Cocaethylene, simultaneous alcohol and cocaine use, and liver fibrosis in people living with and without HIV

Authors

Javier A. Tamargo, Florida International University, Miami, FL, USA. Electronic address: jtamargo@fiu.edu.
Kenneth E. Sherman, University of Cincinnati, Cincinnati, OH, USA. Electronic address: kenneth.sherman@uc.edu.
Rafick-Pierre Sékaly, Emory University, Atlanta, GA, USA; Case Western Reserve University, Cleveland, OH, USA. Electronic address: rafick.sekaly@emory.edu.
Rebeka Bordi, Emory University, Atlanta, GA, USA; Case Western Reserve University, Cleveland, OH, USA. Electronic address: rebeka.bordi@emory.edu.
Daniela Schlatzer, Case Western Reserve University, Cleveland, OH, USA. Electronic address: daniela.schlatzer@case.edu.
Shenghan Lai, University of Maryland, Baltimore, MD, USA. Electronic address: slai@ihv.umaryland.edu.
Jag H. Khalsa, George Washington University, Washington, DC, USA. Electronic address: jagkhalsa2021@gwu.edu.
Raul N. Mandler, National Institute on Drug Abuse, Rockville, MD, USA. Electronic address: mandlerr@nida.nih.gov.
Richard L. Ehman, Mayo Clinic, Rochester, MN, USA. Electronic address: ehman.richard@mayo.edu.
Marianna K. Baum, Florida International University, Miami, FL, USA. Electronic address: baumm@fiu.edu.

Document Type

Journal Article

Publication Date

3-1-2022

Journal

Drug and alcohol dependence

Volume

232

DOI

10.1016/j.drugalcdep.2022.109273

Keywords

Cocaethylene; Cocaine; Liver disease; Liver fibrosis; Substance abuse

Abstract

BACKGROUND: The simultaneous consumption of cocaine and alcohol results in the production of cocaethylene (CE) in the liver, a highly toxic metabolite. Prior research suggests that cocaine use contributes to liver disease and its concomitant use with alcohol may increase its hepatotoxicity, but studies in humans are lacking. We evaluated the role of cocaine, its simultaneous use with alcohol, and CE on liver fibrosis. METHODS: We performed a cross-sectional analysis of the Miami Adult Studies on HIV (MASH) cohort. Cocaine use was determined via self-report, urine screen, and blood metabolites, using liquid chromatography with tandem mass spectrometry. Hazardous drinking was determined with the AUDIT-C and liver fibrosis with the Fibrosis-4 Index (FIB-4). RESULTS: Out of 649 participants included in this analysis, 281 (43.3%) used cocaine; of those, 78 (27.8%) had CE in blood. Cocaine users with CE had higher concentrations of cocaine metabolites in blood and were more likely to drink hazardously than cocaine users without CE and cocaine non-users. Overall, cocaine use was associated with liver fibrosis. CE in blood was associated with 3.17 (95% CI: 1.61, 6.23; p = 0.0008) times the odds of liver fibrosis compared to cocaine non-users, adjusting for covariates including HIV and HCV infection. The effect of CE on liver fibrosis was significantly greater than that of cocaine or alcohol alone. CONCLUSIONS: CE is a reliable marker of simultaneous use of cocaine and alcohol that may help identify individuals at risk of liver disease and aid in the prevention of its development or progression.

APA Citation

Tamargo, Javier A.; Sherman, Kenneth E.; Sékaly, Rafick-Pierre; Bordi, Rebeka; Schlatzer, Daniela; Lai, Shenghan; Khalsa, Jag H.; Mandler, Raul N.; Ehman, Richard L.; and Baum, Marianna K., "Cocaethylene, simultaneous alcohol and cocaine use, and liver fibrosis in people living with and without HIV" (2022). GW Authored Works. Paper 185.
https://hsrc.himmelfarb.gwu.edu/gwhpubs/185

Department

Microbiology, Immunology, and Tropical Medicine