Primary Haemostasis Haemostasis activation Thrombosis

Transcription

Primary Haemostasis Haemostasis activation Thrombosis
Innovation dedicated to Haemostasis
Following platelet activation and plasmatic
coagulation, new molecules appear
circulating in the plasma and the platelet
membrane proteins are modified. An
increase of these markers can reveal a
prothrombotic state.
HAE
tPA
MO
ST
Plasminogen
D
D
Plasmin
Fibrin
IS
AT
D
E
D
A
TXA2
+
RE
GG
GA
IIa
IIa
Fibrin
Nitric oxide
Prostacyclin
APC PS
II
IIa
V
AP
C
TFPI
TFPI
Xa
vWF
PAR1
PLM
T
αA
Insoluble
Fibrin
II
VKA
V
+
FPA
+
FPB
AT
Fibrinogen
Va
PLM
Heparins
Anti-IIa
VWF
IXa VIIIa
XD
αAP
Activated
Platelet
AT
XI
YY
Xa
X
XIIIa
DY
VIII
XY
XIII
DXD
Fibrinogen
Degradation Products
YXD
Fragment D
XX
Fragment Y
YXY
VIII
XXD
IX
Xa TFPI
IIa
X
XIa
Anti-Xa
IX
Fragment E
IIa
VIIa
VII
TF
VIIa
VII
TF
T
IXa VIIIa APC PS
II
XI
FPA
DD
G
VWF
IXa VIIIa APC PS
XIa
Activated
Platelet
Soluble
Fibrin
PLG
AT
XI
T
Xa
Fibrin Monomer
αM
Activated
Platelet
X
anti-Xa
Heparan
sulphate
A
Va
A
VIII
VWF VIII
V
a
X
XIa
a
Released
molecules*
Va
TAFIa
Specific anti-IIa
and anti-Xa drugs
(tc-uPA)
Fibrin
Degradation Products
AT
C
AT
T
PS
sGPVf1
Activated
platelet
AP
Lys
Lys
IIa
XIIa
UK
PAI-1
II
PS
HMWK
C1inh
A
Fibrinogen
IIa
TAFI
IIa
V
AT
Microparticles
+
P2Y1
anti-IIa
PC
IIa
GMP140 or
P selectin
HC II
K
PK
tc-tP
A
Fibrinogen
Historical Multi target
Anticoagulants
ProUK
(sc-uPA)
Fibrinogen
Dermatan
sulphate
N
TIO
GPIb/ Vf2/IX
The parameters:
IX
A
T
The parameters:
X
•Von Willebrand Factor
•Fibrinogen
V
IIa
TF
n
AT
Heparan
sulphate
+
ADP
IIa
IIa
PA
TM
T
+
+
Fibrin
IIa
A
TXA
P2Y12
Fibrin
sc-t
•D-Dimer
Inhibition pathways
Activation pathways
Coagulation
Fibrinolysis
Xa TFPI
VIIa
AT
AT
PAI-1
APC PS
The parameters:
The parameters:
•Antithrombin
•D-Dimer
•INR for VKA monitoring
•Protein C
•Anti-Xa activity direct(rivaroxaban,
apixaban, edoxaban) and indirect (heparins,
fondaparinux…) Xa inhibitors determination
TFPI
•Von Willebrand Factor
•Activated Protein C Resistance
•Fibrin and Fibrinogen Degradation
Products
•ß-Thromboglobulin
•Fibrin Monomers
•Protein S
•Soluble Fibrin Monomer Complexes
•Soluble Glycoprotein V (sGPV)
•Soluble Fibrin Monomer Complexes
•C4b-BP
•Fibrin Monomers
•Platelet Glycoproteins by
Flow Cytometry
•Platelet Factor 4
•Protein Z
•Plasminogen
•Heparin Cofactor II (HCII)
•tPA (Tissue Plasminogen Activator)
•Anti-platelet antibodies by
Flow Cytometry
•ß-Thromboglobulin
•Soluble Glycoprotein V (sGPV)
•Inhibitor of the Extrinsic Pathway (TFPI)
•Antiplasmin
•Soluble Endothelial Protein C Receptor
(sEPCR)
•Soluble Endothelial Protein C Receptor
(sEPCR)
•Plasminogen Activator Inhibitor (PAI)
•Monitoring of P2Y12 ADP receptor
antagonists (clopidogrel, prasugrel,
ticagrelor, cangrelor…)
•Platelet Glycoproteins by
Flow Cytometry
•Lupus Anticoagulants
•Thrombin Activatable Fibrinolysis
Inhibitor (TAFI)
•Monitoring of GpIIb/IIIa antagonists by
Flow Cytometry
•Antiphospholipid Antibodies
•Microparticles
•Thrombin Generation
•Thrombin Generation
•Coagulant Activity Monitoring for
Activated Factor VII
•Microparticles
•Microparticles
•Platelet Factor 4
•Thrombin Generation
•Microparticles
Therapeutic inhibitor
Physiological inhibitor
TF
•Coagulation factors
Xa
The parameters:
•Activated Factor VII - Antithrombin
complex
•Anti-IIa activity for Direct Thrombin
Inhibitors determination (dabigatran,
argatroban, bivalirudin)
•Clotting assay for monitoring
Factors VIII and IX
•Anti-heparin/PF4 antibodies detection
•Thrombin Generation
At the Heart of Haemostasis
4614© 2006 DIAGNOSTICA STAGO - All rights reserved - Non-contractual pictures - 04/2013. Ref. 27854
GPIIb/IIIa
HC II
Haemostasis disorders can be regulated by
a broad panel of anti-thrombotic or antihaemorrhagic treatments. Many assays are
available to measure the activity of these
molecules.
HC II
PLM
TM
Fibrinogen
+
IIa AT
PAI1
E
ADP
Fibrinolysis is the enzymatic process which,
along with vascular repair, leads to the
destruction of the clot to restore normal
blood circulation. An imbalance of the
stability in anti-fibrinolytic factors results in
a Haemostasis disorder.
AT
D
E
Thienopyridines
The onset of plasma coagulation is an
«explosive» event that triggers the generation
of thrombin. Various control pathways
involving a number of different inhibitors
regulate thrombin generation and ensure
that homeostasis is maintained. Anomalies
regarding these inhibitors are the chief
cause of venous and/or arterial thrombosis.
However, thrombosis may also result from the
presence of antiphospholipid antibodies.
P
D
Anti GPIIb/IIIa
Fibrinolysis
Physiological anti-IIa and anti-Xa
A
I-1
FDP
D-Dimer
AS
Thrombosis
AT
The primary Haemostasis corresponds
to the reactions occurring after vascular
damage and leads to the formation of a
stable platelet clot. This is the first stage of
the Haemostasis. To be effective, primary
Haemostasis requires the optimal function
of Von Willebrand Factor and platelets.
Therapeutic
monitoring
T
Haemostasis
activation
A
Primary
Haemostasis
Diagnostica Stago S.A.S.
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92600 Asnières sur Seine (France)
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