What question did this study set out to answer?

Characterize the diverse coagulation abnormalities in acute promyelocytic leukemia to clarify their underlying mechanisms and guide clinical management.

January 1, 1969Archives of Internal Medicine

Coagulation Defects in Acute Promyelocytic Leukemia

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Authors

JRJoseph J. RandNew York Medical College

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Implication

Case series demonstrates complex coagulopathy driven by intravascular clotting and fibrinolysis in acute promyelocytic leukemia, highlighting distinct mechanisms underlying lethal bleeding risks.

Key Points

Characterize the diverse coagulation abnormalities in acute promyelocytic leukemia to clarify their underlying mechanisms and guide clinical management.
Clinical and laboratory evaluation of coagulation parameters in four patients (N=4) with acute promyelocytic leukemia.
Assessment of response to heparin therapy and postmortem examination of intravascular thrombus formation and fibrinolytic activity.
All patients exhibited profound coagulopathies, including hypofibrinogenemia, prolonged prothrombin and thrombin times, and multiple clotting factor deficiencies.
Heparin therapy in one patient raised fibrinogen levels despite persistent factor deficiencies, with autopsy showing widespread intravascular coagulation, whereas another patient demonstrated primary hyperfibrinolysis and a total absence of postmortem thrombi.

Cite This Study

Joseph J. Rand (1969) studied this question.

synapsesocial.com/papers/6a1d8d4f5a0c5c56ea04faf4 https://doi.org/10.1001/archinte.1969.00300110041007

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Implication

Case series demonstrates complex coagulopathy driven by intravascular clotting and fibrinolysis in acute promyelocytic leukemia, highlighting distinct mechanisms underlying lethal bleeding risks.

Coagulation Defects in Acute Promyelocytic Leukemia

Discussion

Member takes

Implication

Key Points

Cite This Study

Coagulation Defects in Acute Promyelocytic Leukemia

Discussion

Member takes

Implication

Key Points

Cite This Study

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