S(n)orting Out the Problem: Fever of Unknown Origin and Unexplained Abnormal Transaminases in a Young Male

Philips, Cyriac Abby; Chooracken, Mathews; Mahadevan, Pushpa; Augustine, Philip

doi:10.7759/cureus.1543

Cited by 1 publication

(2 citation statements)

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“…Cocaine-induced hepatotoxicity is thought to be mainly due to N oxidative metabolites of cocaine and depletion of intra-cellular and mitochondrial glutathione, which impairs the liver’s antioxidant system [ 5 ]. This could underlie the effectiveness of N acetylcysteine in non-acetaminophen drug-induced liver injury [ 13 – 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…Two cases have been reported in the literature in which patients with a history of substance use disorder were diagnosed with acute fulminant liver failure through urine drug screening early in the investigation that revealed cocaine use as the cause [ 13 , 14 ]. Philips et al discussed a patient in a case report akin to ours in which the patient’s self-reported drug use was discovered late, and cocaine was the ultimate cause of drug-induced liver injury [ 15 ]. Thus, relying on self-reported data can lead to limitations, such as missing the window period for detecting drugs on screening tests due to delayed patient reporting.…”

Section: Discussionmentioning

confidence: 99%

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

Patel,

Thomas,

Stacey

2023

Am J Case Rep

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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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Section: Discussionmentioning

confidence: 99%