Denninger MH, de Prost D, for the PPH Study Group. The decrease of fibrinogen is an early predictor of the severity of postpartum hemorrhage. 2007; 5: 266-73. Summary. Background: Postpartum hemorrhage (PPH) is a major source of maternal morbidity. Objectives: This study's objective was to determine whether changes in hemostasis markers during the course of PPH are predictive of its severity. Patients and methods: We enrolled 128 women with PPH requiring uterotonic prostaglandin E2 (sulprostone) infusion. Two groups were defined (severe and non-severe PPH) according to the outcome during the first 24 hours. According to our criteria, 50 of the 128 women had severe PPH. Serial coagulation tests were performed at enrollment (H0), and 1, 2, 4 and 24 hours thereafter. Results: At H0, and through H4, women with severe PPH had significantly lower fibrinogen, factor V, antithrombin activity, protein C antigen, prolonged prothrombin time, and higher D-dimer and TAT complexes than women with non-severe PPH. In multivariate analysis, from H0 to H4, fibrinogen was the only marker associated with the occurence of severe PPH. At H0, the risk for severe PPH was 2.63-fold higher for each 1 gL )1 decrease of fibrinogen. The negative predictive value of a fibrinogen concentration >4 gL )1 was 79% and the positive predictive value of a concentration £2 gL )1 was 100%. Conclusion: These findings indicate that a simple fibrinogen measurement can anticipate the risk of severe bleeding in PPH. J Thromb Haemost

Human abdominal aortic aneurysm (AAA) expansion has been linked to the presence of a mural thrombus. Here we explored the mechanism of the continual luminal renewal of this thrombus and its ability to release biological markers potentially detectable in plasma. We also explored the ability of platelet inhibition to pacify the thrombus and to limit aneurysm progression in an experimental model. Blood samples and mural thrombi were collected in 20 AAA patients. In parallel, segments of sodium dodecyl sulfate-decellularized guinea pig aorta were xenografted onto the abdominal aorta of 30 rats to induce aneurysms. Fifteen rats received abciximab treatment and fifteen received irrelevant immunoglobulins. Procoagulant activity and platelet activation markers (microparticles, sP-selectin, sGPV, sCD40L) were increased threefold to fivefold in eluates from the luminal thrombus layer compared to other layers. All these markers were increased twofold to fivefold in patients' plasma compared to matched controls (P < 0.005). In the rat model, abciximab reduced both thrombus area and aneurysmal enlargement (P < 0.05). Platelet aggregation is probably responsible for the renewal of the thrombus in AAA. The luminal thrombus released markers of platelet activation that could easily be detected in plasma. Platelet inhibition limited aortic aneurysm expansion in a rat model, providing new therapeutic perspectives in the prevention of AAA enlargement.

Shear-induced platelet aggregation is increased in patients experiencing SAT compared with controls receiving dual antiplatelet therapy and to normals receiving no antiplatelet therapy, which suggests increased intrinsic patient-related platelet reactivity in patients with SAT. The predictive value of SIPA for SAT requires prospective investigation.

These results suggest that neutrophil activation plays a key role in the acute activation of coagulation observed during severe heatstroke, despite a rapid and sustained antiinflammatory response. The comparison with a group of patients with severe sepsis suggests some common mechanisms, but more intense responses during heatstroke.