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A. Malignancy navigator

  1. 5-15% tumors overall
  2. Nearly 50% of patients with pancreatic cancers have some thromboembolic event
  3. May be due to activation of platelets by tumors and/or production of procoagulants
  4. May also be related to interference with protein S (or C) function
  5. Migratory thrombophlebitis (Trousseau's Syndrome) not uncommon
  6. Myeloproliferative Disorders

B. Pregnancy navigator

  1. Increased risk of thromboembolic disease
  2. HELLP Syndrome

C. Estrogens navigator

  1. Oral contraceptives
  2. Hormone Replacement Therapy
  3. Normal women have very low risk of thromboemboli
  4. Smoking and other hypercoagulable states greatly increase risk

D. Nephrotic Syndrome navigator

  1. Loss of fibrinolytic components (such as antithrombin III, proteins C or S) through filtration
  2. Hyperlipidemia
  3. Check albumin levels; urine:serum albumin ratio

E. Metabolic Disordersnavigator

  1. Smoking
  2. Hyperlipidemias
  3. Diabetes mellitus
  4. Obesity - probably associated with reduced activity and/or immobilization

F. Immobilizationnavigator

  1. Trauma
  2. Postoperative (immobilization, bed rest)
  3. Obesity
  4. Airplane travel, particularly >8 hours or in persons with genetic predisposition [9]

G. Genetic Variants [2] navigator

  1. Antithrombin (ATIII) - absence, reduction, resistance
  2. Protein C - deficiency may be accompanied by DIC
  3. Protein S
  4. Factor I (Fibrinogen) - increased levels
  5. Factor II (Prothrombin) - G20210A mutation leads to elevated levels [7]
  6. Factor V Leiden Mutation - resistance to activated protein C (G1691A) [3,4]
  7. Factor VII Levels - increased Levels of plasma Factor VII
  8. Factor VII Genotype H6H6
  9. Protein C or S deficiency symptoms may be precipitated by use of warfarin without heparin
  10. Paroxysmal nocturnal hemoglobinuria (PNH): abnormal platelet membrane proteins
  11. Combinations of gene variants appear to increase thromboembolic risks synergistically

H. Homocystinemia and Hyperhomocysteinemia [2] navigator

  1. High homocysteine levels are a mild to severe risk factor for premature vascular disease
  2. Risk factor for arterial > venous thromboemboli - early MI not uncommon
  3. Many patients with high homocysteine have genetic variants in key metabolic genes
  4. Homozygous Genetic Disease
    1. Homzygous cystathionine ß-synthase deficiency associated with severe events
    2. Also includes mental retardation, ectopia lentis, skeletal abnormalities (osteoporosis)

I. Vasculitis and Collagen Vascular Disease navigator

  1. Antiphospholipid Syndrome
  2. Systemic lupus erythematosus - especially with antiphospholipid antibodies
  3. Thromboangiitis obliterans
  4. ANCA Associated Vasculitis
  5. Cryoglobulinemia

J. Hyperviscosity Syndromesnavigator

  1. Sickle Cell Anemia
  2. Polycythemia
  3. Hypergammaglobulinemia (esp IgM)

K. Miscellaneousnavigator

  1. Heparin-Induced Thrombocytopenia (HIT; antibody mediated)
  2. Anti-Neoplastic agents (vascular endothelial damage; HUS/TTP)
  3. Cryofibrinogenemia [8]

L. Thrombotic Storm [6] navigator

  1. Thrombosis perpetuates thrombosis
  2. Most of the above problems are associated with thrombotic storm
  3. Also includes some of the microangiopathic hemolytic anemias
  4. Endothelial and/or platelet abnormalities are involved
  5. Combinations of hypercoagulation risks are additive or synergistic [4]

References navigator

  1. Nachman RL and Silverstein R. 1993. Ann Intern Med. 119(8):819 abstract
  2. Fermo I, D'Angelo V, Paroni R, et al. 1995. Ann Intern Med. 123(10):747 abstract
  3. van der Bom JG, Bots ML, Haverkate F, et al. 1996. Ann Intern Med. 125(4):265 abstract
  4. Price DT and Ridker PM. 1997. Ann Intern Med. 127(10):895 abstract
  5. Iacoviello L, Di Castelnuovo A, de Knijff P, et al. 1998. NEJM. 338(2):79 abstract
  6. Kitchens CS. 1998. Am J Med. 104(4):381 abstract
  7. Martinelli I, Sacchi E, Landi G, et al. 1998. NEJM. 338(25):1793 abstract
  8. Amdo TD and Welker JA. 2004. Am J Med. 115(6):332
  9. Schreijer AJ, Cannegieter SC, Meijers JC, et al. 2006. Lancet. 367(9513):832 abstract