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Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury

Patient: Male, 34-year-old Final Diagnosis: Venous thromboembolism secondary to cocaine use Symptoms: Shortness of breath Clinical Procedure: — Specialty: General and Internal Medicine OBJECTIVE: Unknown etiology BACKGROUND: Pulmonary embolism secondary to deep vein thrombosis (DVT) with cor pulmona...

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Autores principales: Patel, Khyati H., Thomas, Kyle C., Stacey, Stephen K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615112/
https://www.ncbi.nlm.nih.gov/pubmed/37872733
http://dx.doi.org/10.12659/AJCR.941360
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author Patel, Khyati H.
Thomas, Kyle C.
Stacey, Stephen K.
author_facet Patel, Khyati H.
Thomas, Kyle C.
Stacey, Stephen K.
author_sort Patel, Khyati H.
collection PubMed
description Patient: Male, 34-year-old Final Diagnosis: Venous thromboembolism secondary to cocaine use Symptoms: Shortness of breath Clinical Procedure: — Specialty: General and Internal Medicine OBJECTIVE: Unknown etiology BACKGROUND: Pulmonary embolism secondary to deep vein thrombosis (DVT) with cor pulmonale is commonly associated with risk factors including surgery, cancer, and prolonged immobility. Cocaine is known to cause vasoconstriction and has a prothrombotic effect. Prolonged and heavy use of cocaine can also cause inflammation and liver damage. However, data on its potential role in causing pulmonary embolism and direct hepatotoxicity in cases of episodic use are scarce. CASE REPORT: A 34-year-old man with no significant medical history except for episodic cocaine use presented in respiratory distress. Workup revealed submassive pulmonary embolism with pulmonary infarctions complicated by pneumonia, hypoxemic respiratory failure, and anemia. He was treated with anticoagulation and intensive care. On day 5 of hospitalization, the patient had an acute hepatic injury. His alanine aminotransferase level peaked at over 2000 IU/L on day 7, until finally tapering. Liver failure was found to be secondary to cocaine use. Liver enzyme levels improved with supportive care. He was discharged with apixaban and continued liver enzyme monitoring. CONCLUSIONS: When investigating the cause of venous thromboembolism and transaminitis, evaluating cocaine use via patient history or laboratory analysis of cocaine and its metabolites should be considered. Cocaine is known to cause vasoconstriction and has a prothrombotic effect, although data on its potential role in causing pulmonary embolism and direct hepatotoxicity in cases of episodic use are scarce. Further investigation, such as cohort studies, could help strengthen our understanding of the relationship between cocaine use, acute hepatic injury, and pulmonary embolism.
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spelling pubmed-106151122023-10-31 Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury Patel, Khyati H. Thomas, Kyle C. Stacey, Stephen K. Am J Case Rep Articles Patient: Male, 34-year-old Final Diagnosis: Venous thromboembolism secondary to cocaine use Symptoms: Shortness of breath Clinical Procedure: — Specialty: General and Internal Medicine OBJECTIVE: Unknown etiology BACKGROUND: Pulmonary embolism secondary to deep vein thrombosis (DVT) with cor pulmonale is commonly associated with risk factors including surgery, cancer, and prolonged immobility. Cocaine is known to cause vasoconstriction and has a prothrombotic effect. Prolonged and heavy use of cocaine can also cause inflammation and liver damage. However, data on its potential role in causing pulmonary embolism and direct hepatotoxicity in cases of episodic use are scarce. CASE REPORT: A 34-year-old man with no significant medical history except for episodic cocaine use presented in respiratory distress. Workup revealed submassive pulmonary embolism with pulmonary infarctions complicated by pneumonia, hypoxemic respiratory failure, and anemia. He was treated with anticoagulation and intensive care. On day 5 of hospitalization, the patient had an acute hepatic injury. His alanine aminotransferase level peaked at over 2000 IU/L on day 7, until finally tapering. Liver failure was found to be secondary to cocaine use. Liver enzyme levels improved with supportive care. He was discharged with apixaban and continued liver enzyme monitoring. CONCLUSIONS: When investigating the cause of venous thromboembolism and transaminitis, evaluating cocaine use via patient history or laboratory analysis of cocaine and its metabolites should be considered. Cocaine is known to cause vasoconstriction and has a prothrombotic effect, although data on its potential role in causing pulmonary embolism and direct hepatotoxicity in cases of episodic use are scarce. Further investigation, such as cohort studies, could help strengthen our understanding of the relationship between cocaine use, acute hepatic injury, and pulmonary embolism. International Scientific Literature, Inc. 2023-10-24 /pmc/articles/PMC10615112/ /pubmed/37872733 http://dx.doi.org/10.12659/AJCR.941360 Text en © Am J Case Rep, 2023 https://creativecommons.org/licenses/by-nc-nd/4.0/This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Articles
Patel, Khyati H.
Thomas, Kyle C.
Stacey, Stephen K.
Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury
title Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury
title_full Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury
title_fullStr Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury
title_full_unstemmed Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury
title_short Episodic Cocaine Use as a Cause of Venous Thromboembolism and Acute Liver Injury
title_sort episodic cocaine use as a cause of venous thromboembolism and acute liver injury
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615112/
https://www.ncbi.nlm.nih.gov/pubmed/37872733
http://dx.doi.org/10.12659/AJCR.941360
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