In the evaluation of the results of the diagnostic procedures, it is to be considered that long-term overhydration of any origin suppresses the vasopressin secretion and the "washout" effect of the long-term water-diuresis decreases the concentration gradient of the renal medulla leading to blunted sensitivity towards vasopressin. This is, why the differential diagnostics of central, nephrogenic and dipsogenic diabetes insipidus seems sometimes to be enigmatic. Central diabetes insipidus can be excluded only on the basis of proportional parallel increase of plasma osmolality and plasma vasopressin level. Similarly, nephrogenic diabetes insipidus will be excluded when plasma vasopressin increases proportionately with the increase of urinary osmolality. In equivocal cases T1-weighted MRI of the pituitary may be of help in the establishment of an exact diagnosis. As far as possible, the therapy is to be focused on the diabetes insipidus evoking basal diseases. In central diabetes insipidus, diuresis can be decreased by vasopressin substitution. The first choice compound for this purpose is 1-desamino-8-D-arginine-vasopressin. The non-vasopressin containing oral antidiuretics have become outdated in the treatment of central diabetes insipidus. There is no specific treatment for nephrogenic and dipsogenic diabetes insipidus, so far. Nephrogenic diabetes insipidus can be influenced by non-steroidal antiinflammatory agents or diuretics. Their combined administration is even more effective, however, still does not exceed a 50-percent mitigation in diuresis.
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PMID:[Diabetes insipidus: etiology, diagnosis, and therapy]. 1252 Aug 52

Central diabetes insipidus (CDI) is a rare hypothalamus-pituitary disease due to the deficiency of arginine vasopressin (AVP) synthesis from the hypothalamus and/or secretion from the neurohypophysis. The etiology of CDI is unknown in over one third of cases, classified as idiopathic CDI. The aim of this study was 2-fold: 1) to evaluate the occurrence of circulating autoantibodies to AVP-secreting cells (AVPcAb), and 2) to correlate it to clinical (sex, age of disease onset, disease duration, and degree), immunological (clinical history of autoimmune diseases and presence of related organ-specific autoantibodies), and radiological features (neurohypophyseal bright spot, pituitary stalk thickening, and empty sella) in a large cohort of patients with apparently idiopathic CDI or CDI of known etiology. To this purpose, 150 patients with CDI were studied: 64 idiopathic, 6 familial, 12 associated to granulomatous diseases, and 68 secondary to cranial trauma, tumor, or surgery. AVPcAb were measured by an indirect immunofluorescence method. AVPcAb were found in 23.3% of CDI patients: 21 idiopathic (32.8%) and 14 nonidiopathic (16.3%; chi(2) = 13.1; P < 0.001). AVPcAb were independently associated with age less than 30 yr at disease onset (P = 0.001) in patients with idiopathic CDI and with history of autoimmune diseases (P = 0.006 and P = 0.02, respectively) and radiological evidence of pituitary stalk thickening (P = 0.02 and P = 0.003, respectively) in both idiopathic and nonidiopathic CDI. The likelihood of autoimmunity in one patient with apparently idiopathic CDI with age of disease onset less than 30 yr was 53%, it increased to 91% when history of autoimmune diseases was associated and to 99% when pituitary stalk thickening was further associated. In conclusion, autoimmunity is associated with one third of patients with apparently idiopathic CDI, which should therefore be classified as autoimmune CDI. Autoimmune CDI is highly likely in young patients with a clinical history of autoimmune diseases and radiological evidence of pituitary stalk thickening. Conversely, autoimmunity probably represents an epiphenomenon in patients with nonidiopathic CDI.
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PMID:Central diabetes insipidus and autoimmunity: relationship between the occurrence of antibodies to arginine vasopressin-secreting cells and clinical, immunological, and radiological features in a large cohort of patients with central diabetes insipidus of known and unknown etiology. 1267 49

Central diabetes insipidus, characterized by severe polyuria and polydipsia, is a disorder resulting from deficient secretion of the small neuropeptide hormone vasopressin in the neurohypophysis. The standard therapy is daily and life-long administration of vasopressin analog (desmopressin acetate), but gene therapy is potentially alternative to the conventional replacement therapy. To obtain the therapeutic neuropeptide more feasibly, we tried to express vasopressin in nonneuronal tissues using nonviral gene transfer techniques. We found that the unprocessed large precursor form, provasopressin, was predominantly produced in nonendocrine cells transfected with the wild-type vasopressin gene, because of the lack of neuroendocrine cell-specific endopeptidases. In sharp contrast, appropriately processed bioactive vasopressin can be efficiently produced even in nonendocrine cells with a modified vasopressin gene containing a ubiquitous endoprotease furin cleavage site. We also succeeded in maintaining a long-term antidiuretic effect on vasopressin-deficient (Brattleboro) rats by direct introduction of the furin-processible gene into skeletal muscle by electroporation. Altogether, our data clearly show that skeletal muscle is a useful target tissue for continuous delivery of bioactive neuropeptide. Furthermore, our strategies may be applicable to future gene therapies for central diabetes insipidus and other peptide hormone deficiencies.
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PMID:Gene therapy for central diabetes insipidus: effective antidiuresis by muscle-targeted gene transfer. 1452 7

Central diabetes insipidus (CDI) arising in the puerperal period has been attributed mainly to Sheehan's syndrome or to lymphocytic infundibulo-neurohypophysitis. We report the case of a 24-year-old woman who came to our observation for the appearance, 3 weeks after a normal delivery, of a polyuric-polydipsic syndrome. Measurements of urinary volumes, plasma osmolality and urinary osmolality, in conditions of free water intake, water deprivation and a water deprivation-vasopressin administration test, demonstrated CDI. Brain magnetic resonance imaging showed a normal morphology of the adenohypophysis and total absence of the neurohypophysis. Assays of the pituitary hormones were found to be within normal limits. These results, incompatible with a diagnosis of Sheehan's syndrome and lymphocytic infundibulo-neurohypophysis, excluded all the other known causes of acquired CDI. Our diagnosis was therefore of post-gravid idiopathic CDI. Thus, it is possible that in the puerperal period other diseases of the posterior hypophysis may develop, of unknown etiopathogenesis but equally responsible for CDI.
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PMID:A rare case of central post-gravid diabetes insipidus. 1469 Feb 63

Central diabetes insipidus (DI) is a rare but recognized complication of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) that is caused by leukemic infiltration to the hypothalamo-neurohypophyseal system. In rare patients in whom a wide region of the hypothalamus is involved, central DI results in hypodipsic hypernatremia and dehydration. Typical DI symptoms such as polydipsia, polyuria, and marked thirst are concealed in these cases, because the hypothalamic "thirst center" cannot send thirst stimuli to the cerebral cortex. Herein we describe a patient with MDS developing into AML, who presented with hypodipsic hypernatremia and dehydration. A diagnosis of central DI was made on the ground of a low level of serum anti-diuretic hormone (ADH) despite high serum osmolality. A magnetic resonance imaging study revealed attenuation of a physiological "bright spot" of the neurohypophysis. An induction course chemotherapy including regular-dose cytarabine and daunorubicin produced a rapid improvement of hypernatremia. The bone marrow aspirate after two courses of chemotherapy showed complete remission. At that point, ADH release and the "bright spot" were recovered. In order to correctly diagnose central DI in association with hematological malignancies, we should not overlook this atypical type of DI.
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PMID:Myelodysplastic syndrome with central diabetes insipidus manifesting hypodipsic hypernatremia and dehydration. 1505 12

Vasopressin and its analogue, terlipressin, are potent vasopressors that may be useful therapeutic agents in the treatment of cardiac arrest, septic and catecholamine-resistant shock and oesophageal variceal haemorrhage. The aim of this article is to review the physiology and pharmacology of vasopressin and summarise its efficacy and safety in clinical trials and its subsequent therapeutic use. Recent studies indicate that the use of vasopressin during cardiopulmonary resuscitation may improve the survival of patients with asystolic cardiac arrest. Vasopressin deficiency can contribute to refractory shock states associated with sepsis, cardiogenic shock and cardiac arrest. Low doses of vasopressin and terlipressin can restore vasomotor tone in conditions that are resistant to catecholamines, with preservation of renal blood flow and urine output. They are also useful in reducing bleeding and mortality associated with oesophageal variceal haemorrhage. The long-term outcome of the use of these drugs is not known.
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PMID:Vasopressin and terlipressin: pharmacology and its clinical relevance. 1548 59

Lymphocytic hypophysitis may involve the pituitary gland and various hormonal abnormalities. A 72-year-old man presented with euvolemic hyponatremia caused by glucocorticoid deficiency. After glucocorticoid replacement, hypernatremia in the presence of dilute urine was found. Central diabetes insipidus (DI) was confirmed later by a significant increase in urine osmolality after vasopressin administration. Brain magnetic resonance imaging showed a pituitary mass and loss of hyperintense signal in the posterior pituitary gland on T1-weighted imaging. The patient underwent a transsphenoidal adenectomy, and pathological examination of dissected tissues showed a typical finding of lymphocytic hypophysitis. Two months after surgery, the patient's central DI had resolved sufficiently that 1-desamino-8- d -arginine vasopressin therapy was discontinued without polyuria. However, he was kept on glucocorticoid and levothyroxine therapy. In conclusion, lymphocytic hypophysitis may feature a concealed central DI caused by glucocorticoid deficiency-associated hyponatremia.
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PMID:A case of lymphocytic hypophysitis with masked diabetes insipidus unveiled by glucocorticoid replacement. 1569 61

Central diabetes insipidus developed for the first time in a 14-year-old female during the resection of a craniopharyngioma. The water diuresis persisted until a vasopressin analogue (dDAVP) was given. Professor McCance was asked to explain why hypernatraemia developed, to anticipate dangers that might develop in the salt and water area with therapy, and to provide insights into why this patient died, due to the subsequent development of hyponatraemia that caused a lethal rise in intracranial pressure. The team specifically wanted Professor McCance's opinions as to why a PNa of 124 mmol/l was uniquely dangerous for this patient, and this was a particularly challenging conundrum. Nevertheless, with the aid of a mini-experiment, a careful chart review, and creative thinking, he was able to offer a novel solution, and to suggest ways to prevent its occurrence in other patients.
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PMID:Acute and fatal hyponatraemia after resection of a craniopharyngioma: a preventable tragedy. 1605 76

The identification, characterization, and mutational analysis of three different genes-the arginine vasopressin gene (AVP), the arginine vasopressin receptor 2 gene (AVPR2), and the vasopressin-sensitive water channel gene (aquaporin 2 [AQP2])-provide the basis for understanding of three different hereditary forms of "pure" diabetes insipidus: Neurohypophyseal diabetes insipidus, X-linked nephrogenic diabetes insipidus (NDI), and non-X-linked NDI, respectively. It is clinically useful to distinguish two types of hereditary NDI: A "pure" type characterized by loss of water only and a complex type characterized by loss of water and ions. Patients who have congenital NDI and bear mutations in the AVPR2 or AQP2 genes have a "pure" NDI phenotype with loss of water but normal conservation of sodium, potassium, chloride, and calcium. Patients who bear inactivating mutations in genes (SLC12A1, KCNJ1, CLCNKB, CLCNKA and CLCNKB in combination, or BSND) that encode the membrane proteins of the thick ascending limb of the loop of Henle have a complex polyuro-polydipsic syndrome with loss of water, sodium, chloride, calcium, magnesium, and potassium. These advances provide diagnostic and clinical tools for physicians who care for these patients.
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PMID:Molecular biology of hereditary diabetes insipidus. 1609 48


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