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 37-year-old woman undergoing laparoscopic-assisted vaginal hysterectomy experienced seizures and subsequent coma on the first postoperative day. Early recognition of the syndrome of inappropriate antidiuretic hormone with aggressive treatment and avoidance of hypoxia resulted in full recovery without sequelae. Menstruant women are 25 times more likely to die or suffer permanent brain damage from hyponatremic encephalopathy than menopausal women.
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PMID:Syndrome of inappropriate antidiuretic hormone after laparoscopic-assisted vaginal hysterectomy. 905 May

Diabetes insipidus is an uncommon condition characterized by polyuria and polydipsia. The symptoms and biochemical changes of this condition result from either a lack of antidiuretic hormone or renal insensitivity to its effect. Failure to produce or release antidiuretic hormone may result from cranial pathology, including trauma and surgery. The renal insensitivity to antidiuretic hormone that occurs in patients with nephrogenic diabetes insipidus may be caused by genetic factors, drugs (especially lithium) or specific disease processes. Patients may compensate for polyuria and nocturia by excessive water intake but show marked decreases in urine specific gravity and osmolality. Patients with severe and uncompensated symptoms develop marked dehydration, neurologic symptoms and encephalopathy. The water deprivation test is useful in diagnosing diabetes insipidus and in differentiating neurogenic from nephrogenic cases. Neurogenic diabetes insipidus may respond to nasal administration of desmopressin. Nephrogenic diabetes insipidus requires good hydration and monitoring of body chemistry. Thiazides and amiloride may relieve symptoms.
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PMID:Evaluation and management of diabetes insipidus. 914 42

A 66-year-old hypertensive male with acute intracerebral hemorrhage developed acute hyponatremic coma 3 days after the addition of enalapril and a combination of amiloride and a thiazide diuretic to his hypotensive regimen. The patient recovered consciousness and serum sodium normalized 2 days after fluid restriction and withdrawal of both medications. Three weeks later, upon inadvertent reinstitution of enalapril and indapamide, severe hyponatremic encephalopathy promptly recurred; recovery was again rapid following fluid restriction and withdrawal of both medications. This temporal relationship establishes the thiazide diuretic or the angiotensin converting enzyme inhibitor or both as the cause of the profound symptomatic hyponatremia in this patient. Results of simultaneous serum and urine osmolality assays on several occasions were consistent with a decrease in free water clearance, a result of either increased antidiuretic hormone (ADH) secretion or potentiation of its peripheral action, and thiazide-induced natriuresis. The use of a thiazide diuretic in the presence of either of these aberrations of ADH homeostasis most likely explains the profound and rapid development of hyponatremia. Drug-induced disturbances in serum osmolality are a potentially reversible cause of deterioration of the mental state in a patient with an acute cerebrovascular accident.
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PMID:Acute hyponatremic encephalopathy after a cerebrovascular accident. 967 Oct 45

Rathke's cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernig's sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. Magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.
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PMID:Hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report. 1046 7

Hyponatremia in advanced cirrhosis and ascites or congestive heart failure (CHF) is the result of an inappropriate increase in vasopressin secretion, which acts through activation of specific V(2) receptors in the distal renal nephron to increase water reabsorption. This study investigates the efficacy and safety of 3 different doses of the V(2) receptor antagonist, VPA-985, in correcting hyponatremia over a 7-day inpatient study period. Forty-four hospitalized patients (33 patients with cirrhosis, 6 with CHF, and 5 with syndrome of inappropriate antidiuretic hormone (SIADH) were studied on a constant sodium intake, with VPA doses of 25, 125, and 250 mg twice daily or placebo. Serum sodium measurements were repeated after every daily dose, and the next dose withheld for excessive serum sodium rises. Fluid intake was adjusted according to previous 24-hour urinary outputs. Adverse events were based on clinical signs of dehydration or encephalopathy. VPA-985 produced a significant overall aquaretic response compared with placebo, with significant dose related increases in free water clearance (P <.05) and serum sodium (P <.05), without significant changes in orthostatic blood pressure or serum creatinine levels. Five patients (50%) on 250 mg twice daily had to have medication withheld on multiple occasions. End-of-study plasma vasopressin levels increased significantly in the 2 larger dose groups. In conclusion, VPA-985 appears effective and safe in appropriate doses in correcting abnormal renal water handling and hyponatremia in conditions associated with water retention. Higher doses of VPA-985 may produce significant dehydration and will require close monitoring with their use.
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PMID:A vasopressin receptor antagonist (VPA-985) improves serum sodium concentration in patients with hyponatremia: a multicenter, randomized, placebo-controlled trial. 1499 23

Hyponatremia is a common electrolyte disturbance occurring in a broad spectrum of patients, from asymptomatic to critically ill. The disease is defined as a decrease in serum sodium concentration to a level below 136 mmol per liter. The brain damage from hyponatremia can be associated with either hyponatremic encephalopathy or improper therapy of symptomatic hyponatremia both in patients and in experimental models of hyponatremia in rats. This review covers the clinical symptoms of hyponatremia as well as the consequences of its correction. It also summarises the effects of experimental hyponatremia associated with vasopressin on some aspects of cerebral blood flow regulation and the morphology of cerebral tissue.
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PMID:Hyponatremic encephalopathy--some experimental and clinical findings. 1286 95

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.
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PMID:Management of hyponatremia. 1516 58

Portal hypertension can lead to life-threatening hemorrhage, ascites, and encephalopathy. This paper reviews the pathophysiology and multidisciplinary management of portal hypertension and its complications, including the indications for and techniques of the various surgical shunts. Variceal bleeding is the most dreaded complication of portal hypertension. It may occur once the portal-systemic gradient increases above 12 mm Hg, occurs in 30% of patients with cirrhosis, and carries a 30-day mortality of 20%. Treatment of acute variceal bleeding includes resuscitation followed by upper endoscopy for sclerosis or band ligation of varices, which can control bleeding in up to 85% of patients. Medical therapies such as vasopressin and somatostatin can also be useful adjuncts. Shunt therapy, preferably the placement of a TIPS, is indicated for refractory acute variceal bleeding. Recurrent variceal bleeding is common and is associated with a high mortality. Therapies to prevent recurrent variceal bleeding include chronic endoscopic therapy, nonselective beta-blockade, operative or nonoperative (TIPS) shunts, devascularization operations, and liver transplantation. Recommendations and a treatment algorithm are provided, taking into account both the etiology and the manifestations of portal hypertension.
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PMID:Current management of portal hypertension. 1613 97

Hepatorenal syndrome (HRS) is defined as functional renal failure that develops in patients with advanced liver disease. HRS may be either slowly or rapidly progressive (type I and II HRS, respectively). Untreated HRS carries a high mortality. Liver transplantation is the best available treatment for HRS. However, all patients with HRS are not suitable candidates for transplantation. Moreover, an organ is often not available in a timely manner in those who are candidates for transplantation. Treatment with vasoconstrictors (terlipressin, octreotide, and midodrine) and plasma expansion with albumin is beneficial and serves as a bridge to transplantation in such cases. The vasopressin analog, terlipressin, produces a sustained reversal of HRS in about 57% to 78% of the patients. The benefits of terlipressin are seen mainly in those who are also receiving albumin simultaneously. In those who improve, recurrence of HRS is reported to be relatively uncommon in the short and intermediate term. In the United States, terlipressin is not available, and octreotide and midodrine are often used for the medical management of HRS. Unfortunately, there are only limited uncontrolled data to support the use of these drugs for HRS. In those who respond to octreotide and midodrine, the subsequent placement of a transjugular intrahepatic portasystemic shunt (TIPS) has been shown to produce a sustained improvement in renal function. TIPS alone also improves renal functions in selected patients with HRS. The exact role of TIPS in HRS needs further evaluation, as patients with HRS are particularly at risk for complications such as encephalopathy and liver failure. Molecular adsorbent recirculating system (MARS) is an albumin-based dialysis system that has a promising role in the treatment of HRS and liver failure. MARS is a very expensive form of treatment, and further clinical trials are needed to establish its utility. Development of HRS can be prevented by adding albumin to the antibiotic regimen to treat spontaneous bacterial peritonitis and through pentoxifylline administration to the patients with acute alcoholic hepatitis.
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PMID:Hepatorenal syndrome. 1631 61

The management of children with end-stage chronic liver disease and acute liver failure mandates a multidisciplinary approach and intense monitoring. In recent years, considerable progress has been made in developing specific and supportive medical measures, but studies and publications have mainly concerned adult patients. Therapeutic approaches to complications of end-stage chronic liver disease and acute liver failure (e.g. refractory ascites, hepatorenal syndrome, encephalopathy, and cerebral edema) that may be applied to children are reviewed in this article.Mild-to-moderate ascites should be managed by modest salt restriction and oral diuretic therapy in the first instance. Large volume paracentesis associated with colloid volume expansion and diuretic therapy may be effective for acute relief. Treatment of hepatorenal syndrome type 1 with vasopressin analogs (terlipressin) is recommended prior to liver transplantation in order to improve renal function. Prevention and treatment of chronic hepatic encephalopathy are directed primarily at controlling the events that may precipitate hepatic encephalopathy and at reducing ammonia generation and increasing its detoxification or removal. In addition to reduction of gut ammonia production using non-absorbable disaccharides such as lactulose and/or antibacterials such as neomycin, sodium benzoate may be used on a long-term basis to prevent, stabilize, or improve hepatic encephalopathy. The management of hepatic encephalopathy in acute liver failure is considerably more unsatisfactory; treatment is aimed at preventing brain edema and intracranial hypertension. Extracorporeal liver support devices are now used commonly in critically ill children with acute renal failure, advanced hepatic encephalopathy, cerebral edema, intracranial hypertension, and severe coagulopathy. Continuous renal replacement therapy could potentially help support patients until liver transplantation is performed or liver regeneration occurs. The Molecular Adsorbent Recirculating System (MARS or albumin dialysis) is the liver support system most frequently used worldwide in adults and appears to offer distinct advantages over hepatocyte-based systems. There are no specific medical therapies or devices that can correct all of the functions of the liver. Apart from a few metabolic diseases presenting with severe liver dysfunction for which specific medical therapies may preclude the need for liver transplantation, liver transplantation still remains the only definitive therapy in most instances of end-stage chronic liver disease and acute liver failure. Future research should focus on gaining a better understanding of the mechanisms responsible for liver cell death and liver regeneration, as well as developments in hepatocyte transplantation and liver-directed gene therapy.
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PMID:New management options for end-stage chronic liver disease and acute liver failure: potential for pediatric patients. 1649 8


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