Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a patient who developed sulphasalazine-related hepatitis with a subsequent adverse reaction to rectal 5-amino salicylic acid, in the form of pain and fever without associated liver dysfunction, suggesting reactions to both components of sulphasalazine. Included is a review of the literature. Caution should be observed when prescribing 5-amino salicylic acid to sulphasalazine-intolerant patients.
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PMID:Adverse reactions to sulphasalazine and 5-amino salicylic acid in the same patient. 290 50

Serious hepatotoxicity is uncommon with the proper therapeutic use of non-narcotic analgesics but experience with new non-steroidal anti-inflammatory drugs (NSAIDs) is limited. Drugs such as ibufenac, fenclofenac and benoxaprofen were withdrawn from the market because of hepatotoxicity, and liver damage has been reported on occasion with virtually all non-narcotic analgesics. However, a clear pattern of toxicity with characteristic clinical, biochemical and histopathological abnormalities has emerged with relatively few. With the exception of acute hepatic necrosis following overdosage of paracetamol, little is known of the mechanisms of liver injury induced by non-narcotic analgesics. Involvement of the liver in a generalised drug reaction does not imply specific hepatotoxicity. About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity. Liver damage is more severe in a small minority and it may rarely be complicated by disseminated intravascular coagulation and encephalopathy with a fatal outcome. There have also been isolated reports of chronic active hepatitis associated with the use of salicylates. Salicylate hepatitis has been reported most often in young females with connective tissue diseases. Many patients with Reye's syndrome have been given aspirin during the prodromal phase, and this serious condition closely resembles subacute salicylate intoxication in children. Salicylate probably has a causal or contributory role in Reye's syndrome, but many refuse to accept this and the issue is the subject of heated debate. Paracetamol in overdosage causes acute hepatic necrosis, and liver damage has been attributed to its therapeutic use. However, most reports have involved chronic alcoholics who took excessive doses and in these patients the clinical, biochemical and pathological findings were typical of paracetamol overdosage. Many authors have failed to make the distinction between therapeutic use and a therapeutic dose. In other cases liver damage could have been caused by exposure to other agents, viral infection or naturally occurring liver disease. If these cases are excluded, there are very few reports of liver damage associated with the proper therapeutic use of paracetamol. In some cases, the picture resembled chronic active hepatitis but no causal relationship has been established between this condition and paracetamol use. Paracetamol does not cause deterioration in liver function in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of non-narcotic analgesics on the liver. 355 80

Since 1973, when the incidence and pattern of adverse reactions to antituberculosis therapy were described by Rossouw and Saunders, para-amino-salicylic acid, the major cause of drug-induced hepatitis, has been withdrawn from the regimen used in Cape Town and replaced with pyrazinamide (PZA). Our study in the same hospital indicates that although the substitution has resulted in a significant reduction in the incidence of all side-effects (4,1% v. 9%; P less than 0,001), the incidence of hepatitis is unchanged (0,3%). PZA is currently the major cause of hepatitis associated with antituberculosis therapy.
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PMID:Hepatic complications of antituberculosis therapy revisited. 685 25

1 Hepatotoxicity is rare when mild analgesics are used in normal therapeutic doses. 2 The potential of aspirin and salicylates to cause hepatotoxicity has been only recently recognized. 3 Salicylate hepatitis is often asymptomatic, and may only be revealed by finding elevated levels of aminotransferases. 4 Most cases have occurred in children or young adults with connective tissue diseases, who take high doses of salicylates for long periods. 5 Hepatic injury is not recognized as a complication of acute aspirin poisoning. 6 Following overdosage of paracetamol, a toxic intermediate metabolite causes acute hepatic necrosis which may be fatal. 7 Cysteamine, methionine and N-acetylcysteine confer protection against this severe liver damage, but the time between overdosage and treatment is critical. 8 The chronic therapeutic use of paracetamol should be considered a potential but very rare cause of active chronic hepatitis. 9 There is no clear evidence of phenacetin hepatotoxicity in man. 10 Phenylbutazone may cause liver injury and other analgesics can cause hypersensitivity reactions in which the liver is involved.
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PMID:Hepatotoxicity of mild analgesics. 700 91

Salicylate-kodein is a widely used analgesic agent, particularly in outpatient practice. Salicylates have been incriminated in hepatic injury while kodein may induce biliary spasm. We report here a case of granulomatous hepatitis attributed to prolonged intake of this combination, which has never been reported previously to our knowledge.
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PMID:Granulomatous hepatitis induced by aspirin-kodein analgesics. 877 29

The Long-Evans Cinnamon (LEC) rats accumulate excess copper (Cu) in the liver in a manner similar to patients with Wilson's disease (WD) and spontaneously develop acute hepatitis with severe jaundice. Although hydroxyl radicals (*OH) have been proposed to be a cause of hepatitis by the accumulation of Cu, it is not clear whether or not *OH can be produced in the liver of hepatitic LEC rats in vivo and also can be involved in the onset of hepatitis. In the present study, *OH production in plasma and liver of hepatitic LEC rats was quantified by trapping *OH with salicylic acid (SA) as 2, 3-dihydroxybenzoic acid (2, 3-DHBA). The ratios of 2, 3-DHBA/SA were significantly higher in plasma and liver of hepatitic LEC rats than those of Wistar rats and LEC rats showing no signs of hepatitis. Furthermore, the ratios of 2, 3-DHBA/SA in plasma and liver of hepatitic LEC rats were almost the same as those of Wistar rats treated orally with CuSO(4) (0.5 mmol/kg) 2 h before acetylsalicylic acid (ASA) injection. We also evaluated the protective effects of D-mannitol (a *OH scavenger) treatment against acute hepatitis in LEC rats. D-mannitol (500 mg/kg) was administered intraperitoneally to 10-week-old LEC rats for 3 weeks. D-mannitol treatment suppressed the increases in serum aspartate aminotransferase activity and total bilirubin concentration. In addition, D-mannitol treatment significantly reduced hepatic mitochondrial lipid peroxidation, which is thought to be important in the pathogenesis of Cu-induced hepatotoxicity. These observations suggest that accelerated generation of *OH catalyzed by free Cu in the liver may, at least in part, play a role in the pathogenesis of acute hepatitis in LEC rats.
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PMID:In vivo evidence for accelerated generation of hydroxyl radicals in liver of Long-Evans Cinnamon (LEC) rats with acute hepatitis. 1118 25

Cytomegalovirus (CMV) infection in inmunocompetent hosts generally is asymptomatic or may present as a mononucleosis syndrome but rarely can lead to severe organ complications. We report a case of simultaneous hepatic and pericardic CMV infection in a 36-year old immunocompetent man. He was admitted to coronary unit with fever, chest pain radiated to shoulders, changes on electrocardiogram with diffuse ST elevation and modest laboratory elevations in the MB fraction of creatine kinase (CK-MB) of 33.77 microg/L (0.1-6.73), serum cardiac troponin T of 0.904 ng/mL (0-0.4), creatine kinase of 454 U/L (20-195) and myoglobin of 480.4 microg/L (28-72). Routine laboratory test detected an elevation of aminotransferase level: alanine aminotransferase 1445 U/L, aspartate aminotransferase 601 U/L. We ruled out other causes of hepatitis with normal results except IgM CMV. The patient was diagnosed with myopericarditis and hepatitis caused by cytomegalovirus and started symptomatic treatment with salicylic acid. In few days the laboratory findings became normal and the patient was discharged.
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PMID:Cytomegalovirus hepatitis and myopericarditis. 1727 38