Search In this Thesis
   Search In this Thesis  
العنوان
Increased Acquired Activated Protein
C Resistance in Patients with Acute
Leukemia /
المؤلف
Ismaiil,Nada Osama.
هيئة الاعداد
باحث / Nada Osama Ismaiil
مشرف / Manal Fawzy Gabr Ghozlan
مشرف / Doaa Ahmed Gamal Eissa
تاريخ النشر
2016
عدد الصفحات
182p.:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
جراحة
تاريخ الإجازة
1/1/2016
مكان الإجازة
جامعة عين شمس - كلية الطب - الباثولوجيا الاكلينيكية والكيميائية
الفهرس
Only 14 pages are availabe for public view

from 182

from 182

Abstract

Venous thromboembolism is a common problem in
patients with acute leukemia. Depending on the typeof
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 APCRat 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 stateof increased
resistance to APC is statistically associated with thrombosis
and might contribute to the hypercoagulable syndrome in
patients with acute leukemia.