Pregnancy induces a hypercoagulable state peaking at delivery and reverting postpartum. This prospective cohort study evaluated the longitudinal progression of endogenous thrombin potential in 102 high-risk pregnant women in relation to the development of preeclampsia or gestational diabetes mellitus. Samples were collected from gestational weeks 8–15, with follow-ups every 2–12 weeks, and thrombin generation was assessed using Calibrated Automated Thrombography. Eleven women developed preeclampsia, and 19 developed gestational diabetes mellitus. Endogenous thrombin potential values were significantly elevated in patients who developed preeclampsia (2220 ± 357 nM*min, p < 0.001) or gestational diabetes mellitus (2298 ± 377 nM*min, p < 0.001) compared to the rest of the cohort (1995 ± 337 nM*min), with high levels evident from the first trimester—well before clinical symptoms. Notably, preeclampsia patients on acetylsalicylic acid therapy did not show further increases in endogenous thrombin potential, and acetylsalicylic acid intake in gestational diabetes mellitus patients effectively moderated endogenous thrombin potential progression. These findings suggest that higher early-pregnancy endogenous thrombin potential reflects an underlying hemostatic imbalance associated with the subsequent development of preeclampsia and gestational diabetes mellitus. Furthermore, acetylsalicylic acid appears to exert effects beyond its anti-inflammatory properties by moderating endogenous thrombin potential, providing new insights into the early pathophysiology and therapeutic modulation of high-risk pregnancies.
Haidl et al. (Tue,) studied this question.