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
[1]   Synthetic pentasaccharides do not cause platelet activation by antiheparin-platelet factor 4 antibodies [J].
Ahmad, S ;
Jeske, WP ;
Walenga, JM ;
Hoppensteadt, DA ;
Wood, JJ ;
Herbert, JM ;
Messmore, HL ;
Fareed, J .
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS, 1999, 5 (04) :259-266
[2]   Functional heterogeneity of antiheparin-platelet factor 4 antibodies: Implications in the pathogenesis of the HIT syndrome [J].
Ahmad, S ;
Walenga, JM ;
Jeske, WP ;
Cella, G ;
Fareed, J .
CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS, 1999, 5 :S32-S37
[3]   Differential prevalence of anti-heparin-PF4 immunoglobulin subtypes in patients treated with clivarin and heparin: Implications in the HIT pathogenesis [J].
Ahmad, S ;
Untch, B ;
Haas, S ;
Hoppensteadt, DA ;
Misselwitz, F ;
Messmore, HL ;
Walenga, JM ;
Fareed, J .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2004, 258 (1-2) :163-170
[4]  
Ahmad S, 2003, ARCH PATHOL LAB MED, V127, P584
[5]  
Alafify AA, 2005, SAUDI MED J, V26, P1800
[6]   Rapid determination of anti-heparin/platelet factor 4 antibody titers in the diagnosis of heparin-induced thrombocytopenia [J].
Alberio, L ;
Kimmerle, S ;
Baumann, A ;
Taleghani, BRM ;
Biasiutti, FD ;
Lämmle, B .
AMERICAN JOURNAL OF MEDICINE, 2003, 114 (07) :528-536
[7]  
AMIRAL J, 1992, THROMB HAEMOSTASIS, V68, P95
[8]   The biological basis of immune heparin-induced thrombocytopenia [J].
Amiral, J ;
Marfaing-Koka, A ;
Poncz, M ;
Meyer, D .
PLATELETS, 1998, 9 (02) :77-91
[9]  
ANSELL J, 1980, THROMB HAEMOSTASIS, V43, P61
[10]   HEPARIN-INDUCED THROMBOCYTOPENIA AND THROMBOSIS [J].
ASTER, RH .
NEW ENGLAND JOURNAL OF MEDICINE, 1995, 332 (20) :1374-1376