|Background:||L-lactate is the end product of anaerobic glycolysis. It is derived predominantly from white skeletal muscle, brain, skin, renal medulla and erythrocytes. Lactate dehydrogenase catalyses the reduction of pyruvate to lactate.
There are two major clinical settings in which lactic acidosis occurs, conditions associated with hypoxia (e.g. shock, congestive heart failure, myocardial infarction, blood loss and pulmonary oedema) and metabolic or drug/toxin related disorders. Examples of metabolic disorders include diabetes mellitus, hepatic disease and neoplasia. Congenital metabolic disorders include type I glycogen storage disease.
Examples of drugs/toxins which give rise to elevated lactate are methanol, ethanol, epinephrine and acetaminophen. Lactate levels in CSF will generally mirror those in blood/plasma. However, increased lactate levels in CSF in the absence of increased blood/plasma lactate concentration have been reported in cases of bacterial meningitis, cerebral hypoxia, ischemia and in certain inborn errors of metabolism e.g pyruvate dehydrogenase deficiency, mitochondrial myopathies and biotinidase deficiency.
|Reference Ranges:||Plasma: 0.5 – 2.2 mmol/L|
|Specimen Requirements:||Sample type:
|Turnaround Time:||2 hours|