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Table 1.

Demographic data of patient cohort.

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Fig 1.

The progression of soluble fms-like tyrosine kinase-1 (sFlt-1) levels (a), placental growth factor (PlGF) levels (b), and the sFlt-1/PlGF ratio (c) throughout pregnancy within the cohort, inclusive of women who developed PE and GDM.

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Fig 2.

The progression of circulating levels of prothrombin fragments 1 and 2 (F1 + F2) (a), thrombin-antithrombin complexes (TAT) (b), and D-Dimer (c) throughout pregnancy within the cohort, inclusive of women who developed PE and GDM.

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Fig 2 Expand

Fig 3.

Representative thrombin traces showing profiles of women who developed PE, GDM, or the rest of the cohort (Others) and metric parameters derived from these traces.

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Fig 3 Expand

Table 2.

Parameters derived from calibrated automated thrombin generation in patients with PE or GDM, compared to the rest of the cohort (Others).

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Table 2 Expand

Fig 4.

The progression of ETP (a) and Peak height (c) observed in thrombin generation traces during pregnancy among women who developed PE, GDM, or the rest of the cohort (Others).

Shaded areas represent the 95% confidence interval for the regression estimate. The distribution of the means per patient is summarized in boxplots (b, d). Statistical significance is denoted by ***p < 0.001.

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Fig 5.

Change of ETP values (Δ ETP) since the first visit in women who developed PE vs. the rest of the cohort (Others) (a).

Shaded areas represent the 95% confidence interval for the regression estimate. The distribution of the means per patient is summarized in boxplots (b). ns: No statistical significant difference.

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Fig 5 Expand

Fig 6.

Changes in ETP values (Δ ETP) since the initial visit for the entire study cohort (a) and GDM patients (c), comparing patients taking ASA to those who are not.

Shaded areas represent the 95% confidence interval for the regression estimate. The distribution of the means per patient is summarized in boxplots (b, d). Statistical significance is denoted by **p < 0.01, ***p < 0.001.

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Fig 6 Expand