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العنوان
Increased Acquired Activated Protein C Resistance in Patients with Acute Leukemia/
المؤلف
Ismaiil,Nada Osama
هيئة الاعداد
باحث / ندي أسامة اسماعيل
مشرف / منال فوزي غزلان
مشرف / دعاء أحمد جمال عيسي
تاريخ النشر
2016
عدد الصفحات
168.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/1/2016
مكان الإجازة
جامعة عين شمس - كلية الطب - Clinical and Chemical Pathology
الفهرس
Only 14 pages are availabe for public view

from 168

from 168

Abstract

V
enous thromboembolism is a common problem in patients with acute leukemia. Depending on the type of leukemia whether acute myeloid leukemia (AML) or acute lymphoid leukemia (ALL), the VTE incidence ranges from 2.1% up to 12.1%. Even in the absence of symptomatic VTE, many cancer patients present with abnormal blood coagulation tests indicating a hypercoagulable state. Dysfunctional alterations of the protein C pathway may be one mechanism responsible for hypercoagulability in these patients.
Abnormally reduced anticoagulant response of a plasma sample to APC is known as APCR and is aroused by many potential abnormalities in the protein C anticoagulant pathway.
The aim of the present study was therefore to investigate acquired APCR in patients with acute leukemia and correlate it with other clinicolaboratory parameters as well as thrombotic complications.
The study was conducted on 54 newly diagnosed acute leukemia patients, 36 of which were diagnosed as AML and 18 were ALL. 20 age and sex matched healthy individuals were included in the study as control group.
The results of the present study revealed a highly statistical significant increase in APCR in all acute leukemia patients when compared to their matched controls. Also, there is a highly statistical significant increase in APCR in ALL group when compared with the control group alone and a highly statistical significant increase in APCR in AML group when compared with the control group alone. Also a highly statistical significant difference in APCR was detected between AML and ALL patients being higher in AML patients. Additionally our results revealed a significant difference in APCR between different AML subtypes, showing highest APCR among AML M3 patients.
APCR was significantly higher in patients with thrombosis than patients without thrombosis. Additionally APCR at diagnosis was significantly higher compared to its level after chemotherapy. On the other hand, there was no significant difference between APCR in acute leukemia patients with or without cytogenetic abnormalities.
ROC curve was used to detect the best diagnostic cut off level for APCR (expressed as clotting time in seconds) in the prediction of thrombosis in acute leukemia patients and it was <97.9 seconds, with a diagnostic sensitivity of 90.91%, specificity 80%, negative predictive value 97 %, positive predictive value 55.6 %.
In Conclusion, patients with acute leukemia have increased acquired APCR especially those with AML which decreased after cancer therapy. This acquired state of increased resistance to APC is statistically associated with thrombosis and might contribute to the hypercoagulable syndrome in patients with acute leukemia.