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Exploring the Role and Changes of a Disintegrin and Metalloproteinase with a Thrombospondin Type 1 Motif, Member 13 and Von Willebrand Factor Ag in Patients with Acute Myelogenous Leukemia.

Abstract

Background: Acute myeloid leukemia (AML) is a hematologic malignancy associated with significant coagulation abnormalities and endothelial dysfunction. Von Willebrand factor (VWF) and its regulatory protease, a disintegrin and metalloproteinase with thrombospondin type 1 motif member 13 (ADAMTS13), play essential roles in maintaining vascular homeostasis. Disruption of this balance may contribute to thrombotic complications in AML. Methods: This case-control study included 40 newly diagnosed, untreated AML patients and 40 age- and sex-matched healthy controls recruited from Al-Azhar University Hospitals, Cairo, Egypt. Plasma VWF antigen levels and ADAMTS13 activity were measured using enzyme-linked immunosorbent assay (ELISA). Statistical comparisons between groups were performed using appropriate parametric tests, and correlation analysis was conducted to assess the association between both biomarkers. Results: AML patients showed significantly higher plasma VWF antigen levels compared with controls (274.44 ± 139.72% vs. 111.40 ± 31.77%, P < 0.001). In contrast, ADAMTS13 activity was significantly lower in AML patients than in controls (46.70 ± 29.37% vs. 99.01 ± 27.09%, P < 0.001). An inverse correlation was observed between VWF antigen and ADAMTS13 activity (r = -0.28), although this did not reach statistical significance (P = 0.08). Conclusions: Newly diagnosed AML patients demonstrate significant imbalance in the VWF-ADAMTS13 axis, characterized by elevated VWF levels and reduced ADAMTS13 activity. These findings support the presence of early endothelial dysfunction and hemostatic disturbance prior to treatment initiation. Further large-scale prospective studies are needed to determine the prognostic and clinical significance of these biomarkers.

Research topics

  • Complement system in diseases
  • Platelet Disorders and Treatments
  • Blood Coagulation and Thrombosis Mechanisms

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DOI: 10.7417/ct.2026.2117

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