Heparin-induced thrombocytopenia: Impact of bovine versus porcine heparin in HIT pathogenesis

被引:9
作者
Ahmad, Sarfraz [1 ]
机构
[1] Florida Hosp Med Ctr, Inst Canc, Orlando, FL 32804 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
heparin-induced thrombocytopenia; diagnosis; management; treatment; heparin-platelet factor 4 antibodies; bovine vs. porcine heparin; cardiac surgery; platelet activation; immunoglobulin subtypes; pathophysiology; thrombosis; review;
D O I
10.2741/2314
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Heparin-induced thrombocytopenia ( HIT) is a complication of heparin therapy in cardiovascular/ hematologic indications. Heparin is a mixture of sulfated mucopolysaccharide with heterogeneity and is capable of forming multiple complexes with platelet factor 4 ( PF4), released from activated platelets. HPF4 antibodies may cause platelet/ endothelial cell activation to promote HIT pathogenesis. HIT is a clinico-pathologic syndrome and its diagnosis primarily remains a clinical one; however, the serologic confirmation of the presence of HPF4 antibodies is also necessary part of the evaluation. Assays are based on the immunodetection of HPF4 antibodies and/ or their functional ability to activate cells. Currently, there are several assays in use and a few newer/ rapid immunoassays are becoming available. Recent studies have confirmed that HPF4 antibody generation ( seroconversion) is common after cardiac surgery and suggest that patients receiving bovine heparin are more likely to generate functional ( pathogenic) HPF4 antibodies of the IgG subclass. Thus, the use of bovine heparin in cardiovascular surgery should be avoided. A brief account of the currently available options for the management of HIT patients with non- heparin anticoagulants is provided.
引用
收藏
页码:3312 / 3320
页数:9
相关论文
共 58 条
[21]   Biological and clinical features of low-molecular-weight heparin-induced thrombocytopenia [J].
Gruel, Y ;
Pouplard, C ;
Nguyen, P ;
Borg, JY ;
Derlon, A ;
Juhan-Vague, I ;
Regnault, V ;
Samama, M .
BRITISH JOURNAL OF HAEMATOLOGY, 2003, 121 (05) :786-792
[22]   Treatment of heparin-induced thrombocytopenia - A critical review [J].
Hirsh, J ;
Heddle, N ;
Kelton, JG .
ARCHIVES OF INTERNAL MEDICINE, 2004, 164 (04) :361-369
[23]  
HORSEWOOD P, 1991, BLOOD, V78, P1019
[24]  
IQBAL O, 2000, MANAGEMENT BLEEDING, P193
[25]   PORCINE HEPARIN INCREASES POSTOPERATIVE BLEEDING IN CARDIOPULMONARY BYPASS PATIENTS [J].
IVERSON, LIG ;
DUHAYLONGSOD, FG ;
YOUNG, JN ;
ECKER, RR ;
ENNIX, CL ;
MORETTI, RL ;
FARRAR, M ;
HAYES, R ;
LEE, J ;
MAY, IA .
CARDIOVASCULAR DRUGS AND THERAPY, 1990, 4 (01) :269-272
[26]   Functional characterization of antibodies against heparin-platelet factor 4 complex in heparin-induced thrombocytopenia patients in Asian-Indians: relevance to inflammatory markers [J].
Kannan, M ;
Ahmad, S ;
Ahmad, F ;
Kale, S ;
Hoppensteadt, DA ;
Fareed, J ;
Saxena, R .
BLOOD COAGULATION & FIBRINOLYSIS, 2005, 16 (07) :487-490
[27]   HEPARIN-ASSOCIATED THROMBOCYTOPENIA [J].
KING, DJ ;
KELTON, JG .
ANNALS OF INTERNAL MEDICINE, 1984, 100 (04) :535-540
[28]   Danaparoid for heparin-induced thrombocytopenia: an analysis of treatment failures [J].
Kodityal, S ;
Manhas, AH ;
Udden, M ;
Rice, L .
EUROPEAN JOURNAL OF HAEMATOLOGY, 2003, 71 (02) :109-113
[29]   Successful treatment of heparin induced thrombocytopenia (HIT) with fondaparinux [J].
Kuo, KHM ;
Kovacs, MJ .
THROMBOSIS AND HAEMOSTASIS, 2005, 93 (05) :999-1000
[30]   Heparin-induced thrombocytopenia: Molecular pathogenesis [J].
Lee, SH ;
Liu, CY ;
PaoloVisentin, G .
INTERNATIONAL JOURNAL OF HEMATOLOGY, 2002, 76 (Suppl 1) :346-351