Amparo Galán

G‐hydroxybutyrate and acetoacetate as well as lactate and pyruvate are intermediary metabolites normally present in blood. The g‐hydroxybutyrate/acetoacetate ratio is an expression of the mitochondrial oxido‐reduction state. This ketone body ratio can provide a clue to diagnosis and metabolic status in congenital errors of the electron transport chain and pyruvate metabolism. The standardization of these analytical procedures improves the interpretation of the results helping in the difficult diagnosis of mitochondrial diseases in children. This study describes an adaptation to a Dimension R 2 L (Dade Behring, Newark, Delaware, USA) automatic analyser for a method to measure blood ketone bodies (g‐hydroxybutyrate and acetoacetate). The method allows the metabolites to be measured directly in nondeproteinized plasma (fluoride/ethylenediaminetetraacetic acid). This adaptation simplifies the analytical procedure and limits the turnaround time to 20 minutes. With a sample volume of 200 μ l metabolite concentrations ranging from 12 to 1300 μ molL⁻¹ of g‐hydroxybutyrate and from 10 to 450 μ molL⁻¹ of acetoacetate may be measured with a reliable analytical response.

The lack of standardization of methods to measure cardiac markers for coronaria ischaemia, particularly troponin, led us to perform an analytical evaluation of two new immunoassays to quantify CK-MB mass and troponin I using the Dimension R×L automatic analyser. The reliability and analytical intervals of the methods were studied as well as reference values (0.010— 0.228 μg l-1 for troponin I, 0.20—3.90 mg μg l-1 for CK-MB mass) and cuto¡ values (0.77 μg l-1 for troponin I, 5 μg l-1 for CK-MB mass) established. The cutoff values were established from 37 patients with acute myocardial infarction and from 20 with unstable angina. The absence of method cross-reactivity was corroborated using myocardial, brain and skeletal muscle tissue. Both methods were highly specific and showed good reliability and practicability in the diagnosis of coronaria ischaemia after 6 h of precordial pain.