Acute cocaine-induced hepatotoxicity with features of shock liver

Adedinsewo, Demilade; Ajao, Oluwatosin; Okpobrisi, Ofego; Fotzeu, Claudia; Crawford, Marvin

doi:10.5430/crcp.v2n4p36

Cited by 4 publications

(3 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, cocaine may cause hepatocyte damage through two mechanisms: hypoperfusion and oxidative stress. It has been suggested that cocaine reduces hepatic blood flow, causing shock liver, or ischemic hepatitis [10,11]. The findings of shock liver have been associated with cocaine-induced hepatitis in several case reports [9,[11][12][13].…”

Section: Discussionmentioning

confidence: 99%

A Case of Cocaine-Induced Acute Liver Failure Reversed With N-Acetylcysteine

Mitchell¹,

Rogers²

2023

Cureus

View full text Add to dashboard Cite

Acute liver failure (ALF) is a life-threatening injury that is most often caused by drug-induced injury, including acetaminophen overdose, in the United States. The hallmarks of ALF are hepatic encephalopathy and coagulopathy in a patient without an established history of liver disease. While acetaminophen overdose has an antidote, that is N-acetylcysteine (NAC), when given acutely, most other causes of hepatic failure require an urgent liver transplant. In this paper, we report a case of cocaine-induced acute liver failure that was reversed with the administration of NAC. Our case began when a middle-aged male presented to the emergency department complaining of nausea, vomiting, fatigue, and confusion for the past three days. His past medical history was pertinent for a history of opioid use disorder and his physical exam was remarkable for somnolence, asterixis, and periumbilical ecchymoses. His initial lab results showed markedly elevated liver function tests, prolonged coagulation studies, and a urine drug screen that was positive for cocaine. During the patient’s interview, his vital signs became unstable. He was intubated for airway protection and transferred to a tertiary care facility for liver transplant evaluation with the diagnosis of cocaine-induced acute liver failure. There he received NAC, lactulose, rifaximin, and vasopressors. On day two of treatment, his clinical condition greatly improved, and he was extubated. He continued to receive NAC until day five when his liver function tests and coagulopathy improved enough to stop treatment. This case report highlights the clinical benefit of NAC in a case of cocaine-induced acute liver failure, improving the patient’s survival and eliminating his need for a liver transplant.

show abstract

Section: Discussionmentioning

confidence: 99%

A Case of Cocaine-Induced Acute Liver Failure Reversed With N-Acetylcysteine

Mitchell¹,

Rogers²

2023

Cureus

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%

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

“…Together, these findings give pertinence to further research relating to the long‐term damage that cocaine induces in organ systems involved in detoxification. Though there have been clinical reports relating to cocaine‐induced hepatoxicity such as Adedinsewo, Ajao, Okpobrisi, Fotzeu, and Crawford (), a limitation exists in research relating to the molecular mechanisms driving its pathological significance that concentrate on the cell cytoskeleton in the hepatic microenvironment. Research suggests that cocaine may be able to mediate HSC activation through several well‐known pro‐fibrotic mediators such as PDGF and TGF‐β.…”

Section: Future Perspectivementioning

confidence: 99%

Cocaine addicted to cytoskeletal change and a fibrosis high

et al. 2019

View full text Add to dashboard Cite

Cocaine is one of the most widely abused illicit drugs due to its euphoric and addictive properties. Cocaine‐mediated cognitive impairments are the result of dynamic cytoskeletal rearrangements involved in mediating structural and behavioural plasticity. Cytoskeletal changes initiated following cocaine abuse are regulated by the Rho family of GTPases with significant downstream activity in key actin binding proteins. Moreover, signalling via the endoplasmic reticulum chaperone protein, sigma‐1 receptor has highlighted the possibility of cocaine regulated pathology in other organ systems. However, the question of whether upstream stimulation of such a high affinity binding receptor is directly involved in cocaine‐mediated cytoskeletal changes at present remains unknown. In this review, we describe the functional role of key cytoskeletal regulators in response to cocaine‐induced signalling cues. In addition, we ascertain the extent of whether global cytoskeletal modulators involved in cocaine‐induced neurological stimulation can be used as a platform for future studies into elucidating its fibrotic potential within the hepatic microenvironment. A focus on aspects still poorly understood relating to the nonneuronal pathological impact of cocaine is discussed in the sphere of hepatic dysregulation. Lastly, we suggest that cocaine may mediate its pathological capacity via the sigma1 receptor in regulating hepatoxicity, hepatic stellate cells activity, cytoskeletal dynamics, and the transcriptional regulation of key hepato‐fibrogenic modulators.

show abstract

Acute cocaine-induced hepatotoxicity with features of shock liver

Cited by 4 publications

References 14 publications

A Case of Cocaine-Induced Acute Liver Failure Reversed With N-Acetylcysteine

A Case of Cocaine-Induced Acute Liver Failure Reversed With N-Acetylcysteine

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

Cocaine addicted to cytoskeletal change and a fibrosis high

Contact Info

Product

Resources

About