Prostaglandin E2 Metabolite Levels During Diabetic Ketoacidosis
1985
Insulin therapy was withdrawn from 15 well-controlled type I diabetic subjects for no longer than 18 h to examine the sequence with which 13,14-dihydro-15-keto-PGE 2 (PGE-m), glucagon, norepinephrine, and epinephrine increased in circulating blood in diabetic subjects becoming ketoacidotic. Fourteen of 15 patients had increments in PGE-m; 12/12, 12/15, and 13/15 had increments in glucagon, norepinephrine, and epinephrine, respectively. Six of the 15 patients developed mild diabetic ketoacidosis (DKA) by 12–18 h; all had nonmeasurable C-peptide levels. This DKA group had significantly greater increments of PGE-m (835 ± 130 versus 276 ± 111 pg/ml, mean ± SEM, P
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