Session: OR19-Female Reproductive Endocrinology
Room 102 (Moscone Center)
Hypothesis: That pregnancy induces a disproportionate rise in cleaved, low-affinity CBG, with a corresponding relative lack of rise in intact, high-affinity CBG, contributing to the extent of increase in free cortisol.
Methods: Stored plasma samples from pregnant women which had been collected between 1400-1700h, serially through gestation, were assayed. Total (cleaved plus uncleaved) and intact (uncleaved) CBG were assayed in parallel with specific monoclonal antibodies, using our in-house method.2 Total cortisol was assayed using a commercial immunoassay.
Results: 53 samples from 33 women were assayed, encompassing early (<15w, n = 13), mid (16-24w, n = 19), and late (>24w, n = 21) pregnancy.3 Total CBG levels in each interval were (mean ± SE) 1088 ± 167.9, 1117 ± 160 and 1125 ± 155 nmol/L, respectively. Corresponding intact CBG levels were 433.3 ± 27.0, 525.2 ±28.6 and 516.1 ± 46.7 nmol/L. Total cortisol levels increased throughout gestation 328 ± 23, 447 ± 38, 526 ± 33 nmol/L as expected. Cleaved, low affinity CBG comprised 60.2%, 53.0% and 54.1% of total CBG across the three pregnancy intervals.
Conclusion: Cleaved, low cortisol binding affinity CBG comprises over 50% of total CBG in pregnancy compared to approximately 20% CBG in the non-pregnant state.4 The rise in intact high cortisol binding affinity CBG compared to non-pregnant individuals is much less than previously estimated using conventional assays, explaining the unexpectedly high free cortisol relative to total cortisol and total CBG in pregnancy. High affinity CBG levels only rise moderately in pregnancy, less than 2-fold, compared to the non-pregnant state. This allows higher free cortisol levels to be achieved in pregnancy although a role for low affinity CBG in pregnancy is possible.
Nothing to Disclose: MAN, JTH, VLC, NH, PAE, JGL, DJT
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