Thrombophilia classification: Difference between revisions

Jump to navigation Jump to search
Line 21: Line 21:
*''Indeterminate factors:'' Elevated Factor VIII, Elevated Factor IX, Elevated Factor XI, Plasminogen deficiency, Tissue plasminogen activator, Elevated lipoprotein a, Factor VII, Factor XII, Platelet glycoprotein, Plasminogen activator inhibitor, Heparin cofactor II, Thrombomodulin, Histidine-rich glycoprotein
*''Indeterminate factors:'' Elevated Factor VIII, Elevated Factor IX, Elevated Factor XI, Plasminogen deficiency, Tissue plasminogen activator, Elevated lipoprotein a, Factor VII, Factor XII, Platelet glycoprotein, Plasminogen activator inhibitor, Heparin cofactor II, Thrombomodulin, Histidine-rich glycoprotein
|-
|-
| '''Acquired thrombophilia or secondary hypercoagulable state''' || [[Age]], BMI >30 kg/m2, [[Immobilization]], [[Trauma]]/major surgery, [[Orthopedic surgery]], [[Malignancy]], [[Myeloproliferative neoplasm|Myeloproliferative disorders]] ([[polycythemia vera]], [[essential thrombocythemia]], [[hyperviscosity]]),  [[Pregnancy]], [[Estrogen]] and [[testosterone]] ([[oral contraceptive]]s, [[hormone replacement therapy]], and [[selective estrogen receptor modulator]]), [[Obesity]], [[Heart Failure]], [[Cirrhosis]], [[Chronic renal disease]], [[Nephrotic syndrome]], [[Antiphospholipid syndrome]] (APLS) or [[lupus anticoagulant]], [[Heparin-induced thrombocytopenia]] (HIT), [[Disseminated intravascular coagulopathy]] (DIC), [[Paroxysmal nocturnal hemoglobinuria]] (PNH), Autoimmune disorders ([[Vasculitis]], [[Celiac disease]], [[Inflammatory bowel disease]]), [[Thrombotic microangiopathy]], [[Sickle cell disease]], Drug related (chemotherapies including L-aspariginase, [[mitomycin]]; infusion of clotting factors including [[prothrombin]] complex concentrates, [[cryoprecipitate]]; drugs including [[hydralazine]], [[procainamide]], or [[phenothiazines]] can promote lupus anticoagulant formation)  
| '''Acquired thrombophilia or secondary hypercoagulable state''' <ref name="Rosendaal1999">{{cite journal|last1=Rosendaal|first1=FR|title=Venous thrombosis: a multicausal disease|journal=The Lancet|volume=353|issue=9159|year=1999|pages=1167–1173|issn=01406736|doi=10.1016/S0140-6736(98)10266-0}}</ref>
|| [[Age]], BMI >30 kg/m2, [[Immobilization]], [[Trauma]]/major surgery, [[Orthopedic surgery]], [[Malignancy]], [[Myeloproliferative neoplasm|Myeloproliferative disorders]] ([[polycythemia vera]], [[essential thrombocythemia]], [[hyperviscosity]]),  [[Pregnancy]], [[Estrogen]] and [[testosterone]] ([[oral contraceptive]]s, [[hormone replacement therapy]], and [[selective estrogen receptor modulator]]), [[Obesity]], [[Heart Failure]], [[Cirrhosis]], [[Chronic renal disease]], [[Nephrotic syndrome]], [[Antiphospholipid syndrome]] (APLS) or [[lupus anticoagulant]], [[Heparin-induced thrombocytopenia]] (HIT), [[Disseminated intravascular coagulopathy]] (DIC), [[Paroxysmal nocturnal hemoglobinuria]] (PNH), Autoimmune disorders ([[Vasculitis]], [[Celiac disease]], [[Inflammatory bowel disease]]), [[Thrombotic microangiopathy]], [[Sickle cell disease]], Drug related (chemotherapies including L-aspariginase, [[mitomycin]]; infusion of clotting factors including [[prothrombin]] complex concentrates, [[cryoprecipitate]]; drugs including [[hydralazine]], [[procainamide]], or [[phenothiazines]] can promote lupus anticoagulant formation)  
|-
|-
| '''Mixed/Unknown''' || [[Hyperhomocysteinemia]], APC resistance unrelated to Factor V Leiden, Increased [[Factor VIII]] levels, Increased [[Factor XI]] levels, Increased [[Factor IX]] levels,  Increased levels of [[thrombin-activatable fibrinolysis inhibitor]] (TAFI), Decreased levels of free [[tissue factor pathway inhibitor]] (TFPI)   
| '''Mixed/Unknown''' || [[Hyperhomocysteinemia]], APC resistance unrelated to Factor V Leiden, Increased [[Factor VIII]] levels, Increased [[Factor XI]] levels, Increased [[Factor IX]] levels,  Increased levels of [[thrombin-activatable fibrinolysis inhibitor]] (TAFI), Decreased levels of free [[tissue factor pathway inhibitor]] (TFPI)   

Revision as of 18:17, 6 April 2021

Thrombophilia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Thrombophilia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Thrombophilia classification On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Thrombophilia classification

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Thrombophilia classification

CDC on Thrombophilia classification

Thrombophilia classification in the news

Blogs on Thrombophilia classification

Directions to Hospitals Treating Thrombophilia

Risk calculators and risk factors for Thrombophilia classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Asiri Ediriwickrema, M.D., M.H.S. [2] Jaspinder Kaur, MBBS[3]

Overview

Thrombophilia may be classified into three subtypes: inherited or primary hypercoagulable states, acquired or secondary hypercoagulable states, and mixed/unknown.[1][2]

Classification

  • Prothrombotic states which can be origin from venous or both venous and arterial clots might be classified into heritable, acquired or mixed resulting from the interactions between the environment (e.g. oestrogen use, obesity or other lifestyle factors) and genetic factors as elaborated in the following Table 1.[1][2]

Table 1: Classification of thrombophilias

Type of classification Medical conditions
Inherited thrombophilia or primary hypercoagulable state[3] [4]
  • Established genetic factors: Activated protein C resistance (Factor V Leiden), Prothrombin gene mutation (Prothrombin G20210A), Protein C, Protein S deficiency, Antithrombin deficiency
  • Rare genetic factors: Dysfibrinogenemias, Hyperhomocysteinemia
  • Indeterminate factors: Elevated Factor VIII, Elevated Factor IX, Elevated Factor XI, Plasminogen deficiency, Tissue plasminogen activator, Elevated lipoprotein a, Factor VII, Factor XII, Platelet glycoprotein, Plasminogen activator inhibitor, Heparin cofactor II, Thrombomodulin, Histidine-rich glycoprotein
Acquired thrombophilia or secondary hypercoagulable state [5] Age, BMI >30 kg/m2, Immobilization, Trauma/major surgery, Orthopedic surgery, Malignancy, Myeloproliferative disorders (polycythemia vera, essential thrombocythemia, hyperviscosity), Pregnancy, Estrogen and testosterone (oral contraceptives, hormone replacement therapy, and selective estrogen receptor modulator), Obesity, Heart Failure, Cirrhosis, Chronic renal disease, Nephrotic syndrome, Antiphospholipid syndrome (APLS) or lupus anticoagulant, Heparin-induced thrombocytopenia (HIT), Disseminated intravascular coagulopathy (DIC), Paroxysmal nocturnal hemoglobinuria (PNH), Autoimmune disorders (Vasculitis, Celiac disease, Inflammatory bowel disease), Thrombotic microangiopathy, Sickle cell disease, Drug related (chemotherapies including L-aspariginase, mitomycin; infusion of clotting factors including prothrombin complex concentrates, cryoprecipitate; drugs including hydralazine, procainamide, or phenothiazines can promote lupus anticoagulant formation)
Mixed/Unknown Hyperhomocysteinemia, APC resistance unrelated to Factor V Leiden, Increased Factor VIII levels, Increased Factor XI levels, Increased Factor IX levels, Increased levels of thrombin-activatable fibrinolysis inhibitor (TAFI), Decreased levels of free tissue factor pathway inhibitor (TFPI)
Arterial thrombotic disorders APLS and lupus anticoagulant, HIT, DIC, PNH, Cold agglutinins (associated with mycoplasma infections), Vasculitis, Hyperhomocysteinemia, JAK2-positive MPNs like Polycythemia vera and Essential thrombocythemia
Venous thrombotic disorders Superior vena cava thrombosis, Jugular vein thrombosis, Cerebral venous sinus thrombosis, Cavernous sinus thrombosis, Retinal vein occlusion, Budd-Chiari syndrome with hepatic thrombus or cirrhosis and associated splenic vein thrombus

References

  1. 1.0 1.1 Hoffman R, Benz EJ, Shattil SJ, et al. Hematology: Basic Principles and Practice: Elsevier Science Health Science Division; 2004.
  2. 2.0 2.1 Cohoon KP, Heit JA (2014). "Inherited and secondary thrombophilia". Circulation. 129 (2): 254–7. doi:10.1161/CIRCULATIONAHA.113.001943. PMC 3979345. PMID 24421360.
  3. Feero WG (2004). "Genetic thrombophilia". Prim Care. 31 (3): 685–709, xi. doi:10.1016/j.pop.2004.04.014. PMID 15331254.
  4. Khan, Salwa; Dickerman, Joseph D (2006). Thrombosis Journal. 4 (1): 15. doi:10.1186/1477-9560-4-15. ISSN 1477-9560. Missing or empty |title= (help)
  5. Rosendaal, FR (1999). "Venous thrombosis: a multicausal disease". The Lancet. 353 (9159): 1167–1173. doi:10.1016/S0140-6736(98)10266-0. ISSN 0140-6736.

Template:WH Template:WS