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Multiple Choice

Which condition produces the highest elevation of serum lactate dehydrogenase?

Lactate dehydrogenase increases in the blood whenever cells are damaged or destroyed, so conditions with extensive cell turnover or intramedullary destruction can cause large rises. In pernicious anemia, there's ineffective erythropoiesis with marked intramedullary destruction of red cell precursors. This releases large amounts of LDH from immature erythroid cells in the bone marrow (and from destroyed circulating red cells), leading to a particularly high serum LDH level. Muscular dystrophy can raise LDH from muscle injury, but the overall rise is usually not as large as what’s seen with massive erythroid turnover. Myocardial infarction elevates LDH, especially with tissue damage in the heart, but the peak and magnitude are typically less dramatic than the massive intramedullary release seen in pernicious anemia. Acute hepatitis can raise LDH via liver cell injury, but the pattern is liver-dominant and not as striking as the extensive RBC/erythroid precursor destruction in pernicious anemia.

Lactate dehydrogenase increases in the blood whenever cells are damaged or destroyed, so conditions with extensive cell turnover or intramedullary destruction can cause large rises. In pernicious anemia, there's ineffective erythropoiesis with marked intramedullary destruction of red cell precursors. This releases large amounts of LDH from immature erythroid cells in the bone marrow (and from destroyed circulating red cells), leading to a particularly high serum LDH level.

Muscular dystrophy can raise LDH from muscle injury, but the overall rise is usually not as large as what’s seen with massive erythroid turnover. Myocardial infarction elevates LDH, especially with tissue damage in the heart, but the peak and magnitude are typically less dramatic than the massive intramedullary release seen in pernicious anemia. Acute hepatitis can raise LDH via liver cell injury, but the pattern is liver-dominant and not as striking as the extensive RBC/erythroid precursor destruction in pernicious anemia.