Abstract

Serum leucine aminopeptidase activity increases, gradually with the gestation period, but not strikingly high enough during the first trimester to serve as a test for early pregnancy. In trophoblastic disease, particularly in hydatidiform mole, there is no definite elevation of serum leucine uminopeptidase activity. In ectopic gestation, fetal death and abruptio placentae, serum leucine aminopeptidase activity is. markedly depressed. The probable mechanism of this phenomenon is recounted. The serum leucine aminopeptidase activity in cord blood is slightly elevated, but still lower than that of corresponding maternal blood. The possibility that serum leucine uminopeptidase is transmissable through the “placental barrier” is proposed. No significant serum leucine amino peptidase deviation is found among the gynecological disorders, cither neoptastic or non-neoplastic.

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