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Obstet Gynecol. 1999 Aug;94(2):290-4.

Liver function tests and glucose and lipid metabolism in growth-restricted fetuses.

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  • 11st Department of Obstetrics and Gynecology, University of Milano, Clinica Mangiagalli, Italy.



To assess hematologic and biochemical blood variables in growth-restricted fetuses and relate them to biophysical measurements.


Blood was sampled from 22 growth-restricted fetuses. All had normal karyotypes and no congenital infections. Venous pH, partial pressure of oxygen, hematocrit, glucose, uric acid, urea, creatinine, total protein, total and direct bilirubin, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, lactic dehydrogenase, amylase, pseudocholinesterase, creatinine kinase, triglycerides, and cholesterol were measured and compared with our reference range.


Ultrasound measurements of abdominal circumference correlated with fetal pH (r = 0.64), partial pressure of oxygen (r = 0.52), glucose (r = 0.67), total bilirubin (r = -0.54), lactic dehydrogenase (r = -0.48), and triglyceride levels (r = -0.65). Compared with fetuses with present end-diastolic velocities in the umbilical artery, the eight with absent end-diastolic velocities had lower pH (median z score -4.31), partial pressure of oxygen (median z score = -2.39), glucose (median z score = -2.01), and cholesterol (median z score = -2.34), and higher gamma-glutamyltransferase (median z score = 2.43), lactic dehydrogenase (median z score = 3.75), urea (median z score = 1.33), creatinine (median z score = 1.23), and triglyceride levels (median z score = 1.71). Only triglycerides correlated with abdominal circumference, independent of Doppler results.


Growth-restricted fetuses with absent end-diastolic velocities in the umbilical artery had more marked acidemia, hypoxemia, hypoglycemia, and abnormal liver function than those with end-diastolic velocities. Triglyceride levels were inversely related to fetal size independent of Doppler results. High triglyceride levels might reset fetal homeostatic mechanisms, leading to disturbances of lipid metabolism in later life.

[PubMed - indexed for MEDLINE]
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