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)

We studied serum sodium, plasma osmolality and urinary sodium and osmolality on days 1, 3 and 5 of hospitalization of 100 children aged from 1 month to 12 years admitted with a diagnosis of pneumonia. Hyponatraemia (serum sodium concentration < or = 130 mmol/l) was found in 31 patients at the time of admission. The probable cause of hyponatraemia in 94% of cases was the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Symptoms and signs indicative of severe pneumonia were two to three times more frequent and the mean duration of tachypnoea, chest-wall retraction and hospital stay about one and a half times longer in children with hyponatraemia. Four children died (two on day 1, one on day 5 and one on day 8); all four had a serum sodium concentration < or = 125 mmol/l which persisted until death. Of the remaining 27 hyponatraemic children, serum sodium concentrations returned to normal on day 3 in 26, while in one hyponatraemia persisted until day 7. The recovery from hyponatraemia showed a good correlation with improvement in clinical signs of respiratory distress. The SIADH occurred in about one-third of the children hospitalized for pneumonia, and was associated with a more severe disease and a poorer outcome. Perhaps fluid restriction in these cases may improve the outcome.
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PMID:Hyponatraemia and the inappropriate ADH syndrome in pneumonia. 128 78

Studies on two quadriplegic patients who developed severe hyponatremia during episodes of acute respiratory distress were performed to determine whether differences in osmoregulation of vasopressin release could be identified in these patients compared to other quadriplegic subjects previously studied in a similar manner. Both patients were clinically stable and normonatremic, with no signs or symptoms of respiratory distress, when the studies were performed. However, both exhibited evidence of hemodynamic instability in the sitting posture. Linear regression analysis of the plasma vasopressin/plasma osmolality (Pavp:Posm) relationship during infusions of 0.85 M sodium chloride showed no significant differences in either the slope (sensitivity) or abscissal intercept (osmotic threshold) of this relationship compared to that of other quadriplegic subjects when the patients were supine. In contrast, when the patients were studied in the sitting posture there was a marked shift in the relationship of Pavp:Posm indicative of increased sensitivity and reduced osmotic threshold for vasopressin release. The slopes of the Pavp:Posm relationships were 0.249 and 0.178 for the two patients, respectively, compared to 0.092 +/- 0.03 ( +/- SD) for previously studied quadriplegic subjects. Oral water-loading studies performed on one patient revealed marked impairment of urine-diluting ability and free water clearance in the sitting posture compared with observations in similar studies performed when the patient was supine. Impairment of renal water excretion could not be attributed to an effect of vasopressin, which was reduced to unquantifiable levels by water loading. These studies have shown that hemodynamic stress related to autonomic dysfunction in quadriplegic patients may result in marked alteration of osmoregulation of vasopressin release in more severely affected individuals. Such altered osmoregulation, which may also be associated with vasopressin-independent impairment of renal water excretion in the sitting posture, may be a predisposing factor in the development of hyponatremia, especially in the presence of other potent nonosmotic stimuli.
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PMID:Nonosmotic stimuli alter osmoregulation in patients with spinal cord injury. 222 11

We studied the role of arginine-vasopressin (AVP) in the regulation of fluid homeostasis in preterm infants. Group 1 was fed orally, groups 2 and 3 received fluids parenterally, and group 3 developed respiratory distress syndrome (RDS) and had to be ventilated. The infants of group 3 were not able to excrete the administered fluid, gained weight and consecutively developed hyponatremia. 1-min Apgar scores as well as log FiO2 correlated significantly with urinary AVP excretion on day 1. We conclude that nonosmotic stimuli are involved in the release of AVP and therefore disturb fluid homeostasis in severely ill infants with RDS.
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PMID:The role of arginine-vasopressin in the regulation of water metabolism in preterm infants in the first days of life. 344 38

I retrospectively describe 20 episodes of water intoxication in 19 infants, with hypothermia, seizures, and hyponatremia. Overdilution of formula or aggressive supplementation with water or clear juices were documented in 16 of the 20 episodes. Seizures and respiratory distress were severe enough in six cases to require intubation and ventilatory support. Marked diaphoresis was noted as a premonitory symptom to seizures in eight children. The children were an average of 5.1 +/- 4.3 months of age; serum sodium values averaged 118 +/- 4.3 mmol/L. No evidence of excess production of antidiuretic hormone was found. Water intoxication in infants is common, and I discuss its possible relationship to demyelinating disease of the central nervous system.
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PMID:Seizures and hypothermia due to dietary water intoxication in infants. 356 73

We investigated the antidiuretic hormone (ADH) response in 12 infants with bronchopulmonary dysplasia during acute respiratory distress. All of the infants had hypoxemia with air-trapping in the chest at the time of admission to the hospital. None had documented infection. There was a dramatic increase in the plasma levels of ADH during acute respiratory distress, with a subsequent reduction of levels toward normal when the respiratory distress decreased to the preadmission well state. Three of 12 infants manifested hyponatremia at 24 hours after admission, with two of them exhibiting persistent hypertension for up to three days. The mechanism for elevated ADH levels is air-trapping in the chest, causing pulmonary hypovolemia and decreased left atrial filling and/or decreased transmural pressure of the left atrium.
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PMID:Antidiuretic hormone response in children with bronchopulmonary dysplasia during episodes of acute respiratory distress. 375 83

Preterm birth is associated with up to 90% of perinatal deaths. In spite of numerous clinical and preclinical research programs, its incidence has not changed throughout the past decade. An observation that the oxytocin antagonist atosiban delays preterm labor and is significantly more potent than vasopressin(1a) receptors gave rise to research on the role of vasopressin blockade in tocolysis and vasopressin itself in preterm labor. Successful tocolysis allows the introduction of intrauterine steroid treatment of the fetus, which reduces the chance of developing infant respiratory distress syndrome and intracranial hemorrhage. Fetal membranes, decidua and placenta are considered a possible site of initiation of parturition, both term and preterm. Research on the biology of these tissues may shed new light on current concepts of the pathophysiology of preterm labor. We here present a short review on the role of oxytocin, oxytocin receptor blockade and fetal membranes in preterm labor.
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PMID:Oxytocin and fetal membranes in preterm labor: current concepts and clinical implication. 1285 35

Sepsis is physiologically viewed as a proinflammatory and procoagulant response to invading pathogens. There are three recognized stages in the inflammatory response with progressively increased risk of end-organ failure and death: sepsis, severe sepsis, and septic shock. Patients with cirrhosis are prone to develop sepsis, sepsis-induced organ failure, and death. There is evidence that in cirrhosis, sepsis is accompanied by a markedly imbalanced cytokine response ("cytokine storm"), which converts responses that are normally beneficial for fighting infections into excessive, damaging inflammation. Molecular mechanisms for this excessive proinflammatory response are poorly understood. In patients with cirrhosis and severe sepsis, high production of proinflammatory cytokines seems to play a role in the worsening of liver function and the development of organ/system failures such as shock, renal failure, acute lung injury or acute respiratory distress syndrome, coagulopathy, or hepatic encephalopathy. In addition, these patients may have sepsis-induced hyperglycemia, defective arginine-vasopressin secretion, adrenal insufficiency, or compartmental syndrome. In patients with cirrhosis and spontaneous bacterial peritonitis (SBP), early use of antibiotics and intravenous albumin administration decreases the risk for developing renal failure and improves survival. There are no randomized studies that have been specifically performed in patients with cirrhosis and severe sepsis to evaluate treatments that have been shown to improve outcome in patients without cirrhosis who have severe sepsis or septic shock. These treatments include recombinant human activated C protein and protective-ventilation strategy for respiratory failure. Other treatments should be evaluated in the cirrhotic population with severe sepsis including the early use of antibiotics in "non-SBP" infections, vasopressor therapy, hydrocortisone, renal-replacement therapy and liver support systems, and selective decontamination of the digestive tract or oropharynx.
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PMID:Severe sepsis in cirrhosis. 2037 75

The research papers on shock that have been published in Critical Care throughout 2009 are related to four major subjects: first, alterations of heart function and, second, the role of the sympathetic central nervous system during sepsis; third, the impact of hemodynamic support using vasopressin or its synthetic analog terlipressin, and different types of fluid resuscitation; as well as, fourth, experimental studies on the treatment of acute respiratory distress syndrome. The present review summarizes the key results of these studies together with a brief discussion in the context of the relevant scientific and clinical background published both in this and other journals.
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PMID:Year in review 2009: Critical Care--shock. 2112 69

Severe sepsis and septic shock remains the most urgent problem. In severe sepsis and septic shock should be early goal-directed resuscitation of the septic patient during the first 6 hrs after recognition; -appropriate diagnostic studies to ascertain causative organisms before starting antibiotics; -early administration of broad-spectrum antibiotic therapy; -reassessment of antibiotic therapy with microbiology and clinical data to narrow coverage, when appropriate; -a usual 7-10 days of antibiotic therapy guided by clinical response; -source control with attention to the method that balances risks and benefits; -equivalence of crystalloid and colloid resuscitation; aggressive fluid challenge to restore mean circulating filling pressure; -vasopressor preference for norepinephrine and dopamine; -cautious use of vasopressin pending further studies; -avoiding low-dose dopamine administration for renal protection; consideration of dobutamine inotropic therapy in some clinical situations; -stress-dose steroid therapy for septic shock; use of recombinant activated protein C in patients with severe sepsis and high risk for death; -with resolution of tissue hypoperfusion and in the absence of coronary artery disease or acute hemorrhage, targeting a hemoglobin of 7-9 g/dL; -a low tidal volume and limitation of inspiratory plateau pressure strategy for acute lung injury and acute respiratory distress syndrome; -application of a minimal amount of positive end-expiratory pressure in acute lung injury/acute respiratory distress syndrome; -protocols for weaning and sedation, using either intermittent bolus sedation or continuous infusion sedation with daily interruptions/lightening; -avoidance of neuromuscular blockers, if at all possible; -maintenance of blood glucose <150 mg/dL after initial stabilization.
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PMID:[Protocol of the management of patients with severe sepsis and septic shock]. 2322 Nov 37

A 32-year-old man presented with a 10-day history of fever, chills, nausea, vomiting, myalgia, nonproductive cough, and worsening dyspnea after freshwater swimming in the Caribbean 1 week prior to presentation. Shortly after arrival at the hospital, the patient developed severe respiratory distress with massive hemoptysis. Based on serologic workup, he was diagnosed with leptospirosis pulmonary hemorrhage syndrome leading to diffuse alveolar hemorrhage, severe hypoxemic respiratory failure, and multiorgan failure. He received appropriate antibiotic coverage along with hemodynamic support with norepinephrine and vasopressin, mechanical ventilation, and renal replacement therapy in an intensive care unit. Introduction of extracorporeal membrane oxygenation was initiated to provide lung-protective ventilation supporting the recovery of his pulmonary function. Aminocaproic acid was used to stop and prevent further alveolar hemorrhage. He fully recovered thereafter; however, it is uncertain whether it was the use of aminocaproic acid that led to the resolution of his disease.
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PMID:Use of Aminocaproic Acid in Combination With Extracorporeal Membrane Oxygenation in a Case of Leptospirosis Pulmonary Hemorrhage Syndrome. 2846 3


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