Difference between revisions of "Hypercoagulable state (thrombophilia)"
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Revision as of 12:16, 18 August 2023
Guidelines
"How I Treat"
- 2020: May & Moll How I treat unexplained arterial thrombosis
Inherited thrombophilias
- Prothrombin gene mutation (G20210A)
- Factor V Leiden mutation
- Antithrombin III deficiency
- Protein C deficiency
- Protein S deficiency
- Dysfibrinogenemia
Controversial:
- Plasminogen deficiency
- Factor XII deficiency
Acquired thrombophilias and clotting risk factors
- Surgery, foreign bodies such as venous catheters, smoking, obesity, elevated factor VIII, advanced age, male sex, trauma, sedentary state, immobilization, malignancy, myeloproliferative disorders-- polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF), pregnancy, medications--e.g. Bevacizumab (Avastin), Lenalidomide (Revlimid), Thalidomide (Thalomid), Tamoxifen (Nolvadex), oral contraceptive use, heparin--in the case of heparin-induced thrombocytopenia/thrombosis (HIT), congestive heart failure, anatomic/low cardiovascular flow states--e.g. inferior vena cava (IVC) abnormalities, chronic inflammation, inflammatory bowel disease, nephrotic syndrome, paroxysmal noctural hemoglobinuria (PNH)
- Prior venous thromboembolism (VTE)
- Antiphospholipid antibody syndrome (APS)
- Lupus anticoagulant: dilute Russell viper venom time (dRVVT), dilute activated partial thromboplastin time (dAPTT), Staclot LA (hexagonal phase phospholipids), Kaolin clotting time (KCT)
- Anticardiolipin (aCL) antibody IgG, IgM, IgA
- Beta 2 glycoprotein 1 (B2GP1) IgG, IgM, IgA
- Sapporo criteria for APS