scholarly journals Gap junction inhibition prevents drug-induced liver toxicity and fulminant hepatic failure

2012 ◽  
Vol 30 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Suraj J Patel ◽  
Jack M Milwid ◽  
Kevin R King ◽  
Stefan Bohr ◽  
Arvin Iracheta-Vellve ◽  
...  
Keyword(s):  
Gap Junction ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Liver Toxicity ◽  
Drug Induced ◽  
Gap Junction Inhibition

scholarly journals Erratum: Gap junction inhibition prevents drug-induced liver toxicity and fulminant hepatic failure

2014 ◽  
Vol 32 (3) ◽  
pp. 291-291 ◽  
Author(s):  
Suraj J Patel ◽  
Jack M Milwid ◽  
Kevin R King ◽  
Stefan Bohr ◽  
Arvin Iracheta-Velle ◽  
...  
Keyword(s):  
Gap Junction ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Liver Toxicity ◽  
Drug Induced ◽  
Gap Junction Inhibition

1020 Developing a Hepatoprotective Strategy for Preventing Drug-Induced Liver Toxicity and Fulminant Hepatic Failure

2012 ◽  
Vol 142 (5) ◽  
pp. S-941
Author(s):  
Suraj J. Patel ◽  
Kevin R. King ◽  
Stefan Bohr ◽  
Martin L. Yarmush
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Liver Toxicity ◽  
Drug Induced

Oxaprozin-Induced Fulminant Hepatitis

1994 ◽  
Vol 28 (10) ◽  
pp. 1159-1161 ◽  
Author(s):  
Preston P. Purdum ◽  
Stacey L. Shelden ◽  
John W. Boyd ◽  
Mitchell L. Shiffman
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Fulminant Hepatitis ◽  
The Elderly ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Antiinflammatory Drugs ◽  
Drug Induced ◽  
Hepatic Transaminase ◽  
Long Acting ◽  
Work Up

OBJECTIVE: To report oxaprozin-induced fulminant hepatic failure. CASE SUMMARY: A 56-year-old woman was admitted with fulminant hepatic failure. Work-up for potential etiologies was negative except for the use of oxaprozin for the preceding two months. Results of premortem liver biopsy were consistent with drug-induced hepatic injury similar to that previously reported with diclofenac. DISCUSSION: Although the literature describes elevation in hepatic transaminase concentrations associated with oxaprozin, fulminant hepatic failure has not been described previously. CONCLUSIONS: Elevations in hepatic transaminase concentrations and now fulminant hepatic failure have been shown to occur with oxaprozin, as previously seen with other nonsteroidal antiinflammatory drugs (NSAIDs). Transaminitis is a known adverse effect of NSAID use, but is usually mild and reversible with discontinuation of drug. Transaminitis may be more likely to occur in the elderly, in patients receiving concurrent potentially hepatotoxic medications, and possibly with the newer long-acting NSAIDs. The existence of fulminant hepatitis, although rare, supports the need for monitoring liver function enzymes during NSAID therapy.

Levofloxacin-Induced Acute Fulminant Hepatic Failure in a Patient with Chronic Hepatitis B Infection

2005 ◽  
Vol 39 (10) ◽  
pp. 1737-1740 ◽  
Author(s):  
şahin Çoban ◽  
Bilge Ceydilek ◽  
Fuat Ekiz ◽  
Esra Erden ◽  
İrfan Soykan
Keyword(s):  
Hepatitis B ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Hepatitis B Surface Antigen ◽  
Drug Induced ◽  
Upper Respiratory Infection ◽  
Negative Results ◽  
B Virus ◽  
Short Time ◽  
The Relationship

OBJECTIVE: To report a case of possible levofloxacin-induced acute fulminant hepatic failure. CASE SUMMARY: An unconscious 55-year-old woman was hospitalized with the diagnosis of hepatic encephalopathy. The patient had received levofloxacin 500 mg daily for 10 days because of an upper respiratory infection. Her past medical history revealed hepatitis B surface antigen positivity as an asymptomatic hepatitis B virus carrier for 10 years. After hospitalization, treatment included plasmapheresis and supportive care. The patient's consciousness improved on the second day of treatment. Other etiologies of fulminant hepatic failure were ruled out, suggesting levofloxacin-induced fulminant hepatic failure. Although the patient received supportive treatment, her condition gradually deteriorated and she died 12 weeks after admission to our hospital. An objective causality assessment revealed that the adverse event was possibly related to levofloxacin. DISCUSSION: Levofloxacin is widely used because of its broad spectrum of antimicrobial activity. As of August 9, 2005, to our knowledge, only one case of fulminant hepatic failure in relation to levofloxacin has previously been published. We believe that, in our patient, the relationship between levofloxacin and her illness is clear because of the negative results in the etiological studies, the short time between the drug's administration and the development of disease, and the pathologic findings suggestive of drug-induced hepatitis. CONCLUSIONS: Clinicians should be aware of the possibility of severe hepatic injury associated with levofloxacin when prescribing this drug.

scholarly journals Curative Effects of Thiacremonone against Acetaminophen-Induced Acute Hepatic Failure via Inhibition of Proinflammatory Cytokines Production and Infiltration of Cytotoxic Immune Cells and Kupffer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Yu Ri Kim ◽  
Nam Jin Lee ◽  
Jung Ok Ban ◽  
Hwan Soo Yoo ◽  
Yong Moon Lee ◽  
...  
Keyword(s):  
Kupffer Cells ◽  
Immune Cells ◽  
Hepatic Failure ◽  
Liver Toxicity ◽  
Cytotoxic T Cells ◽  
Metabolic Activation ◽  
Acute Hepatic Failure ◽  
Dependent Manner ◽  
Drug Induced ◽  
High Doses

High doses of acetaminophen (APAP;N-acetyl-p-aminophenol) cause severe hepatotoxicity after metabolic activation by cytochrome P450 2E1. This study was undertaken to examine the preventive effects of thiacremonone, a compound extracted from garlic, on APAP-induced acute hepatic failure in male C57BL/6J. Mice received with 500 mg/kg APAP after a 7-day pretreatment with thiacremonone (10–50 mg/kg). Thiacremonone inhibited the APAP-induced serum ALT and AST levels in a dose-dependent manner, and markedly reduced the restricted area of necrosis and inflammation by administration of APAP. Thiacremonone also inhibited the APAP-induced depletion of intracellular GSH, induction of nitric oxide, and lipid peroxidation as well as expression of P450 2E1. After APAP injection, the numbers of Kupffer cells, natural killer cells, and cytotoxic T cells were elevated, but the elevated cell numbers in the liver were reduced in thiacremonone pretreated mice. The expression levels of I-309, M-CSF, MIG, MIP-1α, MIP-1β, IL-7, and IL-17 were increased by APAP treatment, which were inhibited in thiacremonone pretreated mice. These data indicate that thiacremonone could be a useful agent for the treatment of drug-induced hepatic failure and that the reduction of cytotoxic immune cells as well as proinflammatory cytokine production may be critical for the prevention of APAP-induced acute liver toxicity.

scholarly journals Investigation of Inherited Chromosomally Integrated Human Herpesvirus-6A+ and -6B+ in a Patient with Ulipristal Acetate-Induced Fulminant Hepatic Failure

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 62
Author(s):  
Laure Izquierdo ◽  
Clémence M. Canivet ◽  
Eleonora De Martin ◽  
Teresa M. Antonini ◽  
Anne-Marie Roque-Afonso ◽  
...  
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Human Herpesvirus ◽  
Distinct Species ◽  
Mendelian Inheritance ◽  
Hair Follicles ◽  
Drug Induced ◽  
Ulipristal Acetate ◽  
Her Family ◽  
Receptor Modulator

Inherited chromosomally integrated (ici) human herpes virus 6 (HHV-6) is estimated to occur in 0.6–2.7% of people worldwide. HHV-6 comprises two distinct species: HHV-6A and HHV-6B. Both HHV-6A and HHV-6B integration have been reported. Several drugs are capable of activating iciHHV-6 in tissues, the consequences of which are poorly understood. We report herein a case of a woman with iciHHV-6A+ and iciHHV-6B+, who developed ulipristal acetate (a selective progesterone receptor modulator)-induced fulminant hepatic failure that required liver transplantation. We confirmed the presence of ~one copy per cell of both HHV-6A and HHV-6B DNA in her hair follicles using multiplex HHV-6A/B real-time PCR and demonstrated the Mendelian inheritance of both iciHHV-6A and iciHHV-6B in her family members over three generations. Because of the rarity of this presentation, we discuss herein the possible links between reactivated HHV-6 from iciHHV-6A and/or iciHHV-6B and adverse drug reactions, suggesting that iciHHV-6 could be screened before the introduction of any hepatotoxic drugs to exclude HHV-6 active disease or combined idiosyncratic drug-induced liver injury in these patients.

scholarly journals Drug-induced fulminant hepatic failure in pregnancy

2015 ◽  
Vol 8 (4) ◽  
pp. 190-192 ◽  
Author(s):  
Tabassum Firoz ◽  
Douglas Webber ◽  
Hilary Rowe
Keyword(s):  
Liver Disease ◽  
Liver Failure ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Liver Enzymes ◽  
Abnormal Liver Function ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Elevated Liver Enzymes ◽  
In Pregnancy

Liver disease in pregnancy can be classified as predating, co-incidental or unique to pregnancy. Medications are often overlooked as a significant cause of liver disease. We present the case of a 39-year-old patient who presented at 20 weeks with jaundice, elevated liver enzymes, and abnormal liver function progressing eventually to fulminant hepatic failure. The patient was on methyldopa and labetalol from 12 weeks’ gestational age. Liver biopsy was consistent with drug-induced liver injury. Both methyldopa and labetalol have been associated with hepatotoxicity including liver failure. This case highlights the importance of including medications as a cause of liver failure in pregnant patients.

Non-paracetamol drug-induced fulminant hepatic failure among adults in Scotland

2005 ◽  
Vol 17 (2) ◽  
pp. 161-167 ◽  
Author(s):  
Innes D.M. Smith ◽  
Kenneth J. Simpson ◽  
O. James Garden ◽  
Stephen J. Wigmore
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Drug Induced
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