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 syndrome of inappropriate secretion of antidiuretic hormone (ADH) or SIADH has been reported in various disorders. We report a pediatric patient with nasopharynx carcinoma who may have developed a clinical SIADH with severe hyponatremia and generalized seizure during the administration of intravenous hydration. We propose that the inappropriately high plasma level of ADH led to the inability to excrete sufficient amounts of free water during a hyperhydration protocol with a relatively hypotonic fluid, which resulted in acute hyponatremia and central nervous system involvement. To avoid this complication, intravenous hydration before chemotherapy in children with nasopharynx carcinoma should be performed at a slower infusion rate and with a sodium chloride concentration of more than half isotonic.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in nasopharynx carcinoma. 926 Feb 57

In a minority of patients with malignant tumors, signs and symptoms develop that cannot be explained on the basis of the mass effect produced by the primary tumor or its metastases, or production of a hormone normally associated with the tissue type that has given rise to the malignant tumor; these peculiar symptom complexes are known as paraneoplastic syndromes, and may be divided into endocrinologic, dermatologic, hematologic, neurologic, and osteoarticular manifestations. In the head and neck region in particular, the syndrome of inappropriate antidiuretic hormone production (SIADH, or Schwartz-Bartter syndrome) is a well-recognized form of paraneoplastic syndrome that may accompany head and neck malignancies. Most of such tumors are squamous carcinomas, with lesser numbers of olfactory neuroblastomas, small cell neuroendocrine carcinomas, adenoid cystic carcinomas, and undifferentiated carcinomas; sarcoma was reported in only a single instance. The lesions associated with the development of SIADH have most often been located in the oral cavity, and less often in the larynx, nasopharynx, hypopharynx, nasal cavity, maxillary sinus, parapharyngeal space, salivary glands, and oropharynx. Key features of SIADH include serum hypo-osmolality; an unexpectedly high urinary specific gravity; an absence of edema or dehydration; normal adrenal, thyroid, and renal function; hyponatremia; and an elevation of plasma vasopressin.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion associated with head neck cancers: review of the literature. 934 88

To evaluate the pathomechanism of hyponatremia occasionally seen in Duchenne muscular dystrophy (DMD) on intermittent positive pressure ventilation (IPPV), we performed a comparative study on 26 DMD patients, 7 IPPV in trachetomized intermittent positive pressure ventilation (TIPPV), 6 nasal intermittent positive pressure ventilation (NIPPV), 6 cuirass respirator (CR), and 7 spontaneous breathings (SB). We followed fluctuation of serum sodium levels for several years. Since the serum sodium level was gradually reduced with years on mechanical ventilation, we speculated positive relationship between hyponatremia and antidiuretic hormone (ADH) secretion. Serum sodium levels of 135.6 +/- 2.8 mEq/L in average on IPPV (TIPPV + NIPPV) patients was significantly lower than the levels of 137.8 mEq/L +/- 0.98 on CR patients and 138.8 +/- 0.69 mEq/L on SB patients. Plasma ADH levels in IPPV patients were not reduced when plasma osmolarity was less than 280 mOSm/L. Previous reports showed that ADH was inappropriately secreted only during IPPV with positive end expiratory pressure (PEEP). Ours is the first report of inappropriate secretion of ADH during IPPV without PEEP. It becomes clear that inappropriate ADH secretion is one of the causes of hyponatremia in DMD, though the exact mechanism is not clear. We should bear in mind the change of serum electrolyte level in ventilated DMD patients, especially patients on antidepressant known to release of ADH.
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PMID:[Hyponatremia in Duchenne muscular dystrophy on mechanical ventilation]. 961 71

Authors deal in detail with the pathophysiology of the osmolal regulation. Besides hyperosmolality the secretion of antidiuretic hormone (ADH) in increased by hypovolemia and hypotension. Secretion of ADH is lowered in hypoosmolal states. All other mechanisms are preferebly volume regulating and they influence mainly retention and excretion of sodium. Authors discuss homeostatic effects of the renin-angiotensin-aldosteron system, effects of renal failure with prevailing glomerular or tubular function disorder, impact of diuretics, natriuretic peptides, digitalis-like hormone, urodilantin and influence of the other solutes. Disorders of the effective osmolality regulation are frequent in the cerebral affections that originate from trauma, vascular disease, inflammation or tumors. Hypoosmolality and hyponatremia are presented in two different conditions: Inappropriate Vasopressin Secretion Syndrome (IADHS) and Cerebral Salt Wasting Syndrome (CSWS). Quick differential diagnose is important because the treatment of both syndromes is essentially different. Typical cause of hypernatremia is central diabetes insipidus (DI). The group of available calculated renal function parameters is applied in the differential diagnosis of these syndromes. They are creatinin clearance, excretion fraction of water and sodium, electrolyte clearance and electrolyte free water clearance. Investigation of ADH and natriuretic peptide could be even misleading. Pathophysiologic consequence of the state given by inappropriate elevation of one hormone can be the elevation of the second one.
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PMID:[Disturbances of effective osmolality regulation in disorders of the central nervous system and possible methods of monitoring]. 974 51

70-year old man was admitted to the hospital due to the sudden change in his behaviour with the production of unusual echolalic word connections. Arginin-vasopressin (AVP) level (1.16 pg/ml) was found inappropriately higher in relation to the severe serum hypoosmolality (261 mmol/kg) and hyponatraemia (117 mmol/l) with relatively high urinary osmolality (590 mmol/kg) and natriuria (684 mmol/24 h). Diagnosis of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH-type C) was confirmed during the water load test. Magnetic resonance imaging and CT scans revealed in the region of hypophysis intrasellar tumour (diameter of 16 mm) and the stabilized finding of temporal cyst. Substitution of sodium losses with the restricted fluid intake resulted in the correction of water-electrolyte balance and the restoration of normal clinical state.
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PMID:[The syndrome of inappropriate secretion of antidiuretic hormone in hypophyseal tumors]. 982 85

In animal models of the syndrome of inappropriate antidiuresis (SIADH), sustained administration of vasopressin and water results in free-water retention and progressive hyponatremia for several days, which is then followed by escape from the vasopressin-induced antidiuresis. With the onset of vasopressin escape, water excretion increases despite sustained administration of vasopressin, allowing water balance to be re-established and the serum sodium to be stabilized at a steady, albeit decreased, level. Studies from our laboratories have investigated whether this escape phenomenon can be attributed to altered regulation of aquaporin water channels. After four-day pre-treatment with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) by osmotic minipump, rats were divided into control (continued dDAVP) and water-loaded (continued dDAVP plus a daily oral water load) groups. A significant increase in urine volume in the water-loaded rats was observed by the second day of water loading, indicating escape from antidiuresis. The onset of escape coincided temporally with a marked decrease in renal aquaporin-2 protein (measured by semi-quantitative immunoblotting), which began at day 2 and fell to 17% of control levels by day 3. In contrast, there was no decrease in the renal expression of aquaporins 1, 3, or 4. The marked suppression of whole kidney aquaporin-2 protein was accompanied by a concomitant suppression of whole kidney aquaporin-2 mRNA levels. Immunocytochemical localization and differential centrifugation studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact during vasopressin escape. Additional studies have indicated that the observed down-regulation of aquaporin-2 expression also occurs in the renal cortex as well as the inner and outer medullas, and can be reversed simply by water restriction despite maintenance of hyponatremia. Our results therefore suggest that escape from vasopressin-induced antidiuresis is attributable, at least in part, to a vasopressin-independent and osmolality-independent decrease in aquaporin-2 water channel expression in the renal collecting duct. Similar mechanisms likely contribute to the phenomenon of escape from antidiuresis seen clinically in patients with SIADH as well.
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PMID:Studies of renal aquaporin-2 expression during renal escape from vasopressin-induced antidiuresis. 1002 31

The hypertonic saline test is a useful technique for distinguishing partial diabetes insipidus from psychogenic polydipsia, and for the diagnosis of complex disorders of osmoreceptor and posterior pituitary function. However, there is little information concerning its use in childhood. The experience of using this test in five children (11 months to 18 years) who presented diagnostic problems is reported. In two patients, in whom water deprivation tests were equivocal or impractical, an inappropriately low antidiuretic hormone (ADH) concentration (< 1 pmol/l) was demonstrated in the presence of an adequate osmotic stimulus (plasma osmolality > 295 mosmol/kg). In two children--one presenting with adipsic hypernatraemia and the other with hyponatraemia complicating desmopressin treatment of partial diabetes insipidus--defects of osmoreceptor function were identified. Confirming a diagnosis of idiopathic syndrome of inappropriate ADH secretion (SIADH) was possible in a patient with no other evidence of pituitary dysfunction. The hypertonic saline test was well tolerated, easy to perform, and diagnostic in all cases.
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PMID:Hypertonic saline test for the investigation of posterior pituitary function. 1019 58

We experienced four cases with hyponatremia due to SIADH, which seems to be related to inflammation. The plasma Na concentration decreased when the patients had fever and increased plasma CRP level. In such conditions, plasma vasopressin concentration (PAVP) and the plasma interleukin-6 (IL-6) concentration were increased. There was significant correlation between them. The animal experiments were carried out to investigate the role of interleukin in the development of SIADH. Intravenous administrations of IL-1 beta increased AVP, atrial natriuretic hormone (ANH) and ACTH. The changes in AVP and ACTH were abolished by the pretreatment with an intravenous administration of indomatacin. Moreover, the intracerebroventricular administration (ICV) of IL-1 beta also increased AVP, atrial natriuretic hormone (ANH) and ACTH. The pretreatment of indomatacin attenuated the changes in AVP and ACTH. The intravenous administration of IL-1 beta increased the urinary sodium excretion. The pretreatement of HS142-1, an ANH antagonist, abolished the increase in urinary sodium excretion induced by IL-1 beta. These results suggested that the interleukin play an important role in the development of SIADH associated with inflammation.
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PMID:[Hyponatremia and inflammation]. 1037 61

After the story of success of hormone blockers for catecholamines, aldosterone and angiotensin II and their successful implementation into clinical practice another endocrine cardiovascular system has come into focus. It has long been known, that the hormone vasopressin plays an important role in peripheral vasoconstriction, hypertension and in several disease conditions with dilutional hyponatremia in edematous disorders, like congestive heart failure, liver cirrhosis, SIADH and nephrotic syndrome. A series of orally active nonpeptide antagonists against the vasopressin receptor subtypes has recently been synthesized and is now under intensive examination. Nonpeptide V1a-receptor specific antagonists, OPC 21268 and SR 49059, nonpeptide V2-receptor specific antagonists, SR 121463 A and VPA 985, and combined V1a-/V2-receptor antagonists, OPC 31260 and YM 087, have become available for clinical research. AVP-V2-receptor antagonists lead to a dose-dependent diabetes insipidus in animals and man. The term aquaretic drugs (aquaretics) has been coined for these drugs to highlight their different mechanism compared to the saluretic diuretic furosemide. V1a-receptor antagonists might offer new therapeutic advantages in the treatment of vasoconstriction and hypertension. Combined V1a-/V2-receptor antagonists might be beneficial in the treatment of congestive heart failure. Early results are promising and now need to be confirmed in large clinical studies.
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PMID:Nonpeptide vasopressin antagonists: a new group of hormone blockers entering the scene. 1037 39

A 68 year old woman with sporadic Creutzfeldt-Jakob disease is described, who neither showed characteristic EEG abnormalities nor a positive test of the neuronal protein 14-3-3 or neuron specific enolase (NSE) in CSF, despite a clinical presentation with ataxia of cerebellar type, rapidly progressive dementia, myoclonus, and marked hyperintense signal abnormalities in the deep cortical layers and the basal ganglia on T2 and diffusion weighted MRI. Moreover she showed atypical clinical features with a syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) and a peripheral sensorimotor polyneuropathy. Whether these disturbances are independent of Creutzfeldt-Jakob disease or a feature of it is discussed. It has recently been shown that in Creutzfeldt-Jakob disease different clinical and pathological phenotypes correlate with the polymorphism at codon 129 of the prion protein gene (PRNP) and the type of the protease resistant fragment that accumulates in the brain. According to the new classification at least six sporadic variants of Creutzfeldt-Jakob disease exist. The molecular genetic analysis showed heterozygosity of PRNP at codon 129 for methionine and valine and the presence of PrP(CJD) type 2 in the brain of this patient. As a new feature of changes on MRI, striking cortical changes of hyperintense signals are described in diffusion weighted as well as T2 weighted MRI that directly correlate with the histomorphological spongy degeneration of the brain in this region. In cases of rapidly progressive dementia, Creutzfeldt-Jakob disease always needs to be considered even if unusual features are present and current diagnostic criteria are not in favour of this disease.
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PMID:Clinical range and MRI in Creutzfeldt-Jakob disease with heterozygosity at codon 129 and prion protein type 2. 1051 81


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