Causes of elevated lactate dehydrogenase in blood

Increased activity of lactate dehydrogenase under physiological conditions is observed in pregnant women, newborns, and individuals after intense physical activity.

Increased lactate dehydrogenase activity in myocardial infarction is observed 8-10 hours after its onset. Maximum activity is reached 48-72 hours later (usually 2-4 times higher), and it remains elevated for 10 days. These periods may vary depending on the size of the damaged heart muscle. Increased total lactate dehydrogenase activity in patients with myocardial infarction occurs due to a sharp increase in lactate dehydrogenase ₁ and partially lactate dehydrogenase _2. No increase in lactate dehydrogenase activity is observed in patients with angina, which allows the use of lactate dehydrogenase determination within 2-3 days after an angina attack as a highly reliable criterion for the absence of damage to the heart muscle.

Moderate increase in total lactate dehydrogenase activity is observed in most patients with acute coronary insufficiency (without myocardial infarction), myocarditis, chronic heart failure, and congestive liver disease. In patients with cardiac arrhythmias, lactate dehydrogenase activity is usually normal, but when using electropulse therapy, it sometimes increases.

The source of increased lactate dehydrogenase activity may be lung tissue in embolism and pulmonary infarction. The combination of normal AST activity, increased lactate dehydrogenase activity, and increased bilirubin concentration may serve as a diagnostic triad for pulmonary embolism and to differentiate it from myocardial infarction. In pneumonia, enzyme activity may sometimes not increase.

In myopathies (muscular dystrophies, traumatic muscle injuries, inflammatory processes, disorders associated with endocrine and metabolic diseases), an increase in lactate dehydrogenase activity is observed; in neurogenic muscle diseases, lactate dehydrogenase activity does not increase.

In acute viral hepatitis, the activity of lactate dehydrogenase in the blood serum increases in the first days of the icteric period; in mild and moderate forms of the disease, it returns to normal levels fairly quickly. Severe forms of viral hepatitis, and especially the development of liver failure, are accompanied by a pronounced and longer-lasting increase in lactate dehydrogenase.

In mechanical jaundice, in the early stages of bile duct obstruction, lactate dehydrogenase activity is normal; in later stages, an increase in lactate dehydrogenase activity is observed due to secondary liver damage.

In liver carcinomas or metastases of cancer to the liver, an increase in lactate dehydrogenase activity may occur.

In the remission stage of chronic hepatitis and liver cirrhosis, the activity of lactate dehydrogenase in the blood remains within the normal range or is slightly increased. During an exacerbation of the process, an increase in enzyme activity is noted.

An increase in lactate dehydrogenase activity is characteristic of megaloblastic and hemolytic anemia, therefore its determination is used for the differential diagnosis of Gilbert's disease (LDH is normal) and chronic hemolytic anemia (LDH is elevated).

Lactate dehydrogenase activity increases in acute and exacerbation of chronic kidney disease; in chronic kidney disease associated with uremia, it may be normal, but often increases after hemodialysis, which is due to the removal of enzyme inhibitors during this procedure.

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