Loading clinical trials...
Loading clinical trials...
Showing 1-5 of 5 trials
NCT04635111
A study to evaluate the long-term risk of hepatic failure with TURALIO™ (pexidartinib) and the mechanism of liver injury based upon optional liver biopsy information among patients who received or are receiving TURALIO™ (pexidartinib) and experience hepatotoxicity.
NCT00137059
It is widely believed that people who abuse alcohol can sustain a liver injury after taking doses of acetaminophen just above the recommended maximum dose. This study is designed to look at the interaction between acetaminophen, liver injury and alcohol abuse. Subjects will undergo baseline tests to ensure that they do not have liver damage at the time of enrollment. Each subject will be randomly assigned to receive either a therapeutic dose of acetaminophen or a placebo three times a day for four days. Subjects will have blood work drawn on a daily basis to monitor the status of the liver. These tests will include conventional markers of liver injury in addition to a novel biomarker of liver function, a-GST. Previous work in the investigators' group has shown that a-GST is a more sensitive indicator of liver injury following acetaminophen overdose (Sivilotti 1999, Sivilotti 2002 x 2). However, it has never been used to study the alcoholic population. The investigators believe that a-GST may detect a subclinical acetaminophen-induced liver injury that has previously gone unrecognized in the alcoholic population.
NCT00768716
Although acetaminophen is the most commonly used nonprescription drug in the USA, little is known regarding the influence of genes and race/ethnicity on acetaminophen disposition. The investigators long-term goal is to understand the causes of differences in acetaminophen disposition between people that are the result of genetic variation and ethnicity and may predispose individuals to a higher risk of acetaminophen hepatotoxicity. The aim of this particular study is to measure the rate of elimination of acetaminophen via the 3 main pathways (glucuronidation, sulfation and oxidation) in self-identified White-Americans (n=100) and African-Americans (n=100). These rates will then be correlated with selected genetic polymorphisms in genes encoding enzymes involved in acetaminophen metabolism. Two main hypotheses will be tested: 1. African-Americans eliminate acetaminophen more rapidly by glucuronidation than do White-Americans. 2. Elimination via glucuronidation, sulfation, and oxidation in subjects will be significantly correlated with the presence of polymorphisms in the UGT1A6, SULT1A1, and CYP2E1 genes, respectively.
NCT03602274
Paracetamol (acetaminophen, APAP) is the most commonly used antipyretic and painkiller worldwide, but also the leading cause of acute liver failure (ALF) in developed countries after supra-therapeutic doses (half overdoses being unintentional). At therapeutic doses (4g/day), up to one third of healthy volunteers develop liver test elevation and cases of ALF have been described in the presence of suggested risk factors such as malnutrition, fasting and low body weight as a result of glutathione depletion. However, no well conducted study has aimed to prospectively assess the impact of malnutrition/fasting on the toxicity to therapeutic doses of APAP. Considering the widespread use of APAP and the prevalence of malnutrition in hospitalized patients (up to 30%), it is of crucial importance to assess whether these patients are at higher risk of hepatotoxicity. It is indeed likely that cases of liver damage secondary to normal recommended dose are under-estimated in these situations as the dose is not perceived as excessive and not described as such in international guidelines for pain management. The primary objective of our project will therefore be to assess if malnutrition and fasting are risk factors for liver toxicity after therapeutic doses (4g/day) of APAP in surgery patients. The second objective will be to evaluate the pharmacokinetics of APAP and metabolites according to nutrition status in order to establish, if necessary, dose reduction guidelines. Developing and validating an early and easily accessible marker of hepatotoxicity would especially be useful in these putative higher risk and fragile populations in order to improve early detection diagnosis and allow earlier management.
NCT02076685
To improve the treatment outcome in patients with tuberculosis and integrate the pharmacogenetics into clinical practice, the information of NAT2 genotyping was used in re-challenge protocol for isoniazid (INH) titration in patients with anti-tuberculosis medication-induced hepatitis.