Disease relevance of Hepatitis, Toxic

• We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine [1].
• A single injection of D-galactosamine hydrochloride induces acute self-limiting liver disease in rats that morphologically resembles drug-induced hepatitis in human beings [2].
• Antibodies were also present in patients with hepatitis C virus (HCV)-related HCC, but rarely detected in sera from uninfected individuals, those with tumors other than HCC, or those with drug-induced hepatitis [3].
• Rapid progression to liver cirrhosis of toxic hepatitis due to ebrotidine [4].
• Toxic polyneuritis and toxic hepatitis related to long-term perhexiline maleate therapy [5].

High impact information on Hepatitis, Toxic

• Rechallenge with crystalline niacin after drug-induced hepatitis from sustained-release niacin [6].
• Thus, a new example is presented in which a cytochrome P-450 may be a target for autoantibodies in drug-induced hepatitis [7].
• Icteric toxic hepatitis associated with riluzole [8].
• Drug-induced hepatitis and lymphocyte transformation test in presence of prostaglandin inhibitor [9].
• Toxic hepatitis after therapeutic doses of benorylate and D-penicillamine [10].

Chemical compound and disease context of Hepatitis, Toxic

• We describe three cases of toxic hepatitis associated with the chronic ingestion of excessive doses of acetaminophen [11].
• Most cases with antituberculosis drug-induced hepatitis have been attributed to isoniazid [12].
• The third group included drug-induced hepatitis with special antibody:iproniazid-induced hepatitis with antimitochondrial antibody 6 and tienilic acid (ticrynafen)-induced hepatitis with antiliver/kidney microsome antibody 2 (anti-LKM2) [13].
• In drug-induced hepatitis caused by another heterogenous group of drugs, including clometacin, fenofibrate, oxyphenisatin and papaverine, antismooth muscle, antinucleus and antimitochondria antibodies were found in isolation or in different combinations in 70% of cases [13].
• In drug-induced hepatitis caused by a heterogenous group of drugs consisting of ajmaline, aminopterine, isaxonine, isoniazid, perhexiline, phenylbutazone and troleandromycine, antiorganelle antibodies were absent or rare [13].

Biological context of Hepatitis, Toxic

• A study from five hepatology units documenting 157 cases of drug-induced hepatitis and a second study from a laboratory of immunology which tested more than 100,000 sera permitted us to establish the frequency of antiorganelle antibodies and their diagnostic value in drug-induced hepatitis [13].
• Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis [12].
• The results obtained in the present study indicate that the protective effects of S. polycystum extract may be due to the presence of some active compounds that are inhibitory against the free radicals generated during lipid peroxidation in acetaminophen induced toxic hepatitis [14].
• Because the metabolism of rifampin is independent of the acetylation process, rifampin and isoniazid in combination seem to cause a toxic hepatitis that differs from the hepatitis induced by either drug separately [15].
• The objective of this work was to study the gastric emptying (GE) of liquids in fasted and sucrose-fed rats with toxic hepatitis induced by acetaminophen [16].

Anatomical context of Hepatitis, Toxic

• Plasma membrane cytochromes P450 as neoantigens and autoimmune targets in drug-induced hepatitis [17].

Gene context of Hepatitis, Toxic

• To determine whether acetylator status is a risk factor for antituberculosis drug-induced hepatitis, we genotyped NAT2 in 224 incident tuberculosis patients who received antituberculosis treatment [18].
• This epitope is homologous to three-dimensional epitopes detected by autoantibodies directed against hepatic cytochromes P450s in drug induced hepatitis and to an autoepitope on CYP21B associated with adrenal failure [19].
• Serum cobalt-activated acylase and gamma-glutamyl transpeptidase activities in toxic hepatitis [20].
• Dystonia and drug-induced hepatitis in a patient treated with clozapine [21].
• CONCLUSIONS: Famotidine can cause clinical hepatitis, and drug-induced hepatitis can occur after the administration of two different H2-receptor blockers [22].

Analytical, diagnostic and therapeutic context of Hepatitis, Toxic

• The prior oral administration of S. polycystum alcoholic extract showed significant diminution in the severity of toxic hepatitis in acetaminophen-induced rats by maintaining the activities of tricarboxylic acid enzymes with concomitant improvement in the hepatic mitochondrial antiperoxidative status when compared with intoxicated animals [14].
• Dramatic increase in bilirubin after ERCP - pethidine as a possible cause of drug-induced hepatitis [23].

References