Objectives Platelet-fibrin interactions are critical for hemostasis. Thromboelastography (TEG) assesses these dynamics globally. We investigated the role of fibrinogen on TEG-derived clot strength in pregnant women with and without thrombocytopenia, integrating transcriptomic analysis of public datasets to molecularly corroborate our functional findings. Methods A retrospective study was conducted on 140 third-trimester pregnancies (70 with normal platelet counts and 70 with thrombocytopenia) enrolled between 2015 and 2020. TEG parameters, platelet indices, and fibrinogen concentrations were analyzed. In parallel, public transcriptomic datasets were reanalyzed to explore coagulation- and fibrinogen-related pathways during pregnancy. Results Mean platelet volume (MPV), platelet count, fibrinogen, and TEG parameters R-time, K-time, alpha angle, and maximum amplitude (MA) differed significantly between groups (p < .05). MA positively correlated with platelet count (r = 0.873, p < .001) and fibrinogen concentration (r = 0.410, p < .01). In thrombocytopenic women, MA correlated with platelet count (r = 0.736, p < .0001), MPV (r = 0.447, p < .01), and fibrinogen (r = 0.361, p < .01). Multivariate regression confirmed platelet count and fibrinogen as independent predictors of MA (p < .05). Transcriptomic analysis further demonstrated upregulation of fibrinogen subunits (FGB, F13A1) and enrichment of coagulation pathways in pregnancy, consistent with the functional TEG findings. Conclusions Elevated fibrinogen is associated with and may compensate for preserved clot strength in late pregnancy, particularly in thrombocytopenia. Our integrative analysis provides functional and molecular insights into a potential compensatory mechanism, which forms a rationale for future research to evaluate the therapeutic utility of fibrinogen supplementation. These hypothesis-generating findings warrant prospective interventional validation before clinical application.
Xu et al. (Thu,) studied this question.
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