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)

During the winter of 1986-1987, 64 children with respiratory syncytial virus (RSV) infection were admitted to our hospital. The diagnosis was made by direct immunofluorescent antibody technique. Twenty-three children (36%) needed intensive care treatment. Nearly 11 (52%) had a preexisting disease state, identified as a risk factor i.e., prematurity (n = 8), bronchopulmonary dysplasia (n = 2), congenital heart disease (n = 1). Twelve patients (50%) were intubated and ventilated. Conditions for intubation and ventilation were repetitive apnea with or without bradycardia (n = 4), clinical deterioration (n = 3) or hypercarbia (n = 5). Seventy-five percent of the patients who needed intensive care management were under three months of age compared to 34% of the children who were admitted to the clinical ward. The mean age for ventilated patients was 7.9 weeks. The mean duration of ventilation was 5.5 days. Volume controlled ventilation was initially applied to all patients. Pulmonary complications (atelectasis, pneumonia, pneumothorax or adult respiratory distress syndrome) were present in 15 (65%) IC patients. Nine (39%) of them also had symptoms of inappropriate antidiuretic hormone secretion (IADHS). Only two patients had symptoms of IADHS and two others had convulsions. Three children (5%) died as a result of respiratory insufficiency. Two of these infants belonged to the risk group.
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PMID:Respiratory syncytial virus infections in children admitted to the intensive care unit. 281 76

Babies with chronic bronchopulmonary dysplasia (BPD) can sometimes develop pallor, systemic and pulmonary edema, oliguria, and hyponatremia not attributable to cardiopulmonary or renal impairment. These signs and symptoms might, however, be explained by inappropriate control of vasopressin secretion. To test this hypothesis, we measured plasma vasopressin and osmolality, serum sodium and potassium concentrations, urine output and osmolality, and free water clearance in 26 normoxic infants with BPD aged 1-4 months. All of these infants required supplemental oxygen (FiO2 0.41 +/- 0.03, mean +/- 1 SE) to maintain O2 saturation of greater than 88%, and six infants also required mechanical ventilation. As controls, 10 infants of similar age but without BPD were also studied. None of the infants had been discharged from the nursery and was receiving any medications, and all were clinically stable when studied. Compared to control infants, infants with BPD had significantly elevated plasma vasopressin concentrations (control 5.2 +/- 0.9 pg/ml; BPD 42.4 +/- 5.1; mean +/- SE, p less than 0.05). Moreover, infants with BPD had hyponatremia and hypotonic plasma, and both urine output and free water clearance were significantly reduced. These data suggest that some infants with chronic BPD have elevated vasopressin levels that are functionally significant. We speculate that excessive stimulation of vasopressin secretion may explain some of the pulmonary and nonpulmonary signs and symptoms in infants with chronic BPD.
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PMID:Control of water balance in infants with bronchopulmonary dysplasia: role of endogenous vasopressin. 334 Apr 51

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

Elevated levels of vasopressin (AVP) have been found in premature infants with bronchopulmonary dysplasia (BPD), and may be related to abnormalities of water handling, and to non-pulmonary signs of edema. Dexamethasone treatment improves pulmonary function in infants with BPD, and is frequently associated with a significant increase in diuresis and a decrease in weight gain. To determine whether this diuresis is primarily the result of AVP inhibition (potentially induced by steroid treatment), we measured endogenous AVP levels in nine premature babies with BPD [birth weight 802 +/- 141 (SD) g; gestation 26 +/- 2 weeks, age 26 +/- 17 days], before initiation, and 3 and 7 days after the start of dexamethasone therapy (0.5 mg/kg/day). All study infants required mechanical ventilation, and none was receiving diuretics or cardiac inotropes during the study. Results indicated that premature infants with BPD have functionally unmodified AVP levels after 3 and 7 days of dexamethasone therapy (pre-dexamethasone 5.9 +/- 2.1 ng/l vs post-dexamethasone 7.0 +/- 3.0 and 8.0 +/- 1.9 ng/l at 3 and 7 days, respectively). Pulmonary function improved with oxygenation indexes decreasing (pre-dexamethasone 14 +/- 7 vs post-dexamethasone 9 +/- 7 and 7 +/- 4 at 3 and 7 days, respectively). A concurrent reduction in weight gain occurred (pre-dexamethasone 12 +/- 10 g/kg/day vs post-dexamethasone 7 +/- 3 g/kg/day and 3 +/- 1.5 g/kg/day on days 3 and 7, respectively). These data suggest that the improvement in lung function with dexamethasone treatment for BPD in premature infants does not correlate with a diuresis that results from vasopressin inhibition, and potentially induced by dexamethasone.
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PMID:Dexamethasone does not affect vasopressin release in bronchopulmonary dysplasia. 1114 18