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)

To determine factors contributing to life-threatening brain herniation in patients treated for severe diabetic ketoacidosis, we analyzed history, laboratory data, rate and composition of fluid and insulin administration, and time to onset of brain herniation in nine new cases and 33 prior reports. The overall rate of fluid administration was inversely correlated with the time of onset of herniation (r = -0.32, p = 0.04). Only 4 of 40 cases occurred at fluid intakes less than or equal to 4.0 L/m2/day. During treatment, "calculated" serum sodium concentrations fell significantly and were less than 130 mEq/L in 33% of cases at the time of herniation. These data indicate that excessive secretion of vasopressin may exacerbate the brain edema, and that limitation of the rate of fluid administration may be prudent.
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PMID:Factors associated with brain herniation in the treatment of diabetic ketoacidosis. 313 55

Diabetic ketoacidosis is often associated with a temporary increase in protein excretion, but the mechanisms are not completely known. The aim of the present study was to examine the effect of acute experimental moderate ketosis on kidney function and specifically on protein handling using an infusion of 3-hydroxybutyrate in healthy subjects. Seven young healthy males were infused with sodium 3-hydroxybutyrate, the peak blood level attained being 1.96 +/- 0.53 mmol/l (SD). The pH in blood and urine rose significantly from 7.40 +/- 0.03 to 7.45 +/- 0.05 (2p less than 0.01) and from 7.29 +/- 0.79 to 8.51 +/- 0.82 (2p less than 0.01), respectively. Urinary beta-2-microglobulin excretion rose significantly from 0.038 microgram/min x/ divided by 1.9 to 0.082 microgram/min x/ divided by 1.4 (geometric mean x/ divided by tolerance factor) (2p less than 0.01) but urinary albumin excretion was unchanged. No changes were seen in blood pressure, glomerular filtration rate and renal plasma flow. A marked reduction in urine flow from 15 to 5 ml/min was noted, but could not be attributed to changes in plasma arginine-vasopressin, which was reduced before and during infusion due to considerable oral water loading. It is concluded that moderate elevation in blood ketone body levels does not induce albuminuria. It is suggested that the temporary proteinuria present in diabetic ketoacidosis may be related to acidosis per se.
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PMID:Effect of 3-hydroxybutyrate infusion on urinary protein excretion in healthy man. 352 Jul 91

Plasma vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis. During the 24 h period of insulin withdrawal, blood glucose rose from 6.7 +/- 1.0 to 20.7 +/- 2.4 mmol/l, whereas plasma vasopressin was 3.6 +/- 0.5 pg/ml initially and in four patients showed little change. Markedly elevated levels of plasma vasopressin (17.8, 19.8 and 26.6 pg/ml) were observed in three patients following the onset of hypovolaemia, nausea and/or vomiting which are known to stimulate vasopressin release. Free water clearance was negative throughout the study in all patients. Thirst was not noted despite marked hyperglycaemia (16.9 +/- 2.5 mmol/l) until a significant fall in body weight of 0.9 +/- 0.2 kg had occurred (p less than 0.005). We concluded that marked elevation of vasopressin results from non-osmotic stimulation and that the mechanisms of body water conservation are overridden by the glycosuric diuresis.
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PMID:Plasma vasopressin during insulin withdrawal in insulin-dependent diabetes. 702 Dec 77

Among the factors, which may influence on the uric acid metabolism, the excess or deficiency of some hormones apparently induces the abnormal serum uric acid level. We described hyperuricemia and hypouricemia associated with endocrine disorders. Hyperuricemia due to the increased production of uric acid is observed in myopathy associated with hypothyroidism, hyperthyroidism or hypoparathyroidism. Hyperuricemia due to the decreased renal uric acid clearance is associated with hypopituitarism, hypothyroidism, hyperparathyroidism, central diabetes insipidus, nephrogenic diabetes insipidus, Bartter syndrome, and diabetic ketoacidosis. Hypouricemia due to the increased renal uric acid clearance is associated with hypoparathyroidism, primary aldosteronism and inappropriate secretion of antidiuretic hormone (SIADH).
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PMID:[Abnormal serum uric acid level in endocrine disorders]. 897 20

Virtually all hospitalized pediatric patients require some form of intravenous fluid administration. The foundation of current pediatric fluid therapy practice was formulated in the 1950s when pediatricians were dealing with relatively simple dehydration and normal homeostasis could largely be assumed. Recent advances in pediatric medicine have resulted in increased severity of illness and normal physiology can no longer be assumed. The traditional approach to pediatric fluid therapy has been recently challenged by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), cerebral salt wasting syndrome (CSWS), diabetic ketoacidosis (DKA) and hyponatremia caused by the inappropriate use of hypotonic solutions, all of which involve unusual sodium and serum osmolarity dynamics causing life threatening central nervous system (CNS) pathophysiology. In this review, we give an overview of the recent understanding of pediatric fluid therapy. The widespread use of acetate in place of lactate as a bicarbonate precursor and the expanding role of nonalbumin plasma expanders in pediatrics are also discussed as they will play a clinical role in the near future.
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PMID:Recent trends in pediatric fluid therapy. 1531 7