Heparin-induced thrombocytopenia is the most important idiosyncratic drug-induced thrombocytopenia because of its relatively high frequency and association with unexpected arterial and venous thromboembolic complications. Heparin-induced thrombocytopenia is mediated by the formation of an IgG-heparin complex that activates platelets via their IgG Fc receptors. The clinical and laboratory features, prevention, and treatment of heparin-induced thrombocytopenia with and without thrombosis are reviewed.

Heparin and Platelets

Recent reports have documented an increase of thrombotic complications in patients with carcinoma of the breast receiving chemotherapy regimens containing cyclophosphamide, methotrexate, and 5-fluorouracil. The authors studied blood from nine such patients screening for abnormalities that might predispose to thrombosis or indicate that the coagulation cascade had been activated. Six of the patients were in the adjuvant setting, and three had metastatic disease. Samples were collected from each patient before, during, and after completion of the chemotherapy in question. In each patient a statistically significant decline in functional protein C activity (P = 0.001) was demonstrated at midtherapy. In seven of nine patients functional protein C level normalized after the cessation of therapy. No other positive results were found. The authors conclude that the combination of cyclophosphamide, methotrexate, and 5-fluorouracil, when administered to patients with a diagnosis of carcinoma of the breast, causes a reversible decline in the activity of protein C.

Acquired protein C deficiency in patients with breast cancer receiving cyclophosphamide, methotrexate, and 5-fluorouracil.

Reexposure to heparin of patients with heparin-associated antibodies.

There are two types of heparin-induced thrombocytopenia. Type I is more common, has an early onset, and is mild, transient, and benign. Type I is due to direct heparin-induced platelet aggregation and is rarely associated with thromboembolic sequela. Type II is infrequent, has a late onset, and is more severe. Type II is due to an immune-mediated platelet aggregation caused by IgG and IgM that becomes bound to platelets. In Type II, the antibody titers decline over several months; however, early reexposure can result in a catastrophic secondary immune response. Frequently, Type II is associated with life- or limb-threatening thromboembolic complications (white clots), including stroke.

Heparin-induced thrombocytopenia.

Resume Deux cas cliniques de thrombopenie induite par une heparine de bas poids moleculaire (Fraxiparine ®) sont rapportes. Un homme de 35 ans presente un tableau de pancreatite aigue necrosante alcoolique d'evolution rapidement favorable. Apres 12 jours de traitement par Fraxiparine ®, une thrombopenie a 49 G · 1−1 apparait accompagnee d'une aspiration gastrique legerement hemorragique. Le temps de Quick, le temps de cephaline active, le taux de produits de degradation de la fibrine et le taux de D-dimeres sont normaux et la recherche de complexes solubles est negative. La Fraxiparine ® est arretee et le taux de plaquettes revient a la normale en quatre jours. Un homme de 58 ans est hospitalise pour etat de mal asthmatique ; une prevention de la maladie thromboembolique par Fraxiparine ® est entreprise entre le 5e et le 16e jour de son hospitalisation. Au douzieme jour de traitement, la numeration plaquettaire objective une diminution isolee a 122 puis 74 G · 1−1 sans traduction clinique ni trouble de l'hemostase. La numeration plaquettaire se normalise trois jours apres l'arret du traitement. Dans les deux observations, le diagnostic est confirme par la positivite du test d'agregation plaquettaire induite par le plasma du patient en presence de Fraxiparine ®. Nous faisons une revue precise de la litterature sur un effet secondaire rare mais potentiellement grave de l'heparine de bas poids moleculaire qui souligne l'interet de la surveillance preventive de la numeration plaquettaire.

Thrombopénie induite par une héparine de bas poids moléculaire

We investigated the etiology of thrombocytopenia, with or without platelet thrombi, occurring while patients are receiving parenteral heparin We used two in vitro methods to detect possible humoral factors in the sera of patients who became thrombocytopenic while receiving heparin In the presence of heparin, four of four such patients' serum caused platelet aggregation Only serum from the patient most severely affected clinically caused release of platelet factor 3 (PF3) All control sera gave negative results by both methods We propose that platelet aggregation studies may be a sensitive and reliable method of confirming that thrombocytopenia occurring during heparin therapy is due to a humoral factor requiring the presence of heparin

In vitro detection of heparin-induced humoral antiplatelet activity.

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In vitro detection of heparin-induced humoral antiplatelet activity.