Lactate
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| Contents | Physiology Lactate is a 3 carbon intermediary of carbohydrate metabolism which is formed from pyruvate by the reversible action of lactate dehydrogenase. Under normal circumstances it is produced in skeletal muscle, brain and erthrocytes and metabolised in the liver and kidney. The Cori cycle refers to the pathway whereby glycolysis in the muscle produces lactate, which is released into the bloodstream, transported to the liver and converted back to glucose for re-use in the muscle. High levels of lactate may be produced in vigorous exercise. This occurs when energy requirements exceed oxygen supply and is known as oxygen debt. The lactate is rapidly cleared once the muscular activity ceases both by renal and hepatic clearance and by aerobic metabolism in the muscles. The half-life of serum lactate is about 60 minutes in these circumstances. Pathology (top of page)Pathological lactate production occurs when there is inadequate tissue oxygen supply, or if there is defective pyruvate clearance or increased pyruvate production. Type A lactic acidosis occurs when there is obvious tissue hypoxia and Type B when tissue hypoxia is not apparent. See table below. Hypoxia is by far the most common cause of lactic acidosis and can occur with shock from any cause. Other factors which may cause tissue hypoxia include severe asthma, severe anaemia, regional hyoperfusion and carbon monoxide poisoning. The rate of lactate recovery after shock is much slower than after exercise with an average clearance half-life of about 18 hours. Tissue hypoxia is probably a contributing factor in many patients with Type B lactic acidosis. Other mechanisms of lactate accumulation include those causing a block in the further metabolism of pyruvate, eg cyanide, nucleoside analogues, salicylates or mitochondrial cytopathies affecting the electron transport chain, thiamine deficiency reducing the activity of pyruvate dehydrogenase, and defects of gluconeogenic enzymes due to inborn errors or alcohol effects; and those leading to increased production of pyruvate, eg increased glycolysis with adrenaline treatment, and protein breakdown increasing the conversion of alanine to pyruvate in sepsis. The elevated pyruvate then equilibrates via LDH to produce increased lactate levels. In the case of hypoxia, or other causes of inhibition of the electron transport chain, NADH accumulates and the supply of NAD is depleted. This pushes the balance between pyruvate and lactate dramatically in favour of lactate further exacerbating its production in these circumstances. This change also occurs with alcohol abuse with alcohol dehydrogenase depleting NAD and producing NADH. A list of the common causes of elevated lactate is shown in the table. Causes of Lactic Acidosis Type A: (clinical evidence of tissue hypoxia)
Type B: (no clinical evidence of tissue hypoxia)
Reference Interval(s) (top of page) <2.2 mmol/L Lactate is rapidly released from red cells in normal blood tubes. For accurate measurements the following precautions must be observed:
The test is available 7 days/24 hours with the results available within 2 hours of sample arrival in the laboratory. |
The information on this page provided by Dr Graham Jones Further information can be obtained by contacting SydPath on 8382-9100 Last updated 1/11/99 |