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Published on: October 12, 2012
[Major thrombopenia induced by heparin treatment. Apropos of 8 cases]
Major thrombocytopenia occupies a special place among the complications of anticoagulant therapy. Based on a series of 8 personal cases, the authors describe the clinical, biological and physiopathological features of this thrombocytopenia. It occurs in 0.5 to 1 p. 100 of patients on heparin. This figure may not be accurate and thrombocytopenia during heparin therapy occurs almost exclusively in venous thromboembolic disease which it complicated in 4 p. 100 of treated cases. It is detected around the 8th day (between the 4th and 10th day) of treatment and is characterised by thromboembolic events (2 arterial embolisms, 2 pulmonary embolisms, 1 cutaneous necrosis, 1 disseminated intravascular coagulation). Cutaneo-mucous purpura was observed in 1 case. The last two cases in this series were asymptomatic. The thrombocytopenia is peripheral (on average 36,000/mm3) and isolated without any deficiency of the factors of coagulation, except in the case of disseminated intravascular coagulation. A platelet aggregant factor was demonstrated in the plasma of these patients by a thrombo-agglutination technique. This disappeared two months after stopping the heparin. The withdrawal of heparin and relay with oral anticoagulant drugs was associated with a normalisation of the platelet count within 1 to 5 days. Physiopathologically, the high molecular weight fractions of heparin are responsible for this immuno-allergic reaction which leads to the fabrication of a heparin-dependent anti-platelet antibody.
Major thrombocytopenia occupies a special place among the complications of anticoagulant therapy. Based on a series of 8 personal cases, the authors describe the clinical, biological and physiopathological features of this thrombocytopenia. It occurs in 0.5 to 1 p. 100 of patients on heparin. This figure may not be accurate and thrombocytopenia during heparin therapy occurs almost exclusively in venous thromboembolic disease which it complicated in 4 p. 100 of treated cases. It is detected around the 8th day (between the 4th and 10th day) of treatment and is characterised by thromboembolic events (2 arterial embolisms, 2 pulmonary embolisms, 1 cutaneous necrosis, 1 disseminated intravascular coagulation). Cutaneo-mucous purpura was observed in 1 case. The last two cases in this series were asymptomatic. The thrombocytopenia is peripheral (on average 36,000/mm3) and isolated without any deficiency of the factors of coagulation, except in the case of disseminated intravascular coagulation. A platelet aggregant factor was demonstrated in the plasma of these patients by a thrombo-agglutination technique. This disappeared two months after stopping the heparin. The withdrawal of heparin and relay with oral anticoagulant drugs was associated with a normalisation of the platelet count within 1 to 5 days. Physiopathologically, the high molecular weight fractions of heparin are responsible for this immuno-allergic reaction which leads to the fabrication of a heparin-dependent anti-platelet antibody.
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