Antithrombin III deficiency

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M. Khurram Afzal, MD [2], Sogand Goudarzi, MD [3]

Synonyms and keywords: Antithrombin 3 deficiency, Congenital AT-III Deficiancy,

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Antithrombin III deficiency is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism. Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal.

References

Template:WikiDoc Sources CME Category::Cardiology

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Historical Perspective

Discovery

Antithrombin deficiency was first Described in 1965 Olav Egeberg.^[1]
it was observed in an Scandinavian family with multiple venous embolism.

References

↑ Abildgaard U (2001). “[Olav Egeberg–hereditary antithrombin deficiency and thrombophilia]”. Tidsskr Nor Laegeforen. 121 (5): 604–5. PMID 11301618.

Template:WH Template:WS

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD [2]

Overview

Pathophysiology

Physiology

Antithrombin III is a protein in the blood that naturally blocks blood clots from forming. Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of a gene from a parent with the disease.

The abnormal gene leads to low levels of antithrombin III. These low levels of antithrombin III can cause abnormal blood clots (thrombi) that may damage organs.

Pathogenesis

Often, patients with this condition will have a blood clot at a young age and will have a family member who has also experienced a blood clotting episode. In people with this condition, a blood clot may occur without the common risk factors of pregnancy, lack of movement (due to surgery or trauma), or use of oral birth control pills.

Genetics

Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of a gene from a parent with the disease.

The abnormal gene leads to low levels of antithrombin III. These low levels of antithrombin III can cause abnormal blood clots (thrombi) that may damage organs.
The gene for antithrombin is located on human chromosome 1.

References

Template:WikiDoc Sources CME Category::Cardiology

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Causes

Antithrombin III is a protein in the blood that naturally blocks blood clots from forming. Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of a gene from a parent with the disease.

The abnormal gene leads to low levels of antithrombin III. These low levels of antithrombin III can cause abnormal blood clots (thrombi) that may damage organs.

Often, patients with this condition will have a blood clot at a young age and will have a family member who has also experienced a blood clotting episode. In people with this condition, a blood clot may occur without the common risk factors of pregnancy, lack of movement (due to surgery or trauma), or use of oral birth control pills.

References

Template:WikiDoc Sources CME Category::Cardiology

Differentiating Antithrombin III deficiency from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M. Khurram Afzal, MD [2], Sogand Goudarzi, MD [3]

Overview

Antithrombin III deficiency must be differentiated from other diseases that cause symptoms of DVT and pulmonary embolism such as: factor V Leiden mutation, protein C deficiency, protein S deficiency, prothrombin gene mutation, disseminated intravascular coagulation (DIC), antiphospholipid antibody syndrome.

Differential Diagnosis

Differentiating different thrombophilias on the basis of symptoms, physical examination, and laboratory findings

Antithrombin III deficiency must be differentiated from other diseases that cause symptoms of DVT and pulmonary embolism such as:

	Symptoms			Physical examination			Lab Findings		Imaging
Diseases	Clinical manifestations						Para-clinical findings				Gold standard	Additional findings
	Symptoms			Physical examination			Para-clinical findings
	Symptoms of DVT	Symptoms of Pulmonary Embolism	Symptoms of Myocardial Infarction	Tenderness in extremities	Edema in extremities	Warmth in extremities	PT	aPTT	Doppler ultrasound	Chest CT scan
Antithrombin III deficiency^[1]^[2]^[3]	+	+	–	+	+	+	Normal	Normal Reduces the Increase in PTT after administration of heparin	Evidence of deep vein thrombosis (DVT) Should be used for diagnosis and follow up	Occlusion of brachiocephalic vein Large thrombus in superior vena cava	Decreased plasma antithrombin (AT III) activity	Nephrotic syndrome Decreased inhibition of factor II and Xa Antithrombin is a natural anticoagulant that is lost in the urine
Factor V Leiden mutation^[4]^[5]^[6]^[7]^[8]	+	+	+	+	+	+	N/A	↑	Recommended to do weekly Proximal DVT is more commonly observed as compared to distal DVT	Pulmonary embolism	N/A	Inactivates factor Va and factor VIIIa
Protein C deficiency^[9]^[10]^[11]	+	+	–	+	+	+	Normal	Normal / ↑	Hypercoagulation Recurrent venous thromboembolism	Venous thromboembolism Pulmonary embolism	Protein C functional assay ELISA assay: may produce false positive result in cross reaction with rheumatoid factor	Factor VIII elevation in acute phase Functional assay should not be performed if patient is on warfarin Purpura fulminans (skin necrosis) could be a form of presentation Risk of thrombotic skin necrosis following warfarin administration
Protein S deficiency^[11]^[12]^[13]	+	+	–	+	+	+	Normal	Normal / ↑	Hypercoagulation Recurrent venous thromboembolism	Pulmonary embolism Thrombosis of superior mesenteric vein	Protein S free antigen assay	When performing the gold standard test, beware of interference from samples positive for Factor V mutation, protein C deficiency and oral anticoagulants (rivaroxaban) Risk of thrombotic skin necrosis following warfarin administration Suspected in patients with a strong family history of VTE Post phlebitic syndrome Fetal loss
Prothrombin gene mutation^[14]^[15]^[16]	+	+	–	+	+	+	↑	N/A	Proximal DVT is more commonly observed as compared to distal DVT	Pulmonary embolism	Detection of mutation using restriction enzyme and PCR DNA testing for prothrombin G20210A mutation	Mutation causes increased production of prothrombin Increased blood levels of prothrombin lead to venous clots in the circulatory system Hormonal oral contraceptive pills can increase the risk of VTE
Disseminated intravascular coagulation (DIC)^[17]^[18]^[19]	+	+	+/-	+	+	+	↑	↑	Portal vein thrombosis is observed in patients with coexistent hepatitis B	Pulmonary embolism	N/A	Elevated fibrin degradation products (D-dimers) Decreased fibrinogen Decreased factor V and VIII Shistocytes (helmet cells) on peripheral blood smear Portal vein thrombosis
Antiphospholipid antibody syndrome^[20]^[21]^[22]^[23]^[24]	+	+	+/-	+	+	+	N/A	↑	Increased impedance of flow in uterine arteries at 12-20 weeks of gestation	Pulmonary embolism	Antiphospholipid antibody Anticardiolipin antibody Lupus anticoagulant Anti-β2GPI antibody	Both, arterial and venous thrombosis can occur History of spontaneous abortions False positive VDRL Stroke and transient ischemic attack (TIA) are most common forms of presentation of arterial thrombosis

References

↑ Patnaik MM, Moll S (November 2008). “Inherited antithrombin deficiency: a review”. Haemophilia. 14 (6): 1229–39. doi:10.1111/j.1365-2516.2008.01830.x. PMID 19141163.
↑ Al Hadidi, Samer; Wu, Kristi; Aburahma, Ahmed; Alamarat, Zain (2017). “Family with clots: antithrombin deficiency”. BMJ Case Reports: bcr-2017–221556. doi:10.1136/bcr-2017-221556. ISSN 1757-790X.
↑ Konecny F (January 2009). “Inherited trombophilic states and pulmonary embolism”. J Res Med Sci. 14 (1): 43–56. PMC 3129068. PMID 21772860.
↑ Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D (October 2010). “The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease”. J. Thromb. Haemost. 8 (10): 2116–21. doi:10.1111/j.1538-7836.2010.03982.x. PMID 20626623.
↑ Campello E, Spiezia L, Simioni P (December 2016). “Diagnosis and management of factor V Leiden”. Expert Rev Hematol. 9 (12): 1139–1149. doi:10.1080/17474086.2016.1249364. PMID 27797270.
↑ Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV (February 2004). “The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis”. Haematologica. 89 (2): 201–6. PMID 15003896.
↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). “Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis”. Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
↑ Press RD, Bauer KA, Kujovich JL, Heit JA (November 2002). “Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders”. Arch. Pathol. Lab. Med. 126 (11): 1304–18. doi:10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2. PMID 12421138.
↑ Bernard Khor & Elizabeth M. Van Cott (2010). “Laboratory tests for protein C deficiency”. American journal of hematology. 85 (6): 440–442. doi:10.1002/ajh.21679. PMID 20309856. Unknown parameter |month= ignored (help)
↑ Pescatore SL (March 2001). “Clinical management of protein C deficiency”. Expert Opin Pharmacother. 2 (3): 431–9. doi:10.1517/14656566.2.3.431. PMID 11336597.
↑ ^11.0 ^11.1 Gustavo A. Rodriguez-Leal, Segundo Moran, Roberto Corona-Cedillo & Rocio Brom-Valladares (2014). “Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient”. World journal of hepatology. 6 (7): 532–537. doi:10.4254/wjh.v6.i7.532. PMID 25068006. Unknown parameter |month= ignored (help)
↑ Kristi J. Smock, Elizabeth A. Plumhoff, Piet Meijer, Peihong Hsu, Nicole D. Zantek, Nahla M. Heikal & Elizabeth M. Van Cott (2016). “Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories”. Thrombosis and haemostasis. 116 (1): 50–57. doi:10.1160/TH15-12-0918. PMID 27075008. Unknown parameter |month= ignored (help)
↑ Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK (October 2011). “Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy”. Blood Coagul. Fibrinolysis. 22 (7): 619–21. doi:10.1097/MBC.0b013e32834a0421. PMID 21799399.
↑ Cooper PC, Rezende SM (2007). “An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations”. Int J Lab Hematol. 29 (3): 153–62. doi:10.1111/j.1751-553X.2007.00892.x. PMID 17474891.
↑ McGlennen RC, Key NS (2002). “Clinical and laboratory management of the prothrombin G20210A mutation”. Arch Pathol Lab Med. 126 (11): 1319–25. doi:10.1043/0003-9985(2002)126<1319:CALMOT>2.0.CO;2. PMID 12421139.
↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). “Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis”. Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
↑ Venugopal A (September 2014). “Disseminated intravascular coagulation”. Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.
↑ Makruasi N (November 2015). “Treatment of Disseminated Intravascular Coagulation”. J Med Assoc Thai. 98 Suppl 10: S45–51. PMID 27276832.
↑ Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T; et al. (2018). “The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B.” Thromb Res. 161: 7–11. doi:10.1016/j.thromres.2017.11.010. PMID 29178991.
↑ Lim W (2013). “Antiphospholipid syndrome”. Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
↑ Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG (October 2009). “Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis”. J. Thromb. Haemost. 7 (10): 1737–40. doi:10.1111/j.1538-7836.2009.03555.x. PMID 19624461.
↑ Lim W (2013). “Antiphospholipid syndrome”. Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
↑ Garcia D, Erkan D (2018). “Diagnosis and Management of the Antiphospholipid Syndrome”. N Engl J Med. 378 (21): 2010–2021. doi:10.1056/NEJMra1705454. PMID 29791828.
↑ Kornacki J, Wirstlein P, Skrzypczak J (2012). “[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]”. Ginekol Pol. 83 (12): 916–21. PMID 23488294.

Template:WikiDoc Sources CME Category::Cardiology

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Epidemiology and Demographics

Incidence

The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.

Prevalence

The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.
The prevalence of [disease/malignancy] is estimated to be [number] cases annually.

Case-fatality rate/Mortality rate

In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate/mortality rate of [number range]%.
The case-fatality rate/mortality rate of [disease name] is approximately [number range].

Age

Patients of all age groups may develop [disease name].
The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
[Disease name] commonly affects individuals younger than/older than [number of years] years of age.
[Chronic disease name] is usually first diagnosed among [age group].
[Acute disease name] commonly affects [age group].

Race

There is no racial predilection to [disease name].
[Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].

Gender

[Disease name] affects men and women equally.
[Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.

Region

The majority of [disease name] cases are reported in [geographical region].

[Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].

Developed Countries

Developing Countries

References

Template:WH Template:WS

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.

Risk Factors

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

Common Risk Factors

Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
Common risk factors in the development of [disease name] include:
- [Risk factor 1]
- [Risk factor 2]
- [Risk factor 3]

Less Common Risk Factors

Less common risk factors in the development of [disease name] include:
- [Risk factor 1]
- [Risk factor 2]
- [Risk factor 3]

References

Template:WH Template:WS

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

There is insufficient evidence to recommend routine screening for [disease/malignancy].

OR

According to the [guideline name], screening for [disease name] is not recommended.

OR

According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].

Screening

There is insufficient evidence to recommend routine screening for [disease/malignancy].

OR

According to the [guideline name], screening for [disease name] is not recommended.

OR

According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with:

[Condition 1]
[Condition 2]
[Condition 3]

References

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Natural History, Complications and Prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Natural History

Complications

In renal failure, especially nephrotic syndrome, antithrombin is lost in the urine, leading to a higher activity of Factor II and Factor X and in increased tendency to thrombosis.

Blood clots can cause death, especially if they are in the lungs.

Prognosis

Most patients have a good outcome if they stay on anticoagulant medications.

References

Template:WikiDoc Sources CME Category::Cardiology

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1

Related Chapters

Antithrombin

Template:Hematology

Template:WikiDoc Sources CME Category::Cardiology

[pmid11301618-1] Abildgaard U (2001). “[Olav Egeberg–hereditary antithrombin deficiency and thrombophilia]”. Tidsskr Nor Laegeforen. 121 (5): 604–5. PMID 11301618.

[pmid19141163-1] Patnaik MM, Moll S (November 2008). “Inherited antithrombin deficiency: a review”. Haemophilia. 14 (6): 1229–39. doi:10.1111/j.1365-2516.2008.01830.x. PMID 19141163.

[Al_HadidiWu2017-2] Al Hadidi, Samer; Wu, Kristi; Aburahma, Ahmed; Alamarat, Zain (2017). “Family with clots: antithrombin deficiency”. BMJ Case Reports: bcr-2017–221556. doi:10.1136/bcr-2017-221556. ISSN 1757-790X.

[pmid21772860-3] Konecny F (January 2009). “Inherited trombophilic states and pulmonary embolism”. J Res Med Sci. 14 (1): 43–56. PMC 3129068. PMID 21772860.

[pmid20626623-4] Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D (October 2010). “The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease”. J. Thromb. Haemost. 8 (10): 2116–21. doi:10.1111/j.1538-7836.2010.03982.x. PMID 20626623.

[pmid27797270-5] Campello E, Spiezia L, Simioni P (December 2016). “Diagnosis and management of factor V Leiden”. Expert Rev Hematol. 9 (12): 1139–1149. doi:10.1080/17474086.2016.1249364. PMID 27797270.

[pmid15003896-6] Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV (February 2004). “The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis”. Haematologica. 89 (2): 201–6. PMID 15003896.

[pmid23615845-7] Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). “Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis”. Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.

[pmid12421138-8] Press RD, Bauer KA, Kujovich JL, Heit JA (November 2002). “Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders”. Arch. Pathol. Lab. Med. 126 (11): 1304–18. doi:10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2. PMID 12421138.

[9] Bernard Khor & Elizabeth M. Van Cott (2010). “Laboratory tests for protein C deficiency”. American journal of hematology. 85 (6): 440–442. doi:10.1002/ajh.21679. PMID 20309856. Unknown parameter |month= ignored (help)

[pmid11336597-10] Pescatore SL (March 2001). “Clinical management of protein C deficiency”. Expert Opin Pharmacother. 2 (3): 431–9. doi:10.1517/14656566.2.3.431. PMID 11336597.

[:0-11] 11.0 ^11.1 Gustavo A. Rodriguez-Leal, Segundo Moran, Roberto Corona-Cedillo & Rocio Brom-Valladares (2014). “Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient”. World journal of hepatology. 6 (7): 532–537. doi:10.4254/wjh.v6.i7.532. PMID 25068006. Unknown parameter |month= ignored (help)

[12] Kristi J. Smock, Elizabeth A. Plumhoff, Piet Meijer, Peihong Hsu, Nicole D. Zantek, Nahla M. Heikal & Elizabeth M. Van Cott (2016). “Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories”. Thrombosis and haemostasis. 116 (1): 50–57. doi:10.1160/TH15-12-0918. PMID 27075008. Unknown parameter |month= ignored (help)

[pmid21799399-13] Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK (October 2011). “Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy”. Blood Coagul. Fibrinolysis. 22 (7): 619–21. doi:10.1097/MBC.0b013e32834a0421. PMID 21799399.

[pmid17474891-14] Cooper PC, Rezende SM (2007). “An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations”. Int J Lab Hematol. 29 (3): 153–62. doi:10.1111/j.1751-553X.2007.00892.x. PMID 17474891.

[pmid12421139-15] McGlennen RC, Key NS (2002). “Clinical and laboratory management of the prothrombin G20210A mutation”. Arch Pathol Lab Med. 126 (11): 1319–25. doi:10.1043/0003-9985(2002)126<1319:CALMOT>2.0.CO;2. PMID 12421139.

[pmid236158452-16] Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). “Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis”. Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.

[pmid25535423-17] Venugopal A (September 2014). “Disseminated intravascular coagulation”. Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.

[pmid27276832-18] Makruasi N (November 2015). “Treatment of Disseminated Intravascular Coagulation”. J Med Assoc Thai. 98 Suppl 10: S45–51. PMID 27276832.

[pmid29178991-19] Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T; et al. (2018). “The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B.” Thromb Res. 161: 7–11. doi:10.1016/j.thromres.2017.11.010. PMID 29178991.

[pmid24319251-20] Lim W (2013). “Antiphospholipid syndrome”. Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.

[pmid19624461-21] Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG (October 2009). “Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis”. J. Thromb. Haemost. 7 (10): 1737–40. doi:10.1111/j.1538-7836.2009.03555.x. PMID 19624461.

[pmid243192512-22] Lim W (2013). “Antiphospholipid syndrome”. Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.

[pmid29791828-23] Garcia D, Erkan D (2018). “Diagnosis and Management of the Antiphospholipid Syndrome”. N Engl J Med. 378 (21): 2010–2021. doi:10.1056/NEJMra1705454. PMID 29791828.

[pmid23488294-24] Kornacki J, Wirstlein P, Skrzypczak J (2012). “[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]”. Ginekol Pol. 83 (12): 916–21. PMID 23488294.

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Antithrombin III deficiency

Overview

References

Overview

Historical Perspective

Discovery

References

Overview

Pathophysiology

Physiology

Pathogenesis

Genetics

References

Overview

Causes

References

Overview

Differential Diagnosis

References

Overview

Epidemiology and Demographics

Incidence

Prevalence

Case-fatality rate/Mortality rate

Age

Race

Gender

Region

Developed Countries

Developing Countries

References

Overview

Risk Factors

Common Risk Factors

Less Common Risk Factors

References

Overview

Screening

References

Overview

Natural History

Complications

Prognosis

References

Diagnosis

Treatment

Case Studies

Related Chapters

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