Hypercoagulable state (also known as prothrombotic state or thrombophilia) is the propensity to venous thrombosis due to an abnormality in the coagulation system.
It may be inherited or acquired, although in some cases the underlying cause cannot be identified.
Many factors contribute to the hypercoagulable state. Inherited thrombophilia affects up to 10% of the population; acquired risk factors, such as obesity and hormonal therapy, are frequent in the community.
Most patients with heritable thrombophilia remain asymptomatic.
Venous thromboembolism is the most common manifestation of the hypercoagulable state. It can be prevented in some patients through identification of those at risk and appropriate thromboprophylaxis during periods of high risk, such as admission to hospital and following major surgery.
Hypercoagulable state (also known as prothrombotic state or thrombophilia) is the propensity to venous thrombosis due to an abnormality in the coagulation system. It was first described by Rudolf Virchow in the mid-19th century as part of the triad of causative factors for venous thromboembolism (i.e., stasis, vascular injury, and hypercoagulability). It may be inherited or acquired, but in some cases the underlying cause cannot be identified.
History and exam
- history of unprovoked venous thromboembolism
- increasing age
- acute inflammatory state
- antiphospholipid antibodies (aPLs)
- myeloproliferative disorders
- nephrotic syndrome
- Behcet's disease
- HIV infection
- disseminated intravascular coagulation
- paroxysmal nocturnal haemoglobinuria
- heparin-induced thrombocytopenia
- oestrogen-containing oral contraceptive pill/hormone replacement therapy/selective oestrogen receptor modulator therapy
- long-haul flight (>4 hours)
- antithrombin deficiency
- protein C deficiency
- protein S deficiency
- plasminogen deficiency
- elevated fibrinogen
- factor V Leiden
- prothrombin gene mutation (G-20210-A; also referred to as F2 c.*97G>A variant)
- elevated factor VIII levels (>150 U/L)
- elevated levels of factor IX or XI
- sickle cell disease
- elevated levels of thrombin-activatable fibrinolysis inhibitor (TAFI)
- heritable thrombophilia test
- polymerase chain reaction (PCR) for factor V Leiden
- antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies, anti-beta-2 glycoprotein 1 antibodies)
- homocysteine level
- factor VIII level
- PCR for JAK2 mutation
- flow cytometry for paroxysmal nocturnal haemoglobinuria
- heparin-induced thrombocytopenia (HIT) test
- chest x-ray
- abdominal CT
- abdominal ultrasound
- tumour markers
- 24-hour urine collection for protein, or spot urine for protein/creatinine ratio
Lara N. Roberts, MBBS, MD (Res), FRCP, FRCPath
King's Thrombosis Centre
King's College Hospital
LNR declares that she has no competing interests.
Roopen Arya, BMBCh (Oxon), MA, PhD, FRCP, FRCPath
Professor of Thrombosis and Haemostasis
King's Thrombosis Centre
King's College NHS Foundation Trust
RA declares that he has no competing interests.
Beverly Hunt, FRCP, FRCPath, MD
Professor of Thrombosis & Haemostasis
Departments of Haematology, Pathology & Rheumatology
Lead in Blood Sciences
Guy's & St Thomas' NHS Foundation Trust
BH declares that she has no competing interests.
Per Morten Sandset, MD, PhD
Senior Consultant and Head of Department
Oslo University Hospital Ullevål
Department of Hematology
Professor in Hematology
University of Oslo
PMS declares that he has no competing interests.
Michael Bromberg, MD, PhD
Director of Hematologic Malignancies
Medicine and Pharmacology
Temple University School of Medicine
MB declares that he has no competing interests.
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