Induction or spontaneous labor for pregnant patients on anticoagulants?

OBJECTIVE: There are two approaches to peripartum management for pregnant patients undergoing anticoagulation treatments: spontaneous labor or scheduling an induction. A long interval without anticoagulation is a thrombosis risk factor, while a short interval leads to risks of delivery without epidural analgesia or post partum hemorrhage. Our objective was to evaluate the impact of planned induction versus spontaneous labor on obtaining neuraxial analgesia. MATERIALS AND METHODS: A retrospective single-center study was conducted from 2012 to 2020 including all patients on preventive or curative low molecular-weight heparin at the time of delivery, excluding planned cesarean sections. The rates of neuraxial analgesia were compared between two groups: spontaneous labor and induction, as well as the intervals without anticoagulants. RESULTS: 127 patients were included. In the spontaneous labor group, 78% (44/56) received neuraxial analgesia versus 88% (37/42) in the induction group (p = 0.29). For curative dose treatment, the rate of neuraxial analgesia was 45,5% in the spontaneous group versus 78,6% (p = 0.12). The median time without anticoagulation was 34 h [26-46] in the spontaneous labor group and 43 h [34-54] in the induction group (p = 0.01), without an increased incidence of thrombosis. The rate of postpartum hemorrhage did not differ between the two groups. CONCLUSION: Planned induction tended to increase the rate of neuraxial analgesia, without reaching significance, and most women in spontaneous labor accessed analgesia. Peripartum management should be a shared decision with the patient considering the obstetrical and thrombosis risk context for each patient.

The qLabs® FIB system, a novel point-of-care technology for a rapid and accurate quantification of functional fibrinogen concentration from a single drop of citrated whole blood.

Hypofibrinogenemia is often associated with excessive bleeding and requires immediate treatment. The qLabs FIB® is a handheld and easy-to-use point-of-care (POC) device designed for the rapid measurement of functional fibrinogen concentration from a single drop of citrated whole blood. The aim of this study was to evaluate the analytical performances of the qLabs FIB system. Fibrinogen concentrations from 110 citrated whole blood specimen were measured by both the qLabs FIB and the Clauss laboratory reference methods (STA®-Liquid Fib assay on STA-R® Max from Stago). A three-laboratories comparison study was conducted to assess reproducibility and repeatability of the qLabs FIB using plasma quality control material. In addition, single-site assays were conducted to assess the repeatability from citrated whole blood specimen covering the qLabs FIB reportable range. A very strong correlation between the qLabs FIB and the Clauss laboratory reference method was observed (r = 0.95). Using a clinical cut-off value of 2.0 g/L, the area under the receiver operating characteristic curve (ROC) of citrated whole blood was 0.99 and sensibility and specificity were 100 % and 93.5 %, respectively. Percent CVs for reproducibility and repeatability assessed from quality control material, were both <5 %. Repeatability assessed from citrated whole blood specimen showed a CV of 2.6 to 6.5 %. In conclusion, the qLabs FIB system enables a rapid and reliable measurement of functional fibrinogen levels from citrated whole blood and exhibits a strong prediction power at the 2 g/L clinical cut-off when compared to the Clauss laboratory reference. Further clinical studies should demonstrate its ability to quickly confirm the diagnosis of acquired hypofibrinogenemia and help identify patients who may benefit from targeted hemostatic treatment.

[A case of bone marrow necrosis and fat embolism in a sickle-cell disease patient]. / Un cas de nécrose médullaire compliquée d'embolie graisseuse chez un patient drépanocytaire.

We report here a case of bone marrow necrosis and fat embolism syndrome in a 23-year-old sickle-cell disease (HbSS) patient. A brutal and severe bicytopenia conducted to suspect bone marrow necrosis, confirmed by bone marrow aspiration and analysis. This was the first life-threatening medical event for this patient. In the present case, a complex alloimmunization against blood group antigens complicated the treatment because of the risks associated with the transfusion strategy. These rare complications of sickle-cell disease may be fatal, but an efficient symptomatic treatment generally allows for recovery. Medical biologists should be aware of the danger of bone marrow necrosis in sickle-cell disease, so that they can help clinicians and accurately diagnose this serious complication.

Elevated soluble endothelial cell protein C receptor (sEPCR) levels in women with preeclampsia: a marker of endothelial activation/damage?

The endothelial protein C receptor (EPCR) plays a crucial role in the anticoagulant and anti-inflammatory effects of the protein C pathway, whereas its soluble form (sEPCR) exhibits opposite properties. High plasma levels of sEPCR have been observed in subjects carrying the A3 haplotype of PROCR, the EPCR gene. Elevated plasma levels of sEPCR were also recently reported in women with preeclampsia (PE), a multisystemic syndrome involving inflammation, endothelial dysfunction and thrombosis. To determine whether this increase is genetically mediated or acquired, we analyzed sEPCR levels and the A3 haplotype distribution in 145 preeclamptic women and 145 age- and term-matched women with normal pregnancies enrolled in a case-control study. Plasma sEPCR levels were higher in the women with PE than in the controls, and this difference was not due to A3 haplotype over-representation. We observed a positive correlation between sEPCR levels and two markers of endothelium activation/damage (von Willebrand factor and soluble thrombomodulin), and a trend towards a third (sVCAM1). We also found an association between sEPCR levels in the highest quartile and the PE risk. The modest increase of sEPCR levels, together with the correlation with other endothelium activation/damage markers, suggest that it is more an innocent bystander of the endothelium activation/damage than an actor in PE.

Search for an association between V249I and T280M CX3CR1 genetic polymorphisms, endothelial injury and preeclampsia: the ECLAXIR study.

BACKGROUND: Preeclampsia and coronary-artery disease share risk factors, suggesting common pathophysiological mechanisms. CX3CR1/CX3CL1 mediates leukocyte migration and adhesion and has been implicated in the pathophysiology of several inflammatory diseases. M280/I249 variants of CX3CR1 are associated with an atheroprotective effect and reduced endothelial dysfunction. The aim of this study was to search for an association between V249I and T280M polymorphisms of CX3CR1, preeclampsia and endothelial dysfunction. METHODOLOGY/PRINCIPAL FINDINGS: We explored these polymorphisms with real-time polymerase chain reaction in a case-control study (184 white women with preeclampsia and 184 matched normotensive pregnant women). Endothelial dysfunction biomarkers including von Willebrand factor, VCAM-1 and thrombomodulin, as well as the soluble form of CX3CL1 were measured by enzyme-linked immunosorbent assays (ELISA). The I249 and M280 alleles were associated neither with preeclampsia, nor with its more severe form or with endothelial injury. In contrast, we found a trend toward increased CX3CL1 levels in preeclampsia patients, especially in early-onset- preeclampsia as compared to its level in later-onset- preeclampsia. CONCLUSIONS/SIGNIFICANCE: This is the first study to characterize the CX3CR1 gene polymorphisms in patients with preeclampsia. We found no differences in genotype or haplotype frequencies between patients with PE and normal pregnancies, suggesting that maternal CX3CR1 V249I and T280M polymorphisms do not increase susceptibility to preeclampsia. Further studies should be performed to directly evaluate the pathophysiological role of CX3CL1, a molecule abundantly expressed in endometrium, which has been shown to stimulate human trophoblast migration.

[Practical management of HFE hemochromatosis]. / Prise en charge de l'hémochromatose HFE.

HFE-linked, or type 1, hemochromatosis is by far, in the causasians, the most frequent form of chronic iron overload of genetic origin. Its practical management has been recently defined by the French Agency "Haute Autorité de santé". It rests upon a new classification of phenotypic expression. This staging comprises 5 grades according to the combined results of plasma transferrin saturation, ferritinemia and clinical data. The extension of the initial work-up as well as the follow-up modalities is adapted to the staging. A liver biopsy remains indicated only in case of suspected cirrhosis. Venesection therapy is the reference treatment. It is indicated when grade is > or = 2 (i.e. when both transferrin saturation and ferritinemia are increased). The phlebotomy volume should be adapted to the patient's weight. The goal of depletion treatment is to obtain and maintain ferritinemia < or = 50 microg/L. Venesections, especially for maintenance therapy, can be performed at home, which requires a close coordination between the various medical and paramedical partners. Family screening, based upon HFE test, transferrin saturation and serum ferritin, is highly recommended.