Metabolic Studies in Diabetic Acidosis

Franks, M

doi:10.1001/archinte.1948.00220190050005

Cited by 64 publications

(6 citation statements)

References 16 publications

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“…The amount of phosphate infused was similar to that employed by Franks et al 3 The urinary loss of phosphorus during the first days of treatment was about 30 mmol, which compares well with the previously reported 26 mmol excreted before insulin treatment. 2 Phosphate excretion was augmented when phosphate infusions were given; therefore, the amount excreted within the first 3 days almost equaled the amount infused.…”

Section: Discussionsupporting

confidence: 85%

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Prevention of Hypophosphatemia by Phosphate Infusion During Treatment of Diabetic Ketoacidosis and Hyperosmolar Coma

1980

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To assess the effect of phosphate replacement therapy on the course of diabetic coma, 24 patients with severe diabetic ketoacidosis and 16 patients with nonketotic 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. Nonketotic 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. DIABETES 29: 87-95, February 1980.T he occurrence of excessive urinary phosphorus excretion in patients with uncontrolled diabetes mellitus has been recognized for more than 100 yr. 1 Severe phosphorus depletion ensued when insulin was withdrawn from diabetic subjects, 2 and marked hypo-

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Section: Discussionsupporting

confidence: 85%

“…3 Thus, earlier recommendations for treatment of diabetic coma included the administration of phosphate-containing infusions. 4 " 6 However, a clinical benefit of phosphate therapy was not observed in other studies.…”

mentioning

confidence: 99%

Prevention of Hypophosphatemia by Phosphate Infusion During Treatment of Diabetic Ketoacidosis and Hyperosmolar Coma

1980

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“…The finding of the increased circulating concentration of phosphorus encountered during optimal insulin therapy is paradoxical since insulin itself has been shown to cause a shift of phosphorus from the extracellular space to the intracellular space [1,2]. If this action of insulin on cellular flux of phosphorus were the only mechanism, one would have anticipated a fall in serum phosphorus concentration.…”

Section: Discussionmentioning

confidence: 99%

“…It is commonly believed that the administration of insulin lowers the circulating concentration of phosphorus by promoting cellular influx from the extracellular fluid [1,2]. This effect is particularly apparent during the treatment of diabetic ketoacidosis [2].…”

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The effect of chronic insulin therapy on phosphate metabolism in diabetes mellitus

Raskin

Pak

1981

Diabetologia

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Plasma and urine phosphate concentrations were improved in 21 patients with diabetes mellitus during "optimal" metabolic control as compared with "suboptimal" control. During the "suboptimal" control phase the daily insulin dosage averaged 38 +/- 22 (SD) U/day and the mean plasma glucose levels averaged 17.1 +/- 1.8 mmol/l, while during the "optimal" control phase the daily insulin dosage averaged 84 +/- 59 U/day and the mean plasma glucose level was 6.2 +/- 1.4 mmol/l. The institution of rigid diabetic control over 4-10 days significantly raised serum phosphorus from 1.12 +/- 0.16 to 1.26 +/- 0.19 mmol/l (p less than 0.001), and decreased urinary phosphorus excretion from 686 +/- 125 to 588 +/- 88 mg/day (p less than 0.001). These changes were associated with significant reductions in urinary calcium, urinary glucose, plasma immunoreactive glucagon and serum parathyroid hormone. This diminution in urinary phosphorus loss may have been due to diminished glycosuria but equally could have been influenced by a direct action of insulin on the renal tubule or suppression of glucagon and parathyroid hormone secretion. Under the conditions of this study, reduced urinary phosphorus may have been sufficient to cause a rise in serum phosphorus despite the known effects of insulin on the cellular influx of phosphorus.

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