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)

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.
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PMID:[The physiopathology of ascites]. 46 62

A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.
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PMID:Inappropriate secretion of antidiuretic hormone after cerebral injury. 106 6

The rare association of diabetes mellitus and vasopressin sensitive diabetes insipidus found in 5 patients attending the Institute of Endocrinology and Metabolic Diseases in a ten-year period is reported. Suspicious signs and criteria for diagnosis were discussed and a brief review made on the pathogenesis and treatment of this association.
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PMID:Diabetes mellitus and vasopressin sensitive diabetes insipidus. 744 14

The endocrine response to stress is complex. Elevations in the serum concentrations of the "classic" stress hormones, epinephrine and cortisol, occur following many kinds of physiologic challenge and are accompanied by elevations in corticotropin, GH, and glucagon levels. These changes are probably responsible for the hyperglycemia and hypercatabolism common to most critical illness. If volume depletion is present, vasopressin, renin, and aldosterone secretion are also likely to be stimulated. These hormones, if present in excess, may produce fluid retention and hyponatremia. In some critically ill patients, there is a dissociation of renin and aldosterone production called hyperreninemic hypoaldosteronism, but the clinical importance of this syndrome is poorly understood. Thyroid hormone metabolism is commonly affected by critical illness, which results in characteristic abnormalities of thyroid function testing known as the euthyroid sick syndrome. The reproductive axis is exquisitely sensitive to physiologic stress; hypogonadotropic hypogonadism is a common finding in critical illness. The ongoing challenge to the clinician is to determine whether seemingly abnormal hormone measurements in critically ill patients reflect an appropriate homeostatic response to severe illness or, instead, whether they denote an independent metabolic disorder that might actually cause or contribute to the patient's unstable condition. In view of the exceedingly complex (and poorly understood) interactions involved in the human response to a severe illness, a thoughtful approach to the whole patient is essential and far preferable to indiscriminate hormone testing. Such testing, at best, may be uninterpretable in light of the clinical circumstances or, at worst, may lead to therapeutic misadventures.
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PMID:The endocrine response to critical illness. 780 93

Hyponatremia is a common metabolic disorder in clinical practice and is associated with significant morbidity and mortality, especially among the elderly. Hyponatremia resulting from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has been reported in association with neoplasia (including a few reports in patients with head and neck malignancies) and may represent a paraneoplastic condition. Patients with SIADH present with signs and symptoms that cannot be explained by the primary tumour mass effect or its metastases. We describe a 67-year-old male patient with oral squamous-cell carcinoma of recent recurrence admitted because of symptomatic severe hyponatremia resulting from SIADH and discuss the principles of the diagnostic approach and appropriate management.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion due to recurrent oral cancer. 1625

Over the past 2 decades, exercise-associated hyponatraemia (EAH) has emerged as an important complication of prolonged endurance physical activities. Data collected since the first reports of EAH have strongly implicated a dilutional hyponatraemia from inappropriate retention of body water as the primary cause of EAH. Although high rates of fluid consumption clearly contribute to the pathogenesis of EAH, a review of the available data does not support the view that EAH can be ascribed solely to excess drinking. Because the kidney is exquisitely sensitive to low plasma levels of the antidiuretic hormone arginine vasopressin (AVP) and because many non-osmotic stimuli to AVP secretion normally occur during prolonged endurance exercise activity, it is more likely that a combination of higher than normal fluid intakes in the setting of modest elevations of plasma AVP levels from a variety of potential stimuli during prolonged physical activity accounts for the majority of cases of EAH. In any individual, the degree to which AVP secretion is stimulated and whether it can be suppressed with sufficient fluid ingestion, will determine their susceptibility to EAH as a result of fluid ingestion both before and after physical activity, accounting for the high degree of individual variability in the occurrence of this potentially life-threatening metabolic disorder.
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PMID:Renal function and vasopressin during marathon running. 1746 34

Acute intermittent porphyria is a metabolic disorder rarely seen in prepubertal children. A delay in diagnosis of acute intermittent porphyria is common because of variable and nonspecific symptoms. We report an 8-year-old boy with right hemimegalencephaly and intractable seizures, who presented with dark-colored urine, hypertension, increasing lethargy, fluctuating seizures, and poor oral intake. He subsequently developed hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion. His urinalysis was negative for red blood cells, and a random urine porphobilinogen level was elevated. Further biochemical and molecular testing confirmed the diagnosis of acute intermittent porphyria. His antiepileptic medications were discontinued and hemin administered, with dramatic clinical improvement. The diagnosis of acute intermittent porphyria was challenging because of his underlying neurologic condition. This case highlights the variable presentation of acute intermittent porphyria and emphasizes the importance of considering the diagnosis even in young patients with underlying neurologic conditions when they present with nonspecific neurovisceral symptoms or with unexplained neurologic deterioration.
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PMID:Acute intermittent porphyria: a diagnostic challenge. 2219 Apr 98

Acute intermittent porphyria (AIP) is an autosomal dominant metabolic disorder caused by deficiency of the heme biosynthetic enzyme hydroxymethylbilane synthase (approved gene symbol HMBS), also known as porphobilinogen deaminase (PBGD). AIP is characterised by intermittent attacks of abdominal pain, vomiting, and neurological complaints. The highly variable symptomatic presentation of AIP causes confusion with other diseases and results in a high misdiagnosis rate (68% in China) and delayed effective treatments. Based on biochemical and genetic analysis of two Chinese families, a new and a previously reported HMBS mutation were identified in patients with AIP and syndrome of inappropriate antidiuretic hormone (SIADH). The novel HMBS mutation is the 655G>C point mutation (A219P). In addition, the 973C>T point mutation (R325X), which had been previously reported in two Danish families, was identified.
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PMID:Novel A219P mutation of hydroxymethylbilane synthase identified in a Chinese woman with acute intermittent porphyria and syndrome of inappropriate antidiuretic hormone. 2578 8