A 64-year-old male patient with hemophilia A was scheduled for the surgical removal of a pulmonary mass. Preoperative evaluation revealed that the coagulation factor Ⅷ (FⅧ) activity was 0.5%, with an F Ⅷ inhibitor level of 32 BU/ml; the R value could not be detected on the thromboelastogram. Thoracoscopic lobectomy was successfully completed. On the day of the operation and the first day after the operation, 6 mg of recombinant activated coagulation factor Ⅶ (rFⅦa) was intravenously administered every 6 h. On postoperative day 1, the patient’s blood pressure dropped and the HGB gradually declined from 102 g/L to 65 g/L. Chest X-ray revealed a large amount of pleural effusion on the left side, and urgent thoracoscopic thoracic exploration was performed. A total of 3200 mL fresh blood was cleared, and a thoracic drainage tube was placed. On postoperative day 2, the rFⅦa dose was increased to 6 mg, which was intravenously administered every 4 h, and concentrated red cells were intermittently infused to correct anemia. Four days later, due to the inability to obtain rFⅦa, PCC (50 IU/kg every 8 hours) was administered. Additionally, treatment with methylprednisolone (40 mg/d) and cyclophosphamide (200 mg, every 2 weeks) was initiated to remove FⅧ inhibitors. The thoracic drainage tube was removed on postoperative day 9, and the patient was successfully discharged 3 weeks later.

Objective:To analyze the levels of thrombin generation and activated protein C resistance (APC-R) in lupus anticoagulant (LA)-positive patients, and to assess their effectiveness in predicting thrombotic risk in these patients.Methods:Retrospective case-control study. A total of 185 patients with positve LA [91 males, 94 females; age (47.59±19.14) years] in Ruijin Hospital of Shanghai Jiaotong University School of Medicine from November 1st, 2024 to March 31st, 2025 were included. Patients were stratified into thrombotic ( n=91) and non-thrombotic groups ( n=94) based on clinical diagnosis and imaging evidence of thrombosis. The basic characteristics and routine laboratory coagulation levels of LA-positive patients were analyzed. Post-test plasma samples were collected from 43 cases with positive or strongly positive LA, categorized into thrombotic ( n=23) and non-thrombotic ( n=20) groups. Additionally, plasma was collected from 80 healthy controls [40 males and 40 females, age (38.37±15.74) years]. Using simple random sampling method, plasma samples from 10 selected males and 10 selected females were mixed to make 1 group of healthy control, thus accordingly resulted in a total of 4 healthy control groups. Thrombin generation assays (TGA) were then employed to measure prothrombin generation and activated protein C resistance (APC-R) levels in the healthy control, non-thrombotic, and thrombotic groups. One-way analysis of variance was utilized to compare thrombin generation and APC-R levels across these groups. Results:Among the routine laboratory coagulation indexes, the median levels of activated partial thromboplastin time (APTT), fibrin degradation product (FDP) and protein C (PC) in thrombotic group were 30.9 (28.8, 35.5) s, 2.5 (1.3, 2.8) mg/L, and 107.0 (93.0, 127.0)%, respectively, which were significantly higher compared with the non-thrombosis group (all P<0.05). However, between the thrombotic and non-thrombotic group, no statistically significant differences were observed for the levels of prothrombin time (PT), thrombin time (TT), fibrinogen (Fg), or D-dimer (D-D) ( P>0.05). The TGA results showed that the total thrombin generation, the maximal thrombin generation and APC-R levels of patients in the thrombotic group were (1 118.72±387.34) nmol/L·min, (106.01±59.00) nmol/L and (0.33±0.22), respectively, which were significantly higher compared with those in the non-thrombotic group (all P<0.05). Conclusion:Significantly increased thrombin generation and enhanced APC-R were present in the LA-positive patients with thrombosis, indicating the important values of thrombin generation and APC-R in assessing thrombosis risk among this population.

Objective:To compare the accuracy of one-stage clotting assay and chromogenic substrate assay for testing an extended half-life recombinant FⅧ and to explore standardized conversion models between methods.Methods:Observational study. FⅧ activity (FⅧ:C) in plasma samples with theoretical values of 1 000, 800, 600, 500, 400, and 300 IU/L was measured using both one-stage clotting assay (employing Siemens Actin FSL reagent, Werfen SynthASil reagent, Stago PTT-A reagent) and the chromogenic substrate assay from Hyphen Biomed. Differences in FⅧ:C measured by the various methods were compared using the SNK test. Recovery rates were calculated to evaluate the accuracy of each assay. Sample activity was verified using the thrombin generation assay (TGA). Correlations between activities determined by the different assay systems were assessed using linear regression analysis.Results:Observational study. FⅧ activity (FⅧ:C) in diluted plasma samples with theoretical values of 1 000, 800, 600, 500, 400, and 300 IU/L was measured using both one-stage clotting assay (employing Siemens Actin FSL reagent, Werfen SynthASil reagent, Stago PTT-A reagent) and the chromogenic substrate assay from Hyphen Biomed. Differences in FⅧ:C measured by the various methods were compared using the SNK test. Recovery rates were calculated to evaluate the accuracy of each assay. Sample activity was verified using the thrombin generation assay (TGA). Correlations between activities determined by the different assay systems were assessed using linear regression analysis.Conclusion:Some marked one-stage clotting assay system has limitations in the clinical detection of extended half-life recombinant FⅧ. While the chromogenic substrate assay provides more accurate results. The one-stage clotting assay values can undergo cross-assay correction for FⅧ:C using a standardized conversion coefficient, which can further elevate the accuracy of monitoring hemophilia treatment efficacy.

Congenital coagulation factor Ⅶ deficiency is a rare autosomal incomplete recessive disorder caused by a defect in the coagulation factor Ⅶ (FⅦ) gene, with an incidence of approximately 1 in 500 000. Antiphospholipid antibody syndrome is relatively common and is a common cause of acquired thrombosis. However, the combination of the latter and the former is extremely rare in clinical practice, which brings difficulties to diagnosis and treatment. This article reported the laboratory examination, diagnosis and treatment of a patient with congenital coagulation factor Ⅶ deficiency and antiphospholipid syndrome after portal vein thrombosis, and reviewed the relevant literature.

A 64-year-old male patient with hemophilia A was scheduled for the surgical removal of a pulmonary mass. Preoperative evaluation revealed that the coagulation factor Ⅷ (FⅧ) activity was 0.5%, with an F Ⅷ inhibitor level of 32 BU/ml; the R value could not be detected on the thromboelastogram. Thoracoscopic lobectomy was successfully completed. On the day of the operation and the first day after the operation, 6 mg of recombinant activated coagulation factor Ⅶ (rFⅦa) was intravenously administered every 6 h. On postoperative day 1, the patient’s blood pressure dropped and the HGB gradually declined from 102 g/L to 65 g/L. Chest X-ray revealed a large amount of pleural effusion on the left side, and urgent thoracoscopic thoracic exploration was performed. A total of 3200 mL fresh blood was cleared, and a thoracic drainage tube was placed. On postoperative day 2, the rFⅦa dose was increased to 6 mg, which was intravenously administered every 4 h, and concentrated red cells were intermittently infused to correct anemia. Four days later, due to the inability to obtain rFⅦa, PCC (50 IU/kg every 8 hours) was administered. Additionally, treatment with methylprednisolone (40 mg/d) and cyclophosphamide (200 mg, every 2 weeks) was initiated to remove FⅧ inhibitors. The thoracic drainage tube was removed on postoperative day 9, and the patient was successfully discharged 3 weeks later.

Objective:To analyze the levels of thrombin generation and activated protein C resistance (APC-R) in lupus anticoagulant (LA)-positive patients, and to assess their effectiveness in predicting thrombotic risk in these patients.Methods:Retrospective case-control study. A total of 185 patients with positve LA [91 males, 94 females; age (47.59±19.14) years] in Ruijin Hospital of Shanghai Jiaotong University School of Medicine from November 1st, 2024 to March 31st, 2025 were included. Patients were stratified into thrombotic ( n=91) and non-thrombotic groups ( n=94) based on clinical diagnosis and imaging evidence of thrombosis. The basic characteristics and routine laboratory coagulation levels of LA-positive patients were analyzed. Post-test plasma samples were collected from 43 cases with positive or strongly positive LA, categorized into thrombotic ( n=23) and non-thrombotic ( n=20) groups. Additionally, plasma was collected from 80 healthy controls [40 males and 40 females, age (38.37±15.74) years]. Using simple random sampling method, plasma samples from 10 selected males and 10 selected females were mixed to make 1 group of healthy control, thus accordingly resulted in a total of 4 healthy control groups. Thrombin generation assays (TGA) were then employed to measure prothrombin generation and activated protein C resistance (APC-R) levels in the healthy control, non-thrombotic, and thrombotic groups. One-way analysis of variance was utilized to compare thrombin generation and APC-R levels across these groups. Results:Among the routine laboratory coagulation indexes, the median levels of activated partial thromboplastin time (APTT), fibrin degradation product (FDP) and protein C (PC) in thrombotic group were 30.9 (28.8, 35.5) s, 2.5 (1.3, 2.8) mg/L, and 107.0 (93.0, 127.0)%, respectively, which were significantly higher compared with the non-thrombosis group (all P<0.05). However, between the thrombotic and non-thrombotic group, no statistically significant differences were observed for the levels of prothrombin time (PT), thrombin time (TT), fibrinogen (Fg), or D-dimer (D-D) ( P>0.05). The TGA results showed that the total thrombin generation, the maximal thrombin generation and APC-R levels of patients in the thrombotic group were (1 118.72±387.34) nmol/L·min, (106.01±59.00) nmol/L and (0.33±0.22), respectively, which were significantly higher compared with those in the non-thrombotic group (all P<0.05). Conclusion:Significantly increased thrombin generation and enhanced APC-R were present in the LA-positive patients with thrombosis, indicating the important values of thrombin generation and APC-R in assessing thrombosis risk among this population.

Objective:To compare the accuracy of one-stage clotting assay and chromogenic substrate assay for testing an extended half-life recombinant FⅧ and to explore standardized conversion models between methods.Methods:Observational study. FⅧ activity (FⅧ:C) in plasma samples with theoretical values of 1 000, 800, 600, 500, 400, and 300 IU/L was measured using both one-stage clotting assay (employing Siemens Actin FSL reagent, Werfen SynthASil reagent, Stago PTT-A reagent) and the chromogenic substrate assay from Hyphen Biomed. Differences in FⅧ:C measured by the various methods were compared using the SNK test. Recovery rates were calculated to evaluate the accuracy of each assay. Sample activity was verified using the thrombin generation assay (TGA). Correlations between activities determined by the different assay systems were assessed using linear regression analysis.Results:Observational study. FⅧ activity (FⅧ:C) in diluted plasma samples with theoretical values of 1 000, 800, 600, 500, 400, and 300 IU/L was measured using both one-stage clotting assay (employing Siemens Actin FSL reagent, Werfen SynthASil reagent, Stago PTT-A reagent) and the chromogenic substrate assay from Hyphen Biomed. Differences in FⅧ:C measured by the various methods were compared using the SNK test. Recovery rates were calculated to evaluate the accuracy of each assay. Sample activity was verified using the thrombin generation assay (TGA). Correlations between activities determined by the different assay systems were assessed using linear regression analysis.Conclusion:Some marked one-stage clotting assay system has limitations in the clinical detection of extended half-life recombinant FⅧ. While the chromogenic substrate assay provides more accurate results. The one-stage clotting assay values can undergo cross-assay correction for FⅧ:C using a standardized conversion coefficient, which can further elevate the accuracy of monitoring hemophilia treatment efficacy.

Congenital coagulation factor Ⅶ deficiency is a rare autosomal incomplete recessive disorder caused by a defect in the coagulation factor Ⅶ (FⅦ) gene, with an incidence of approximately 1 in 500 000. Antiphospholipid antibody syndrome is relatively common and is a common cause of acquired thrombosis. However, the combination of the latter and the former is extremely rare in clinical practice, which brings difficulties to diagnosis and treatment. This article reported the laboratory examination, diagnosis and treatment of a patient with congenital coagulation factor Ⅶ deficiency and antiphospholipid syndrome after portal vein thrombosis, and reviewed the relevant literature.

Objective:To investigate the inhibitory effect of esomeprazole on proliferation and chemosensitizing effect of breast cancer cells.Methods:Human MBA-MD-231, MCF-7 breast cancer cell line and human Huh7 liver cancer cell line were cultured by conventional methods; cells were treated with different concentrations of esomeprazole, and CCK8 kit was used to detect the proliferation of different tumor cells after stimulation. Cells were treated with different concentrations of esomeprazole, and the effects of esomeprazole on cell cycle of different cells were analyzed by flow cytometry. Cells were treated with different concentrations of paclitaxel and epirubicin combined with esomeprazole, and CCK8 kit was used to detect the proliferation of different tumor cells after stimulation. Measurement data were expressed as mean ± standard deviation ( ± s), and analysis of variance was used for comparison among multiple groups. Results:CCK8 results showed that esomeprazole could inhibit the proliferation of MBA-MD-231 cells, MCF-7 cells and Huh7 cells in a dose-dependent manner. Flow cytometry results showed that cells in G 0/G 1 phase were significantly increased by esomeprazole treatment. Esomeprazole can enhance the inhibitory effect of paclitaxel and epirubicin on the proliferation of MBA-MD-231 cells and MCF-7 cells, and improve the chemosensitivity. Conclusion:Esomeprazole blocks breast cancer cell MBA-MD-231, MCF-7 and liver cancer cell Huh7 in G 0/G 1 phase, thereby inhibiting cell proliferation. Esomeprazole can enhance the inhibitory effect of chemotherapeutic drugs on the proliferation of MBA-MD-231 and MCF-7 cells.

The detection of coagulation factor Ⅷ activity plays an important role in the diagnosis, typing, efficacy monitoring and detection of inhibitor titer in hemophilia A, acquired hemophilia A and von Willebrand disease. However, due to the diversity of detecting systems, the difference of reagent composition, the existence of interfering substances and other influence factors, the detection of coagulation factor Ⅷ activity in the laboratories in China still needs to be improved.