PMID- 15670034
OWN - NLM
STAT- MEDLINE
DCOM- 20050630
LR  - 20230829
IS  - 1538-7933 (Print)
IS  - 1538-7836 (Linking)
VI  - 3
IP  - 2
DP  - 2005 Feb
TI  - A potential pharmacogenomic strategy for anticoagulant treatment in non-ST 
      elevation acute coronary syndromes: the role of interleukin-1 receptor antagonist 
      genotype.
PG  - 287-91
AB  - OBJECTIVES: Our aim was to determine a pharmacogenomic approach to heparin use in 
      non-ST elevation acute coronary syndromes, specifically the impact of interleukin 
      (IL)-1 receptor antagonist polymorphisms upon von Willebrand factor (vWF) 
      responses to unfractionated heparin (UFH) and low molecular weight heparin 
      (LMWH). BACKGROUND: In acute coronary syndromes (ACS), identification of specific 
      biological or genetic targets to direct pharmacological treatment remains a 
      challenge. vWF has been shown to predict future cardiovascular risk and the 
      response to anticoagulant treatments during non-ST elevation ACS. IL-1 receptor 
      antagonist (IL-1RN) polymorphisms predict the change in vWF between 24 and 48 h 
      (Delta vWF) during non-ST elevation ACS. METHODS: We genotyped at the IL-1 locus, 
      67 patients with non-ST elevation ACS who received either LMWH or UFH, and 
      measured vWF levels at 24 and 48 h. RESULTS: LMWH was superior to UFH in reducing 
      the rise in vWF between 24 and 48 h in the cohort as a whole. However, when 
      patients were stratified by IL-1RN genotype, LMWH was superior to UFH in reducing 
      Delta vWF only in allele *2 carriers (0.51 iU mL(-1) vs. 1.37, P < 0.01), but not 
      in non-carriers (- 0.03 iU mL(-1) vs. 0.15, P = NS). CONCLUSION: IL-1RN genotype 
      may be a useful marker to identify patients that benefit from LMWH in non-ST 
      elevation ACS.
FAU - Ray, K K
AU  - Ray KK
AD  - Cardiovascular Research Unit, Clinical Sciences Centre North, Northern General 
      Hospital, Sheffield, UK. kkray@partners.org
FAU - Francis, S
AU  - Francis S
FAU - Crossman, D C
AU  - Crossman DC
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Thromb Haemost
JT  - Journal of thrombosis and haemostasis : JTH
JID - 101170508
RN  - 0 (Anticoagulants)
RN  - 0 (Heparin, Low-Molecular-Weight)
RN  - 0 (IL1RN protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (von Willebrand Factor)
RN  - 9005-49-6 (Heparin)
SB  - IM
MH  - Acute Disease
MH  - Aged
MH  - Anticoagulants/*therapeutic use
MH  - Coronary Disease/*drug therapy/genetics
MH  - Electrocardiography
MH  - Female
MH  - Genotype
MH  - Heparin/*therapeutic use
MH  - Heparin, Low-Molecular-Weight/therapeutic use
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Male
MH  - Middle Aged
MH  - Pharmacogenetics/*methods
MH  - Polymorphism, Genetic
MH  - Sialoglycoproteins/*genetics/physiology
MH  - Time Factors
MH  - Treatment Outcome
MH  - von Willebrand Factor/analysis/drug effects
EDAT- 2005/01/27 09:00
MHDA- 2005/07/01 09:00
CRDT- 2005/01/27 09:00
PHST- 2005/01/27 09:00 [pubmed]
PHST- 2005/07/01 09:00 [medline]
PHST- 2005/01/27 09:00 [entrez]
AID - S1538-7836(22)13056-4 [pii]
AID - 10.1111/j.1538-7836.2005.01125.x [doi]
PST - ppublish
SO  - J Thromb Haemost. 2005 Feb;3(2):287-91. doi: 10.1111/j.1538-7836.2005.01125.x.