Activated protein C resistance: Difference between revisions

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Activated Protein C Resistance
 
{{Infobox medical condition
| name            = Activated protein C resistance
| image          =[[File:Protein_C_anticoagulant.jpg|250px]]
| caption        = Protein C anticoagulant pathway
| field          = [[Hematology]]
| symptoms        = [[Deep vein thrombosis]], [[pulmonary embolism]]
| complications  = [[Thrombophilia]], [[venous thromboembolism]]
| onset          = Varies
| duration        = Chronic
| causes          = [[Factor V Leiden]] mutation, other genetic mutations
| risks          = Family history, [[pregnancy]], [[oral contraceptive]] use
| diagnosis      = [[Activated protein C resistance test]], [[genetic testing]]
| differential    = [[Antiphospholipid syndrome]], [[prothrombin gene mutation]]
| treatment      = [[Anticoagulation therapy]]
| medication      = [[Warfarin]], [[heparin]]
| frequency      = Common in individuals of European descent
}}
Activated Protein C Resistance


[[File:Protein_C_anticoagulant.jpg|thumb|right|Protein C, a key component in the anticoagulation pathway]]
[[File:Protein_C_anticoagulant.jpg|thumb|right|Protein C, a key component in the anticoagulation pathway]]

Latest revision as of 03:44, 4 April 2025


Activated protein C resistance
Synonyms N/A
Pronounce N/A
Specialty N/A
Symptoms Deep vein thrombosis, pulmonary embolism
Complications Thrombophilia, venous thromboembolism
Onset Varies
Duration Chronic
Types N/A
Causes Factor V Leiden mutation, other genetic mutations
Risks Family history, pregnancy, oral contraceptive use
Diagnosis Activated protein C resistance test, genetic testing
Differential diagnosis Antiphospholipid syndrome, prothrombin gene mutation
Prevention N/A
Treatment Anticoagulation therapy
Medication Warfarin, heparin
Prognosis N/A
Frequency Common in individuals of European descent
Deaths N/A


Activated Protein C Resistance
Protein C, a key component in the anticoagulation pathway

Activated Protein C Resistance (APCR) is a hemostatic disorder characterized by a reduced anticoagulant response to activated protein C (APC). This condition is most commonly associated with the Factor V Leiden mutation, which leads to a hypercoagulable state and an increased risk of venous thromboembolism.

Pathophysiology[edit]

Activated protein C is a crucial component of the coagulation cascade, functioning to inactivate Factor Va and Factor VIIIa, thereby reducing thrombin generation and clot formation. In individuals with APCR, the ability of APC to inactivate these factors is impaired, leading to a prothrombotic state.

Factor V Leiden[edit]

The most common cause of APCR is the Factor V Leiden mutation, a single nucleotide polymorphism in the F5 gene that results in a substitution of arginine with glutamine at position 506. This mutation renders Factor V resistant to cleavage by APC, thus diminishing its anticoagulant effect.

Clinical Manifestations[edit]

Patients with APCR are at an increased risk for developing deep vein thrombosis (DVT) and pulmonary embolism (PE). The risk is particularly elevated in individuals who are homozygous for the Factor V Leiden mutation. Other potential complications include cerebral vein thrombosis and recurrent pregnancy loss.

Diagnosis[edit]

The diagnosis of APCR is typically made through functional assays that measure the anticoagulant response to APC. Genetic testing for the Factor V Leiden mutation can confirm the diagnosis.

Management[edit]

Management of APCR involves anticoagulation therapy to prevent thrombotic events. Warfarin and direct oral anticoagulants (DOACs) are commonly used. In certain situations, such as surgery or pregnancy, prophylactic anticoagulation may be indicated.

Related pages[edit]