ObjectiveThis 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).MethodsTotally, 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.ResultsThe 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.ConclusionSerum 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.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12959-025-00810-z.

IntroductionAntithrombin (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.MethodsOur 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.ResultsThe 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.ConclusionThis 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.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12959-025-00802-z.

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.

BackgroundAntiphospholipid syndrome (APS) is a prothrombotic autoimmune disorder in which perioperative factors—particularly cardiopulmonary bypass—may amplify hypercoagulability. Evidence and consensus guidance for APS management around cardiovascular surgery remain limited.Case summaryA 37-year-old man with a large, highly mobile thrombus in the ascending aorta underwent surgical thrombectomy under cardiopulmonary bypass. Preoperative testing showed only leukocytosis, slightly shortened activated partial thromboplastin time (APTT) and mild D-dimer elevation; all other findings were unremarkable. Ten days postoperatively, removal of a nontunneled right internal jugular central venous catheter (CVC) was unexpectedly impeded by catheter-related thrombosis (CRT) despite prophylactic anticoagulation. Noninvasive maneuvers failed to free the catheter, necessitating open surgical extraction. Subsequent evaluation revealed widespread venous thromboses and confirmed APS, likely underlying both the arterial event and the rapidly developing catheter-associated thrombosis. Aggressive multimodal therapy—including methylprednisolone, enteric-coated aspirin, warfarin, rituximab, unfractionated heparin, and fibrinogenase—achieved clinical stabilization and prevented further events.ConclusionThis case highlights the challenges in timely diagnosing APS and the management complexity of rapid, postoperative thrombus formation. Clinicians should maintain a high index of suspicion for early postoperative hypercoagulability—even when routine coagulation screens are unrevealing—escalate promptly when CVC removal meets resistance, and consider APS-tailored antithrombotic strategies. The possibility that fibrin sheaths and catheter-associated thrombosis can evolve quickly, even after short indwelling times, warrants vigilance and early multidisciplinary intervention. It also raises concern that, in this context, standard direct oral anticoagulants (DOACs) may be less effective.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12959-025-00815-8.

Antithrombin (AT) III is a key physiological anticoagulant, and its hereditary deficiency represents one of the most severe forms of inherited thrombophilia. However, as a rare disorder, AT III deficiency is frequently underdiagnosed due to the limitations of current clinical algorithms. In this study, we describe two cases of hereditary AT III deficiency accompanied by multiple venous thromboembolic events: a 39-year-old male with extensive lower limb deep venous thrombosis (DVT) involving the iliac, femoral, and popliteal veins, and a 21-year-old female with intermediate-high risk pulmonary embolism (PE). Laboratory evaluation revealed reduced AT III activity levels of 51.9% and 52.7%, respectively. Quantitative ELISA analysis further confirmed a corresponding reduction in AT antigen levels. Both patients showed suboptimal responses to initial low-molecular-weight heparin treatment but responded favorably to oral rivaroxaban. Genetic testing identified two nonsense mutations in the SERPINC1 gene: NM_000488.4:c.906dupT (p.Glu303Ter), a previously unreported variant, and NM_000488.4:c.481 C > T (p.Arg161Ter), reported here for the first time in an Asian individual. Family analyses confirmed that the variants were inherited from the proband’s parents, who had a history of venous thromboembolism (VTE). These findings underscore the importance of assessing AT activity in patients with unexplained thrombotic events, particularly at a young age, and support the use of genetic testing to guide personalized anticoagulation strategies in AT III deficiency.

Venous thromboembolism (VTE) is a common complication among hospitalized patients, hence VTE prophylaxis is essential. Low body weight patients are at an increased risk of bleeding however there are no guideline recommendations regarding dose adjustment in this population. We performed a meta-analysis to determine whether dose reduction for VTE prophylaxis in low-body weight patients reduces the risk of bleeding, without compromising its efficacy. We searched electronic databases from inception to October 2024. We did a random-effects meta-analysis using RevMan 5.4. Data were pooled to obtain a risk ratio (RR) with 95% confidence interval (CI). Heterogeneity and publication bias were assessed with statistic and funnel plot, respectively. Risk of bias was assessed using ROBINS-I and certainty of evidence was assessed using GRADE. Seven observational studies with 5,575 individuals were included. Pooled analyses revealed no significant difference in risk of total bleeding [RR 0.78, 95% CI 0.48–1.26] and major bleeding [RR 0.62, 95% CI 0.33–1.15] with reduced dose compared to standard dose anticoagulation, however with high heterogeneity (I2 = 64%). Excluding studies with baseline characteristics increasing risk of bleeding in the reduced dose group, sensitivity analysis showed that dose reduction significantly decreases the risk of total [RR 0.49, 95% CI 0.30–0.82] and major bleeding [RR 0.42, 95% CI 0.22–0.80], with low heterogeneity (I = 0). In terms of efficacy, there is not enough evidence to show that anticoagulation dose reduction increases risk of VTE [RR 0.74, 95% CI 0.32–1.73]. Among low body weight patients, dose reduction for VTE prophylaxis may reduce risk of bleeding, especially major bleeding, without compromising its efficacy in preventing VTE, hence it can be considered in this population. Randomized controlled trials are needed to further support this recommendation.

BackgroundCurrent therapeutic interventions for Sickle Cell Disease (SCD) have improved patient survival; however, the clinical determinants of elevated autoantibody prevalence and related complications in patients with SCD remain insufficiently elucidated.ObjectiveThis study aimed to examine the frequency of lupus anticoagulant (LA), anticardiolipin antibody (aCL), and anti-beta2 glycoprotein I antibodies (anti- β2GPI) in patients with SCD at steady state phase to evaluate their possible correlations with hematological factors and clinical complications.MethodsThis cross-sectional study involving 92 SCD patients in a steady state phase was conducted. Blood specimens were obtained for complete blood count (CBC), in conjunction with the identification of IgG for aCL and anti-β2GPI utilizing enzyme-linked immunosorbent assay (ELISA) and the assessment of LA through the Diluted Russell Viper Venom Time (dRVVT).ResultsThe prevalence of LA, aCL, and anti-β2GPI (IgG) in SCD patients at steady state was 29.4%, 16.3%, and 5.4%, respectively. A correlation was found between LA and chronic leg ulcers, history of thrombosis, decreased platelet counts (PLT), and increased mean platelet volume (MPV) in SCD patients. Furthermore, aCL (IgG) exhibited a significant association with chronic leg ulcers, history of thrombosis, elevated Hemoglobin (Hb) levels, increased red blood cell count (RBC), and higher red cell distribution width (RDW) in SCD patients at steady state phase.ConclusionThis research elucidates the incidence of LA and aCL in SCD patients during steady state, linking these autoantibodies to hematological parameters and clinical complications; thus, prospective assessments of aPL in SCD patients are essential.