To assess the effect of phosphate replacement therapy on the course of diabetic coma, 24 patients with severe diabetic ketoacidosis and 16 patients with non-ketotic hyperosmolar coma were randomly assigned either to standardized conventional treatment alone or combined with phosphate infusions. Insulin and fluid therapy produced a rapid fall of plasma phosphorus; almost all patients not receiving phosphate infusions developed marked hypophosphatemia within 12 h. Hypophosphatemia was prevented by administration of 62 ± 5 mmol (range 35–140) sodium phosphate. Initial red blood cell 2,3-diphosphoglycerate (2,3-DPG) concentrations were markedly decreased in ketoacidotic patients. The recovery of 2,3-DPG upon institution of therapy was accelerated when phosphate replacement infusions were given. The increase in 2,3-DPG during the first 48 h was 56% greater (P < 0.02) when phosphate was administered, but later the difference between the two treatment groups disappeared. Non-ketotic hyperosmolar coma patients revealed normal 2,3-DPG concentrations on admission, and a similar decline of plasma phosphorus occurred, as in ketoacidosis, during treatment. 2,3-DPG levels remained unaffected by phosphate therapy. While plasma calcium levels declined during the initial 48 h in both groups, transient postinfusion hyperphosphatemia was noted in 7 of 17 patients. A favorable effect of phosphate therapy on the clinical course of diabetic ketoacidosis or hyperosmolar coma could not be demonstrated.
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Original Contributions|
February 01 1980
Prevention of Hypophosphatemia by Phosphate Infusion During Treatment of Diabetic Ketoacidosis and Hyperosmolar Coma
Ulrich Keller;
Ulrich Keller
Department of Internal Medicine, University Hospital
CH-4031 Basel, Switzerland
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Willie Berger
Willie Berger
Department of Internal Medicine, University Hospital
CH-4031 Basel, Switzerland
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Citation
Ulrich Keller, Willie Berger; Prevention of Hypophosphatemia by Phosphate Infusion During Treatment of Diabetic Ketoacidosis and Hyperosmolar Coma. Diabetes 1 February 1980; 29 (2): 87–95. https://doi.org/10.2337/diab.29.2.87
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