Thromb Haemost 2017; 117(10): 1868-1874
DOI: 10.1160/TH17-03-0212
Cellular Haemostasis and Platelets
Schattauer GmbH

Platelet count recovery and seroreversion in immune HIT despite continuation of heparin: further observations and literature review

Andrew W. Shih
1  Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
3  McMaster Centre for Transfusion Research, McMaster University, Hamilton, Ontario, Canada
,
Jo-Ann I. Sheppard
2  Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
,
Theodore E. Warkentin
2  Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
3  McMaster Centre for Transfusion Research, McMaster University, Hamilton, Ontario, Canada
4  Department of Medicine, McMaster University, Hamilton, Ontario, Canada
› Author Affiliations
Further Information

Publication History

Received: 27 March 2017

Accepted after major revision: 16 June 2017

Publication Date:
08 November 2017 (online)

Summary

One of the standard distinctions between type 1 (non-immune) and type 2 (immune-mediated) heparin-induced thrombocytopenia (HIT) is the transience of thrombocytopenia: type 1 HIT is viewed as early-onset and transient thrombocytopenia, with platelet count recovery despite continuing heparin administration. In contrast, type 2 HIT is viewed as later-onset (i. e., 5 days or later) thrombocytopenia in which it is generally believed that platelet count recovery will not occur unless heparin is discontinued. However, older reports of type 2 HIT sometimes did include the unexpected observation that platelet counts could recover despite continued heparin administration, although without information provided regarding changes in HIT antibody levels in association with platelet count recovery. In recent years, some reports of type 2 HIT have confirmed the observation that platelet count recovery can occur despite continuing heparin administration, with serological evidence of waning levels of HIT antibodies (“seroreversion”). We now report two additional patient cases of type 2 HIT with platelet count recovery despite ongoing therapeutic-dose (1 case) or prophylactic-dose (1 case) heparin administration, in which we demonstrate concomitant waning of HIT antibody levels. We further review the literature describing this phenomenon of HIT antibody seroreversion and platelet count recovery despite continuing heparin administration. Our observations add to the concept that HIT represents a remarkably transient immune response, including sometimes even when heparin is continued.