 |
||||||||||||||||||||||||||||
 |
||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||
Lactic dehydrogenase (LD) catalyzes the conversion of lactate to pyruvate and is present in high concentrations in the cytoplasm of almost all cells. Since LD is found in every tissue in the body, the diagnostic value of an elevated level without additional laboratory investigation is limited. Diseases of most organs including myocardial infarction, hepatic necrosis, skeletal muscle disease, renal disease, pulmonary infarction, malignancy, megaloblastic anemia, and hemolysis increase serum levels of LD. In liver disease, AST and ALT are usually much more elevated than LD. The half life of cardiac LD is about three days, while the half life of LD released from skeletal muscle and liver is about ten hours. LD is no longer recommended for evaluation of acute myocardial infarction and has been removed from the acute cardiac injury panel. Late presenters should be evaluated with cardiac troponin I rather than LD. Heparin therapy can elevate serum LD. Specimens that are not promptly centrifuged will have slightly elevated LD levels, due to leakage from red blood cells. Usually these specimens also have decreased glucose. Hemolysis results in more significant increases. Reference range is 300 - 600 IU/mL (Vitros analyzer). Specimen requirement is one SST tube of blood. |
||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||
|
||
