Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hepatic Drug Excretion: Influencing Factors01:16

Hepatic Drug Excretion: Influencing Factors

The biliary system of the liver, crucial for bile secretion and drug excretion, comprises intrahepatic bile ducts that merge to form the common hepatic duct. This duct, carrying hepatic bile, combines with the cystic duct, draining the gallbladder and forming the common bile duct, which empties into the duodenum. Bile, produced by hepatic cells lining the bile canaliculi, is composed primarily of water, bile salts, pigments, electrolytes, and lesser amounts of cholesterol and fatty acids. Bile...
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess the...
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Beclin 1 mRNA strongly correlates with Bcl-XLmRNA expression in human hepatocellular carcinoma.

Cancer investigation·2007
Same author

Validation and comparison of indexes for fibrosis and cirrhosis prediction in chronic hepatitis C patients: proposal for a pragmatic approach classification without liver biopsies.

Journal of viral hepatitis·2006
Same author

Human pancreatic mucinous cystadenoma is characterized by distinct mucin, cytokeratin and CD10 expression compared with intraductal papillary-mucinous adenoma.

Histopathology·2006
Same author

Multiple mixed adenoma-focal nodular hyperplasia of the liver associated with spontaneous intrahepatic porto-systemic shunt: a new type of vascular malformation associated with the multiple focal nodular hyperplasia syndrome?

Histopathology·2006
Same author

Interferon-alpha suppresses liver cell proliferation in patients with chronic hepatitis C virus infection.

Journal of viral hepatitis·2005
Same author

Safety and efficacy of peginterferon plus ribavirin in patients with chronic hepatitis C and bridging fibrosis or cirrhosis.

Journal of viral hepatitis·2005

Related Experiment Video

Updated: Jul 11, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
09:03

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Published on: February 3, 2012

Pirprofen-induced fulminant hepatitis.

G Danan, P Trunet, J Bernuau

    Gastroenterology
    |July 1, 1985
    PubMed
    Summary

    Fulminant hepatitis, a severe liver condition, was observed in two patients after prolonged use of pirprofen, a nonsteroidal anti-inflammatory drug. Early monitoring of liver enzymes is recommended for patients on long-term pirprofen therapy.

    More Related Videos

    Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms
    11:36

    Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms

    Published on: May 29, 2020

    Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
    09:44

    Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

    Published on: November 27, 2019

    Related Experiment Videos

    Last Updated: Jul 11, 2026

    The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
    09:03

    The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

    Published on: February 3, 2012

    Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms
    11:36

    Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms

    Published on: May 29, 2020

    Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
    09:44

    Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

    Published on: November 27, 2019

    Area of Science:

    • Hepatology
    • Clinical Pharmacology
    • Toxicology

    Background:

    • Pirprofen is a novel nonsteroidal anti-inflammatory drug (NSAID).
    • Drug-induced liver injury (DILI) is a significant concern with NSAIDs.
    • Fulminant hepatitis is a rare but life-threatening form of DILI.

    Observation:

    • Two female patients, aged 69 and 61, developed fulminant hepatitis after 7 and 9 months of pirprofen use, respectively.
    • Hepatitis onset was not associated with hypersensitivity reactions.
    • Liver pathology revealed massive centrilobular hepatic cell necrosis and microvesicular steatosis.

    Findings:

    • Pirprofen can induce severe hepatotoxicity, including fulminant hepatitis.
    • The liver injury pattern includes extensive hepatocellular necrosis and microvesicular steatosis.
    • One patient succumbed to liver failure, highlighting the potential lethality of this adverse reaction.

    Implications:

    • Clinicians should consider pirprofen-induced hepatitis in patients presenting with acute liver failure.
    • Monitoring of serum aminotransferase levels is crucial for patients on pirprofen for over two months.
    • Prompt drug discontinuation upon detecting elevated liver enzymes may prevent severe outcomes.