MONITORING KETOSIS
‘In a patient initially presenting in ketoacidosis the ketones, as measured by nitroprusside reaction, may be only weakly positive, whereas they are in fact high.’
availability of carbohydrates such as starvation, frequent vomiting, diabetes mellitus, glycogen storage disease oralkalosis. High fat, low carbohydrate diets are ketogenic and increase ketone bodies in circulation. Ketogenic diets and prolonged exercise are also associated with physiological ketosis. Ketogenic diets, which are used in certain weight- reduction programmes and which have been used to treat patients with refractory epilepsy, contain at least 50% of their calories as fat. This degree of fat content is nearly twice as high as that found in the typical diet of individuals in developed nations. Prolonged exercise is also
associated with mild hyperketonemia, with ketone body levels not uncommonly rising to the range of 1-2 mmol/L. Diabetes mellitus and alcohol consumption are the most common causes of ketoacidosis in adults. Diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar nonketotic state (HHNS) are two serious, acute metabolic complications of diabetes. Ketoacidosis can also be
precipitated following binge drinking and withdrawal in chronic alcoholics. Ketosis can also occur following ingestion of isopropyl alcohol and salicylates. After DKA, alcoholic ketoacidosis is the most common cause of ketoacidosis in adults. It is a relatively common syndrome in chronic alcohol abusers and binge drinkers. Alcoholic ketoacidosis (AKA) is generally associated with a period of excessive alcohol consumption, followed by withdrawal and minimal food intake.
Urine ketone tests are positive in
approximately 30% of first morning specimens from pregnant women. During periods of glucose deficiency ketone bodies play a key role in sparing glucose utilisation and reducing proteolysis. Unlike most other tissues the brain cannot utilise fatty acids for energy when blood glucose levels become compromised. In this case ketone bodies provide the brain with an alternative source of energy, amounting to nearly two thirds of the brain’s energy requirements during prolonged fasting and starvation.1
Ketone
bodies stimulate insulin release in vitro, generate oxygen radicals and cause lipid peroxidation. Lipid peroxidation and the generation of oxygen radicals may play a role in vascular disease in diabetes.
Ketone bodies in body fluids The nitroprusside test in the form of the semi-quantitative Acetest and Ketostix is commonly used to determine ketones in urine but is insensitive to ßHB. It is important, therefore, to remember that a negative nitroprusside test does not rule out ketoacidosis. The semi-quantitative determination of ketone bodies in blood is more sensitive but still does not detect ßHB. The reaction is shown in Figure 2. Serum or plasma samples should only
Stanbio Laboratory, an EKF Diagnostics company has developed the ß-Hydroxybutyrate LiquiColor Reagent System to improve the detection of clinically significant ketosis.
Figure 2: Determination of Ketone Bodies in serum or urine.
Na-nitroprusside + Acetoacetic acid or acetone (glycine, Na2
HPO4 , lactose) ––––––––– Purple complex Figure 3: Determination of ßHB.
ßHB + NAD ––––––––– Acetoacetic acid + NAHD + H+ NADH + NBT (colourless) ––––––––– NBT (reduced -blue) + H+
be analysed with the Acetest tablets. When a positive is initially detected samples should be serially diluted until a negative is obtained. The Ketostix test gives a positive reaction within 15 seconds with a specimen containing at least 50 mg of
‘During periods of glucose deficiency ketone bodies play a key role in sparing glucose utilisation and reducing proteolysis.’
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www.triplered.com NOVEMBER 2012 THE CLINICAL SERVICES JOURNAL 47
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