Thrombosis Journal最新文献

Objective: This study evaluated the predictive value of serum homocysteine (HcY) and potassium ion (K⁺) for short-term prognosis of patients with acute cerebral infarction (ACI) undergoing intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA).

Methods: Totally, 140 ACI patients receiving intravenous thrombolysis using rt-PA were finally included and classified into early neurological deterioration (END) and non-END groups. Serum levels of HcY and electrolytes were detected. The 90-day prognosis of patients after thrombolysis was analyzed. Influencing factors for END and poor short-term prognosis in rt-PA-treated ACI patients were identified using stepwise regression models. Correlations of serum HcY and K⁺ with modified Rankin scale (mRS) scores were analyzed, and values of serum HcY and K⁺ in assessing END and poor prognosis of ACI patients were determined.

Results: The END group had higher age, atrial fibrillation, neutrophil ratio, CysC, FIB, FPG, TNF-ɑ, IL-6 and HcY levels, and National Institutes of Health Stroke Scale scores on admission but lower serum calcium ion and K⁺ concentrations than the non-END group. In ACI patients, serum HcY and K⁺ levels significantly correlated with mRS scores. Serum HcY and K⁺ levels were independent influencing factors for END and poor short-term prognosis of rt-PA-treated ACI patients. Combination of serum HcY and K⁺ could assist in predicting END and poor short-term prognosis in ACI patients.

Conclusion: Serum HcY and K⁺ levels are closely linked to END and short-term prognosis in ACI patients after intravenous thrombolysis using rt-PA and can be used as novel biomarkers for short-term prognosis in ACI patients.

Introduction: Antithrombin (AT) deficiency, often caused by mutations in the SERPINC1 gene, is a well-established risk factor for venous thromboembolism (VTE), which can lead to serious complications such as deep vein thrombosis (DVT), pulmonary embolism (PE), and cerebral venous sinus thrombosis (CVST). Syndecan-4 (SDC4), an endothelial cell membrane protein, enhances AT's anticoagulant function by facilitating its interaction with the vascular endothelium, thereby supporting hemostatic balance.

Methods: Our team enrolled a patient diagnosed with CVST, and subsequent genetic testing identified the SERPINC1 p.Phe155del variant. This study sought to elucidate the interaction between AT mutations and SDC4 in VTE pathogenesis using clinical case analyses, molecular docking, co-immunoprecipitation (Co-IP), and immunofluorescence assays.

Results: The patient was diagnosed with Type I hereditary AT deficiency, with a five-generation family pedigree constructed. Molecular docking simulations showed the SERPINC1 p.Phe155del variant weakened the protein's interaction with SDC4. Cell-level co-immunoprecipitation and immunofluorescence results were consistent with molecular docking findings, confirming that the SERPINC1 p.Phe155del mutant binds less strongly to SDC4 than the wild-type.

Conclusion: This reduced binding may underlie hereditary AT deficiency and increased venous thrombosis risk. The findings from this research deepen understanding of the connection between hereditary hypercoagulable states and VTE -with CVST as one possible clinical manifestation-offering new insights to inform clinical diagnosis and treatment.

Type 3 von Willebrand disease (VWD) is the rarest and most severe form of VWD, resulting from a complete loss of function of the von Willebrand factor (VWF). This disease presents bleeding symptoms that are characteristic of primary hemostasis disorders and hemophilia-like bleeding. We present a case series of the first three patients diagnosed with type 3 VWD in Ethiopia. All three patients presented with episodes of frequent epistaxis, easy bruising, and prolonged bleeding from minor injuries. Comprehensive laboratory evaluation revealed severe anemia, markedly prolonged activated partial thromboplastin time (aPTT), complete absence of VWF, and profoundly decreased clotting factor VIII (FVIII) activity in all patients, thereby establishing the diagnosis of type 3 VWD. Patients are currently managed with frequent fresh frozen plasma, cryoprecipitate, and tranexamic acid (TXA) due to the unavailability of VWF replacement therapy in the country. For treatment response, clinical follow-up with serial aPTT monitoring was performed. Under this supportive regimen, both the frequency of mucosal bleeding episodes and the need for fresh frozen plasma (FFP) and cryoprecipitate transfusions have decreased, with transfusions required at intervals of approximately every 3-4 weeks. Thorough assessment, accurate diagnosis, and proper classification of VWD are crucial because they significantly affect patient management and treatment modalities. Type 3 VWD is often underdiagnosed and undertreated in developing countries because of the lack of available diagnostic laboratory investigations and VWF-containing concentrates.