Thromb Haemost 1957; 01(02): 158-168
DOI: 10.1055/s-0038-1656169
Originalarbeiten – Original Article – Travaux Originaux
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The Reduction of Platelet Cofactor II (Autoprothrombin II) Activity with Anticoagulants

Shirley A. Johnson
1   Department of Physiology and Pharmacology, Wayne State University College of Medicine, Detroit, Michigan
2   Department of Surgery, Presbyterian-St. Luke’s Hospital, Chicago, Illinois
,
Walter H. Seegers
1   Department of Physiology and Pharmacology, Wayne State University College of Medicine, Detroit, Michigan
2   Department of Surgery, Presbyterian-St. Luke’s Hospital, Chicago, Illinois
,
J. L Koppel
1   Department of Physiology and Pharmacology, Wayne State University College of Medicine, Detroit, Michigan
2   Department of Surgery, Presbyterian-St. Luke’s Hospital, Chicago, Illinois
,
John H. Olwin
1   Department of Physiology and Pharmacology, Wayne State University College of Medicine, Detroit, Michigan
2   Department of Surgery, Presbyterian-St. Luke’s Hospital, Chicago, Illinois
› Author Affiliations

This investigation was supported by a research grant from the Michigan Heart Association, and a grant from Mrs. Cleona Parker McAdoo.
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Publication History

Publication Date:
05 June 2018 (online)

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Summary

The total platelet cofactor activity in plasma and the platelet cofactor II activity in serum was measured. The normal variations are high. Some individuals have less serum platelet cofactor II than found in certain cases of PTC “deficiency”; and when the serum platelet cofactor II concentration was reduced to zero with the use of anticoagulants, there was no bleeding tendency observed. With the use of Sintrom and phenylindanedione, the total platelet cofactor activity of plasma was reduced and the platelet cofactor II activity of serum was reduced to near zero. With the latter drug platelet cofactor II of serum was still low 10 days after the drug was withdrawn. With Sintrom given intermittently the fluctuations in prothrombin concentration are noticeably more rapid than the changes in platelet cofactor II. In a preliminary study of other drugs, there were indications that platelet cofactor II concentration is not altered with some anticoagulants even though the prothrombin concentration is reduced. Apparently, the platelet cofactor II changes which occur are characteristic for each anticoagulant. The platelet cofactor I levels of the plasma are not appreciably, and most likely not at all altered by the drugs studied.