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• W2146263025 endingPage "1487" @default.
• W2146263025 startingPage "1482" @default.
• W2146263025 abstract "We have previously found that activation of coagulation in patients with various hematological malignancies was apparently not initiated by tissue factor (TF). Acquired activated protein C (APC) resistance may be another mechanism responsible for such hypercoagulation, and has been demonstrated in patients with solid tumors, but not in patients with hematological malignancy.To investigate acquired APC resistance in a hypercoagulable cohort of patients with hematological malignancies.Blood samples from 93 patients with acute myeloid leukemia (AML), chronic lymphatic leukemia, multiple myeloma, or non-Hodgkin's lymphoma, were analyzed before start and after completion of cancer therapy. APC resistance was measured using calibrated automated thrombography. The APC sensitivity ratio (APC-SR) was calculated as the ratio of the endogenous thrombin potential (ETP) determined in plasma probed with either APC or buffer.Untreated patients were found to have higher APC-SR than healthy controls, and patients with AML had higher APC-SR as compared to the other diagnoses, both findings being consistent with acquired APC resistance. The acquired APC resistance was partly ameliorated with cancer treatment. Decreased levels of protein S and TF pathway inhibitor were inversely correlated to APC resistance.APC resistance may contribute to the hypercoagulable state in hematological malignancies." @default.
• W2146263025 created "2016-06-24" @default.
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• W2146263025 date "2008-09-01" @default.
• W2146263025 modified "2023-10-18" @default.
• W2146263025 title "Increased acquired activated protein C resistance in unselected patients with hematological malignancies" @default.
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• W2146263025 doi "https://doi.org/10.1111/j.1538-7836.2008.03060.x" @default.
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