Clinical and Interpretive

Measurement of lactate dehydrogenase (LDH) is useful in the investigation of a variety of diseases involving the heart, liver, muscle, kidney, lung, and blood and in monitoring changes in tumor burden after chemotherapy. Lactate dehydrogenase elevations in patients with cancer are too erratic to be of use in the diagnosis of cancer.

Lactate dehydrogenase activity is present in all cells of the body with highest concentrations in heart, liver, muscle, kidney, lung, and erythrocytes. Serum LDH is elevated in a number of clinical conditions.

Marked elevations in lactate dehydrogenase activity can be observed in megaloblastic anemia, untreated pernicious anemia, Hodgkin’s disease, abdominal and lung cancers, severe shock, and hypoxia.

Moderate to slight increases in LDH levels are seen in myocardial infarction (MI), pulmonary infarction, pulmonary embolism, leukemia, hemolytic anemia, infectious mononucleosis, progressive muscular dystrophy (especially in the early and middle stages of the disease), liver disease, and renal disease.

In liver disease, elevations of LDH are not as great as the increases in aspartate amino transferase (AST) and alanine aminotransferase (ALT).

Increased levels of the enzyme are found in about one third of patients with renal disease, especially those with tubular necrosis or pyelonephritis. However, these elevations do not correlate well with proteinuria or other parameters of renal disease.

On occasion a raised LDH level may be the only evidence to suggest the presence of a hidden pulmonary embolus.

Red blood cells contain much more lactate dehydrogenase (LDH) than serum. A hemolyzed specimen is not acceptable. LDH activity is one of the most sensitive indicators of in vitro hemolysis. Causes can include transportation via pneumatic tube, vigorous mixing, or traumatic venipuncture.

While increases in serum LDH also are seen following a myocardial infarction, the test has been replaced by the determination of troponin.