PMID- 18291250
OWN - NLM
STAT- MEDLINE
DCOM- 20080319
LR  - 20231024
IS  - 1532-7361 (Electronic)
IS  - 0039-6060 (Linking)
VI  - 143
IP  - 3
DP  - 2008 Mar
TI  - Contemporary standards for the diagnosis and treatment of heparin-induced 
      thrombocytopenia (HIT).
PG  - 305-12
LID - 10.1016/j.surg.2007.09.036 [doi]
AB  - BACKGROUND: Heparin binding to platelet factor 4 (PF4) generates a new antigenic 
      epitope. In an unpredictable fashion, as many as approximately 17% of patients 
      treated with unfractionated heparin (UFH) and approximately 8% treated with 
      low-molecular-weight heparin (LMWH) subsequently develop the anti-heparin-PF4 
      antibodies that mediate heparin-induced thrombocytopenia and thrombosis (HIT). 
      Very few of those patients with circulating anti-heparin-PF4 antibodies, however, 
      progress to develop clinical HIT (referred to previously as Type II HIT). Only 
      20% of those who harbor antibodies ( approximately 3% of those exposed to 
      heparin) will manifest the thrombocytopenia subsequently. Even fewer patients 
      (0.03% to 0.09% of those exposed to heparin) experience the marked platelet 
      activation and morbid thromboses characteristic of the HIT syndrome. The 
      pathogenesis of heparin-induced thrombocytopenia (HIT) remains elusive. The 
      pathophysiologic understanding to date has revolved around pathogenic 
      anti-heparin-PF4 antibodies that trigger platelet activation, release of platelet 
      procoagulant microparticles, and resultant thrombosis. The clinical diagnosis of 
      HIT is confusing because current assays to detect anti-heparin-PF4 antibodies do 
      not correlate well with the disease. Currently available assays lack either 
      adequate sensitivity and interlaboratory reproducibility (ie, functional 
      serotonin release assays) or specificity (ie, enzyme-linked immunosorbent assays 
      or ELISAs). CONCLUSIONS: Fortunately, the treatment for HIT is not confusing. The 
      purposes of this review are as follows: (1) to examine the relevant clinical 
      definition of HIT, (2) to explore our current understanding as to the 
      pathogenesis of HIT, and (3) to present an algorithm for the identification and 
      treatment of the HIT syndrome.
FAU - Baldwin, Zachary K
AU  - Baldwin ZK
AD  - Division of Vascular Surgery, Department of Surgery, School of Medicine, 
      University of California, San Francisco, Calif 94143, USA. 
      baldwinz@surgery.ucsf.edu
FAU - Spitzer, Austin L
AU  - Spitzer AL
FAU - Ng, Valerie L
AU  - Ng VL
FAU - Harken, Alden H
AU  - Harken AH
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20071221
PL  - United States
TA  - Surgery
JT  - Surgery
JID - 0417347
RN  - 0 (Anticoagulants)
RN  - 9005-49-6 (Heparin)
SB  - IM
CIN - Surgery. 2008 Jun;143(6):835. PMID: 18549904
MH  - Anticoagulants/*adverse effects
MH  - Heparin/*adverse effects
MH  - Humans
MH  - Thrombocytopenia/chemically induced/diagnosis/therapy
RF  - 12
EDAT- 2008/02/23 09:00
MHDA- 2008/03/20 09:00
CRDT- 2008/02/23 09:00
PHST- 2007/05/01 00:00 [received]
PHST- 2007/08/22 00:00 [revised]
PHST- 2007/09/06 00:00 [accepted]
PHST- 2008/02/23 09:00 [pubmed]
PHST- 2008/03/20 09:00 [medline]
PHST- 2008/02/23 09:00 [entrez]
AID - S0039-6060(07)00633-2 [pii]
AID - 10.1016/j.surg.2007.09.036 [doi]
PST - ppublish
SO  - Surgery. 2008 Mar;143(3):305-12. doi: 10.1016/j.surg.2007.09.036. Epub 2007 Dec 
      21.