Extreme Elevation of Alkaline Phosphatase in a Pregnancy Complicated by Uncontrolled Chronic Hypertension and Its Association With Placental Pathology

Alkaline phosphatase (ALP) is an enzyme produced primarily by cells of liver, bone, kidney, small intestine and placenta, each detect-able by a specific isoenzyme. It appears in maternal serum in the sec-ond trimester and increases progressively with gestational age. Review of the literature has linked markedly elevated serum ALP levels with adverse obstetric and perinatal outcomes, including preterm labor, hypertensive disorders of pregnancy and low birth weight. The exact mechanism of this association is unknown, but an overwhelm-ing majority of literature suggests placental dysfunction as the primary cause. We describe a 38-year-old G5P2022 female who began prenatal care at 10 + 0/7. She started on labetalol 100 mg BID at 17 + 0/7. At 35 + 5/7, she had persistent severely elevated blood pressure, with ALP of 2,826 U/L. She was admitted for observation, and labetalol titrated to 300 mg BID. The maximum value of ALP was 3,429 U/L at 36 + 5/7. Serum isoenzyme assay revealed solely placental origin. Labor induction was done at 37 + 0/7 followed by delivery of a 3,315 g neonate, with a displaced clavicular fracture in the absence of shoulder dystocia. Placental pathology revealed diffuse villous edema and chorionic plate vessel with dense embedded mural thrombus. Our case represents an association between extreme elevation of ALP in pregnancy and placental dysfunction, confirmed by placental pathology. Close monitoring of the absolute value and degree of rise in ALP may hold significant clinical importance in predicting impaired placental function and ultimately in determining the timing of delivery.