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Cocaine use increases oxidative stress (mitochondria‐specific 8‐oxo‐hydroxy‐guanosine (8‐oxo‐dg) and oxidized glutathione) in HIV infection: mechanism of hepatic fibrogenesis (639.9)
Author(s) -
Campa Adriana,
Sherman Kenneth,
Greer Pedro,
Stewart Tiffanie,
Martinez Sabrina,
Fleetwood Christina,
Ramamoorthy Venkataraghavan,
Dizon Kimberly,
Li Yinghui,
Baum Marianna
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.639.9
Subject(s) - oxidative stress , glutathione , medicine , cohort , viral load , alcohol , human immunodeficiency virus (hiv) , gastroenterology , pharmacology , endocrinology , chemistry , immunology , biochemistry , enzyme
Objective: Cocaine is hepatotoxic in animal models. We examined the effect of cocaine on oxidative stress as one of the mechanisms of liver fibrosis. Methods: With consent we followed 266 HIV+ adults from the MASH cohort for one year using urine toxicology, questionnaires on cocaine and alcohol use. Fib‐4, CD4 cell count, viral load, mitochondrial 8‐oxo‐DG and glutathione were obtained. Results: Cocaine was used by 29% of the cohort and 85.2% were on antiretroviral therapy (ART). Mean age was 47.2 years, 64% were male, and 70.3% African American. Cocaine users had lower ART use (78% vs. 88%, P=0.05), higher viral load (2.76±1.28 vs.2.38±1.1 log 10 copies/mL, P =0.0196) and lower BMI (26.4±5.6 vs. 28±5.1 kg/m 2 , P =0.026) than non‐users. Over one year, using Mixed Models, cocaine users had faster liver fibrosis progression using FIB‐4 (OR=2.52, 95%CI 1.15, 5.54, P=0.021), increased 8‐oxo‐DG (β=0.051, SE=0.02, P =0.047) and oxidized glutathione (β=2.18, SE=1.08, P=0.044), adjusting for gender, age, ART, CD4 count, BMI and alcohol. Conclusions: Cocaine use increases oxidative stress independent of alcohol, ART and CD4 count, linking cocaine use with the mechanisms for liver fibrosis. Funded by: NIDA and NIAAA