Thromb Haemost 1980; 43(01): 061-065
DOI: 10.1055/s-0038-1650013
Original Article
Schattauer GmbH Stuttgart

Heparin Induced Thrombocytopenia: a Prospective Study

Jack Ansell
The Departments of Medicine, Veterans Administration Hospital, Boston, Massachusetts and University of Massachusetts Medical Center, Worcester, Massachusetts, U.S.A.
,
Nicholas Slepchuk Jr.
The Departments of Medicine, Veterans Administration Hospital, Boston, Massachusetts and University of Massachusetts Medical Center, Worcester, Massachusetts, U.S.A.
,
Raminder Kumar
The Departments of Medicine, Veterans Administration Hospital, Boston, Massachusetts and University of Massachusetts Medical Center, Worcester, Massachusetts, U.S.A.
,
Aaron Lopez
The Departments of Medicine, Veterans Administration Hospital, Boston, Massachusetts and University of Massachusetts Medical Center, Worcester, Massachusetts, U.S.A.
,
Luzbella Southard
The Departments of Medicine, Veterans Administration Hospital, Boston, Massachusetts and University of Massachusetts Medical Center, Worcester, Massachusetts, U.S.A.
,
Daniel Deykin
The Departments of Medicine, Veterans Administration Hospital, Boston, Massachusetts and University of Massachusetts Medical Center, Worcester, Massachusetts, U.S.A.
› Author Affiliations
Further Information

Publication History

Received 25 October 1979

Accepted 30 January 1980

Publication Date:
13 July 2018 (online)

Summary

Thrombocytopenia occurred in 11.6% of 43 patients prospectively randomized to receive either bovine lung or porcine mucosal heparin. Four patients received bovine heparin and developed mild to moderate thrombocytopenia after eight to twelve days which resolved when therapy was stopped in one to six days. One patient received porcine heparin and developed mild thrombocytopenia after four days. The thrombocytopenia resolved in one day in spite of continued heparin therapy.

Serial blood samples from the five thrombocytopenic patients were studied for their in vitro effect upon normal platelets. These samples induced a high release of serotonin from normal platelets or caused normal platelets to aggregate in the presence of additional heparin. Release or aggregation coincided with or occurred shortly after nadir platelet counts were reached and returned toward normal following cessation of heparin.

Our data constitute the first prospective study of heparin induced thrombocytopenia in which serial blood samples were studied before, during and following the onset of thrombocytopenia. They strongly support the presence of a heparin dependent co-factor, presumably an antibody, as the cause for thrombocytopenia.

 
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