Liver Function Tests in Nonparenteral Cocaine Users

R, Kothur; Marsh, Franklin; Posner, Gerald

doi:10.1001/archinte.1991.00400060068011

Cited by 23 publications

(6 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Amphetamines have an extensive hepatic metabolism and the generation of a toxic metabolite may be the cause of hepatic injury [163]. Cocaine can lead to a range of liver abnormalities and its metabolites are involved in oxidative stress and lipid peroxidation in hepatocytes [164,165]. …”

Section: Dysregulation Of Matrix Metalloproteinases and Role Of Fimentioning

confidence: 99%

Molecular Mechanisms of Liver Fibrosis in HIV/HCV Coinfection

Mastroianni

Lichtner

Mascia

et al. 2014

IJMS

View full text Add to dashboard Cite

Chronic hepatitis C virus (HCV) infection is an important cause of morbidity and mortality in people coinfected with human immunodeficiency virus (HIV). Several studies have shown that HIV infection promotes accelerated HCV hepatic fibrosis progression, even with HIV replication under full antiretroviral control. The pathogenesis of accelerated hepatic fibrosis among HIV/HCV coinfected individuals is complex and multifactorial. The most relevant mechanisms involved include direct viral effects, immune/cytokine dysregulation, altered levels of matrix metalloproteinases and fibrosis biomarkers, increased oxidative stress and hepatocyte apoptosis, HIV-associated gut depletion of CD4 cells, and microbial translocation. In addition, metabolic alterations, heavy alcohol use, as well drug use, may have a potential role in liver disease progression. Understanding the pathophysiology and regulation of liver fibrosis in HIV/HCV co-infection may lead to the development of therapeutic strategies for the management of all patients with ongoing liver disease. In this review, we therefore discuss the evidence and potential molecular mechanisms involved in the accelerated liver fibrosis seen in patients coinfected with HIV and HCV.

show abstract

Section: Dysregulation Of Matrix Metalloproteinases and Role Of Fimentioning

confidence: 99%

Molecular Mechanisms of Liver Fibrosis in HIV/HCV Coinfection

Mastroianni

Lichtner

Mascia

et al. 2014

IJMS

View full text Add to dashboard Cite

show abstract

“…Our patient presented with fulminant hepatitis that manifested with all of the above-mentioned symptoms secondary to acute cocaine toxicity in the setting of β-blocker use. Cocaine has been reported to cause hepatotoxicity in humans [1][2][3][4][5][6] as well as several animal models. [7][8][9][10][11] Two previous studies found cocaine use to be associated with hepatic dysfunction manifested by elevation in liver enzymes.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9][10][11] Two previous studies found cocaine use to be associated with hepatic dysfunction manifested by elevation in liver enzymes. 3,4 Silva et al studied this correlation, specifically in the setting of acute cocaine use. 3 Cocaine-induced periportal hepatocyte damage has been attributed to oxidative stress 12,13 with damage to endoplasmic reticulum and mitochondria seen in the early stages of toxicity.…”

Section: Discussionmentioning

confidence: 99%

Reversible Fulminant Hepatitis Secondary to Cocaine in the Setting of β-Blocker Use

Sharma

Kapoor

Chaudhari

et al. 2020

Journal of Investigative Medicine High Impact Case Reports

View full text Add to dashboard Cite

Background. Fulminant hepatitis is acute hepatic injury with severe decline in hepatic function manifested by encephalopathy, hypercoagulable state, jaundice, renal failure, hypoglycemia, or a constellation of these symptoms in patients without preexisting liver disease. Etiologies include viral infections, hepatotoxic drugs, autoimmune diseases, vaso-occlusive diseases, sepsis, and malignant infiltration. Case Report. A 56-year-old man presented with acute heart failure in the setting of cocaine use. The patient subsequently developed fulminant hepatic failure manifested by acute hypoglycemia, elevated liver enzyme, and worsening liver function, which resolved over 1 week with supportive care. The patient was on β-blocker, which was stopped during the admission. He was again admitted on several different occasion for cocaine-induced acute heart failure but did not develop hepatic failure as his β-blocker was discontinued. Discussion. Cocaine has been known to cause hepatotoxicity in humans. However, our patient developed fulminant hepatic failure in the setting of concomitant cocaine and β-blocker use likely secondary to unopposed α-adrenergic activity and ischemic hepatopathy. The patient did not develop hepatic failure on subsequent admissions with cocaine use after discontinuation of β-blockers.

show abstract

“…Nonparenteral cocaine users can have mild elevation of transaminases and alkaline phosphatase. Physical and mental deterioration, depresseion, agitation, nervousness, tired but unable to sleep, loss of the smell sense, nosebleeds, difficulty in swallowing, chronically runny nose [7,8].…”

Section: Drugs Risk Factors Clinical Symptomsmentioning

confidence: 99%