Year: 2025
Type: article
Study design: Observational Study
Abstract: Background: One of the more life-threatening complications related to acute leukemia is thrombosis. The potential for this consequence to exacerbate the disease's progression has been stated on multiple occasions. One probable cause was the prothrombotic condition brought on by a breakdown in anticoagulant and fibrinolytic systems. Aim of the work: This study's objective was to evaluate Antithrombin III, Protein C, Protein S, and D-dimer levels in patients with acute leukemia, acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML), in comparison with normal subjects. Subjects and methods: Ninety participants were split into two groups for this investigation. The patient group consisted of 30 individuals with ALL and 30 individuals with AML. Thirty healthy individuals who did not exhibit any clinical or biochemical signs of acute leukemia made up the control group. From August 2022 through March 2024, all participants were examined at Al-Hussien Hospital, Al-Azhar University. Results: There was a statistically significant distinction between the control group and acute leukemia patients in this study with respect to anti-thrombin III, protein C, protein S, and D-dimer. Furthermore, with the exception of Protein S, no statistically significant differences were found between AML and ALL. At ALL, the protein S level was decreased compared to AML. Conclusion: In summary, acute leukemia was associated with decreased levels of natural anticoagulants (ATIII, PC, and PS) and increased D-dimer levels, indicating a hypercoagulable state. These alterations were influenced by many factors, including mainly the disease itself and the effects of chemotherapy. So, a suitable anticoagulant therapy as a prophylactic measure could be proposed in acute leukemia patients.
Institutions: Al-Azhar University, Al-Azhar University, Al Azhar University
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W7117466728
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