Protein-C deficiency presenting as Pulmonary embolism and Deep vein thrombosis: A case report

Plasma protein-C is a naturally occurring anticoagulant and its deficiency, either homozygous or heterozygous, predisposes the individual to a state of thrombosis, particularly venous thromboembolism, and manifests as deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction (MI), or stroke. Protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is inherited as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. We describe a young patient with protein-C deficiency who experienced recurrent pulmonary embolism as well as deep vein thrombosis due to thrombotic occlusion without underlying major risk factors. Pulse Vol.16, 2024 P: 43-46

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Journal
Pulse
Published
2024-10-21
DOI
https://doi.org/10.3329/pulse.v16i1.77071
Citations
1
Primary Topic
Blood Coagulation and Thrombosis Mechanisms
Type
article
Field-Weighted Citation Impact
0.45
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article

Protein-C deficiency presenting as Pulmonary embolism and Deep vein thrombosis: A case report

Mohammad Mahfuzur Rahman, B Ahmed, Kaniz Fatema
1 citations
Pulse
Blood Coagulation and Thrombosis Mechanisms
0.45
article

Protein-C deficiency presenting as Pulmonary embolism and Deep vein thrombosis: A case report

Mohammad Mahfuzur Rahman, B Ahmed, Kaniz Fatema
article en
1 citations

Abstract

Plasma protein-C is a naturally occurring anticoagulant and its deficiency, either homozygous or heterozygous, predisposes the individual to a state of thrombosis, particularly venous thromboembolism, and manifests as deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction (MI), or stroke. Protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is inherited as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased risk for venous thrombosis and pulmonary embolism. We describe a young patient with protein-C deficiency who experienced recurrent pulmonary embolism as well as deep vein thrombosis due to thrombotic occlusion without underlying major risk factors. Pulse Vol.16, 2024 P: 43-46

PulseVol. 16(1)
Women Medical College (PK), Square Hospitals (BD), Dhaka Medical College and Hospital (BD)
Openalex Percentile: Top 27%
Blood Coagulation and Thrombosis Mechanisms
0.45
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