Heparin‐induced thrombocytopenia: Association with a platelet aggregating factor and arterial thromboses

Abstract

Eleven patients with heparin-induced thrombocytopenia were studied. Thrombocytopenia appeared 3-16 days following the initiation of prophylactic or therapeutic doses of heparin. The mean lowest platelet count recorded was 48,000/mm3. When heparin was stopped, recovery from thrombocytopenia began within 24 hours and was complete by ten days. Two patients developed fatal thromboses, and two others had myocardial infarctions while thrombo-cytopenic. In the serum of seven patients, including three of the four with arterial thrombosis, a heparin-dependent platelet aggregating factor was present. The factor caused release of platelet 14C serotonin but did not lyse platelets. It was present in the globulin fraction of all positive sera, and in one serum studied it was isolated in the IgG/IgA immunoglobulin fraction. The factor was not present in 16 normal sera or in the sera of 15 nonthrombocytopenic patients receiving heparin. Our observations suggest that heparin-induced thrombocytopenia is common and that, in some patients it may be accompanied by severe arterial thrombosis. In vivo platelet aggregation is a possible explanation for the thrombocytopenia and the thrombosis in this disorder.

Treatment and Prevention of Heparin-Induced Thrombocytopenia

“…110 In the second report, one out of 11 patients with suspected HIT received a platelet transfusion and had an inadequate increase in platelet count (but no thrombotic events). 111 More recently, a case series reported 37 patients with PF4-ELISA-confi rmed HIT who received one or more platelet transfusions during a 1-year period at a single center. 112 No thrombotic complications developed in any of the patients following platelet transfusion, and three deaths within a few days of transfusion were deemed unrelated to transfusion.…”

“…110,111 In the fi rst report, two out of fi ve patients with suspected HIT received a single platelet transfusion, one of whom developed arterial thromboembolism post transfusion (while still receiving heparin). 110 In the second report, one out of 11 patients with suspected HIT received a platelet transfusion and had an inadequate increase in platelet count (but no thrombotic events).…”

Heparin-induced thrombocytopenia: a historical perspective

“…During the latter half of the 1970s, at least 7 groups of investigators [10][11][12][13][14][15][16] reported patients who resembled those of Rhodes and colleagues. Together, these studies provided further evidence of an Submitted February 14, 2008; accepted March 31, 2008.…”

“…A common feature of these reports was evidence of platelet activation induced by patient serum, plasma, or purified immunoglobulin. [11][12][13][14][15][16][17] HIT: an immune disorder or a consumptive coagulopathy?…”

“…A common feature of these reports was evidence of platelet activation induced by patient serum, plasma, or purified immunoglobulin. [11][12][13][14][15][16][17] HIT: an immune disorder or a consumptive coagulopathy?Doubts persisted regarding the immune basis of HIT. After all, Rhodes and colleagues had also noted that when their patients were deliberately rechallenged with heparin several months after their episode of HIT, thrombocytopenia failed to recur.…”