Distinct phenotype of hepatotoxicity associated with illicit use of anabolic androgenic steroids
Author
dc.contributor.author
Robles Díaz, M.
Author
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González Jiménez, A.
Author
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Medina Cáliz, I.
Author
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Stephens, C.
Author
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García Cortés, M.
Author
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García Muñoz, B.
Author
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Ortega Alonso, A.
Author
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Blanco Reina, E.
Author
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González Grande, R.
Author
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Jiménez Pérez, M.
Author
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Rendon, P.
Author
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Navarro, J. M.
Author
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Gines, P.
Author
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Prieto, M.
Author
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García Eliz, M.
Author
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Bessone, F.
Author
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Brahm Barril, Javier
Author
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Paraná, R.
Author
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Lucena, M. I.
Author
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Andrade, R. J.
Admission date
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2015-08-08T22:01:44Z
Available date
dc.date.available
2015-08-08T22:01:44Z
Publication date
dc.date.issued
2015
Cita de ítem
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Aliment Pharmacol Ther 2015; 41: 116-125
en_US
Identifier
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DOI: 10.1111/apt.13023
Identifier
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https://repositorio.uchile.cl/handle/2250/132530
General note
dc.description
Artículo de publicación ISI
en_US
Abstract
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Background
We have observed an increase in hepatotoxicity (DILI) reporting related to
the use of anabolic androgenic steroids (AAS) for bodybuilding.
Aim
To characterise phenotype presentation, outcome and severity of AAS DILI.
Methods
Data on 25 cases of AAS DILI reported to the Spanish (20) and LatinAmerican
(5) DILI Registries were collated and compared with previously
published cases.
Results
AAS DILI increased from representing less than 1% of the total cases in
the Spanish DILI Registry in the period 2001–2009 to 8% in 2010–2013.
Young men (mean age 32 years), requiring hospitalisation, hepatocellular
injury and jaundice were predominating features among the AAS cases.
AAS DILI caused significantly higher bilirubin values independent of type
of damage when compared to other drug classes (P = 0.001). Furthermore,
the cholestatic AAS cases presented significantly higher mean peak bilirubin
(P = 0.029) and serum creatinine values (P = 0.0002), compared to the
hepatocellular cases. In a logistic regression model, the interaction between
peak bilirubin values and cholestatic damage was associated with the development
of AAS-induced acute kidney impairment (AKI) [OR 1.26 (95%
CI: 1.035–1.526); P = 0.021], with 21.5 9ULN being the best bilirubin cutoff
point for predicting AKI risk (AUCROC 0.92). No fatalities occurred.
Conclusions
Illicit recreational AAS use is a growing cause of reported DILI that can
lead to severe hepatic and renal injury. AAS DILI is associated with a distinct
phenotype, characterised by considerable bilirubin elevations independent
of type of damage. Although hepatocellular injury predominates, acute
kidney injury develops in cholestatic cases with pronounced jaundice.