Liver function tests in non-parenteral cocaine users

Tabasco-Minguillan, J.; Novick, David M.; Kreek, Mary Jeanne

doi:10.1016/0376-8716(90)90124-w

Cited by 11 publications

(7 citation statements)

References 23 publications

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“…Another study showed additive, dose‐related detrimental effects of cocaine and alcohol on neurobehavioural performance after 1–3 days of abstinence, with these effects persisting after 4 weeks of abstinence (Bolla, Funderburk & Cadet 2000). A study which was concerned primarily with liver function showed that those who used the combination displayed more irritability and greater memory loss than those who used cocaine alone, but this study did not include an alcohol‐only comparison group (Tabasco‐Minguillan, Novick & Kreek 1990).…”

Section: Resultsmentioning

confidence: 99%

Effects of concurrent use of alcohol and cocaine

2002

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The combination of alcohol and cocaine is popular among drug users, perhaps because of more intense feelings of 'high' beyond that perceived with either drug alone, less intense feelings of alcohol-induced inebriation and tempering of discomfort when coming down from a cocaine 'high'. A review is presented of the medical literature on psychological and somatic effects and consequences of combined use of alcohol and cocaine in man. The search was carried out with Medline, the Science Citation Index/Web of Science and Toxline. Exclusion and inclusion criteria for this search are identified. There is generally no evidence that the combination of the two drugs does more than enhance additively the already strong tendency of each drug to induce a variety of physical and psychological disorders. A few exceptions must be noted. Cocaine consistently antagonizes the learning deficits, psychomotor performance deficits and driving deficits induced by alcohol. The combination of alcohol and cocaine tends to have greater-than-additive effects on heart rate, concomitant with up to 30% increased blood cocaine levels. Both prospective and retrospective data further reveal that co-use leads to the formation of cocaethylene, which may potentiate the cardiotoxic effects of cocaine or alcohol alone. More importantly, retrospective data suggest that the combination can potentiate the tendency towards violent thoughts and threats, which may lead to an increase of violent behaviours.

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Section: Resultsmentioning

confidence: 99%

Effects of concurrent use of alcohol and cocaine

2002

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“…However, there is increasing clinical evidence that, besides these major sites, the liver is also a target organ of cocaine-related toxicity. Although a recent report indicates that cocaine use is rarely associated with significant liver function test abnormalities (Tabasco-Minguillan et al 1990), several other studies document that high doses of cocaine can precipitate massive hepatic necrosis as reflected by profound increases in serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT) and bilirubin levels, and by perivenous, midzonal or periportal parenchymal necrosis (Marks and Chapple 1967;Perino et al 1987;Kanel et al 1990;Kokko 1990;Wanless et al 1990). Collectively, these recent studies indicate that cocaine is potentially hepatotoxic in humans.…”

Section: Introductionmentioning

confidence: 97%

Biomechanisms of cocaine-induced hepatocyte injury mediated by the formation of reactive metabolites

Boelsterli

Göldlin

1991

Arch Toxicol

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Cocaine is an intrinsic hepatotoxin in laboratory animals, and there is growing evidence that high doses of cocaine can precipitate hepatic necrosis in humans. The rodent model of cocaine hepatotoxicity is commensurate with the concept that a multistep mainly cytochrome P-450 dependent N-oxidative pathway is responsible for the expression of hepatocellular injury. Among the possible biomechanisms by which cocaine exerts its cytotoxic effects, direct oxidative damage by reactive oxygen species generated by redox cycling during the metabolic cascade seems most important. The role of the ensuing lipid peroxidation and protein thiol oxidation is less clear. Similarly, the functional role of irreversible (covalent) binding of a not yet defined electrophilic cocaine intermediate to hepatocellular proteins remains enigmatic so long as the critical molecular targets have not been identified. Finally, glutathione plays a pivotal protective role against cocaine-induced hepatic injury. Interactions with ethanol or inducers of the expression of the cytochrome P-450IIB subfamily can potentiate cocaine hepatotoxicity. Thus, the net amount of the ultimate reactive species seems to determine the severity of the hepatic lesions and to be responsible for the marked interspecies, interstrain, and sex differences. Recent advances in culture techniques of hepatocytes and precision-cut liver slices from various species including man have made it possible to correlate cocaine biotransformation with cytotoxicity and to selectively study the putative cellular mechanisms. Clearly, more studies are necessary to further illuminate our understanding of the role of the biochemical and molecular events precipitating hepatic necrosis during cocaine-mediated hepatotoxicity.

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“…18 Clinical hepatotoxicity after cocaine use is also well documented. [19][20][21][22] Our patient's LFTs were slightly elevated at baseline and peaked at approximately 3 times the upper limit of normal before study withdrawal. The highest LFT values obtained were 2 months after study withdrawal, at which time AST and ALT values were both 4 times the upper limit of normal.…”

Section: Discussionmentioning

confidence: 93%

Elevations in Creatine Kinase and Hepatic Transaminases in an HIV-Positive Patient

Klibanov¹,

Berg-Wolf²,

Kerper³

et al. 2006

Infectious Diseases in Clinical Practice

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Objective: To describe a patient who experienced elevations in creatine kinase and hepatic transaminases after initiation of ezetimibe. Case Summary: A 45-year-old HIV-positive man, who is also status post-renal transplant, and is coinfected with hepatitis C, was initiated on ezetimibe. The patient was stable on protease inhibitor-based antiretroviral therapy, cyclosporine/sirolimus-based immunosuppression, and pravastatin before initiation of ezetimibe. While on therapy with ezetimibe, the patient also abused cocaine. He experienced asymptomatic elevations in liver function tests and creatine kinase concentrations, which declined after ezetimibe discontinuation. Discussion: Explanations for the patient's laboratory abnormalities include cyclosporine/ezetimibe drug-drug interaction, additive toxicity of ezetimibe and pravastatin, cocaine use, and hepatic insufficiency associated with hepatitis C, contributing to higher drug exposure and toxicity. Conclusion: Liver function tests and creatine kinase concentrations should be monitored closely in patients who are taking ezetimibe, especially if they are also on multiple other medications or if substance abuse is suspected. (Infect Dis Clin Pract 2006;14:181-184)

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Liver function tests in non-parenteral cocaine users

Cited by 11 publications

References 23 publications

Effects of concurrent use of alcohol and cocaine

Effects of concurrent use of alcohol and cocaine

Biomechanisms of cocaine-induced hepatocyte injury mediated by the formation of reactive metabolites

Elevations in Creatine Kinase and Hepatic Transaminases in an HIV-Positive Patient

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