Abstract
Two patients with underlying thromboembolic disorders developed severe thrombocytopenia while receiving heparin sodium; 1 of these developed recurrence of thrombocytopenia and possible heparin-induced pulmonary emboli when heparin was restarted. In a prospective study of patients receiving heparin in a coronary care unit (CCU), 9 of 37 patients developed transient mild thrombocytopenia (platelet count range 88,000-150,000/cu mm). Heparin added to citrated platelet-rich plasma caused platelet aggregation in the two original patients, in 3 of 6 CCU patients tested, and in 17 of 87 other subjects, with maximum aggregation at concentrations of heparin likely to be present in vivo during therapy. Evidence is discussed that suggests that heparin may cause or aggravate thrombosis by causing platelet aggregation. Occurrence of severe heparin-induced thrombocytopenia is well documented, and mild transient thrombocytopenia may be more common than has been recognized. Studies of heparin efficacy should take these responses into account.

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