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Urinary ketone measurement has become an established investigation in the management of children with diabetes mellitus.1 ,2 However, in the context of diabetic ketoacidosis (DKA), current paediatric clinical guidelines3 ,4 fall short of providing reliable quantitative recommendations regarding the measurement of ketonuria. Ketonuria occurs as plasma levels of ketone bodies rise above 0.1–0.2 mM, as in the case of DKA.5 More recently it has become possible to measure capillary ketone levels with handheld, near-patient ketone meters. While the use and availability of these devices have steadily increased, their incorporation into hospital and national paediatric guidelines has been limited. This is despite the fact that the American Diabetes Association6 no longer recommends the use of urinary ketone measurement, favouring capillary ketone measurement instead. In this review article, we present the strengths and limitations of this new technology in paediatric practice.
The physiological role of ketone bodies (acetone, acetoacetate and β-hydroxybutyrate (β-HB)) is to act as an alternative energy source for the brain in the fasted state.2 ,5 When glycogen stores are depleted in hepatocytes, acetyl-coenzyme A is diverted into the synthesis of ketone bodies. In the brain, they are converted back into acetyl-coenzyme A for use in the Krebs cycle. Ketogenesis has evolved as a physiological response to the fasting individual. However, it can become pathological in DKA, where an inappropriately low plasma insulin concentration simulates the intrahepatic fasting environment, causing inappropriate ketogenesis and subsequent metabolic acidosis. The principle ketone bodies in the plasma are β-HB and acetoacetate. In DKA, the ratio of β-HB to acetoacetate rises from 1:1 to as much as 10:1.7 Once ketogenesis is switched …
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