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)

Hycanthone was given to 15 patients with metastatic cancer in order to determine the maximum tolerable dose. The drug was administered in 5-day courses at 3-week intervals. The starting dose was 30 mg/m2/day and the highest dose level reached was 90 mg/m2/day. The most common (13 patients) side effect was nausea and/or vomiting. The dose-limiting toxicity was toxic hepatitis manifested as elevation in serum transaminases in eight of 15 patients and an increase in serum bilirubin in three patients. Hepatotoxicity was dose-related and was observed in two of 25 courses given at the dose level of less than or equal to 70 mg/m2 compared to seven of nine courses given at the dose level of greater than or equal to 80 mg/m2. Because of an unacceptable incidence of hepatotoxicity at higher doses, 70 mg/m2/day x 5 appears to be a safe dose for phase II studies.
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PMID:Phase I study of hycanthone. 35 76

One hundred and twenty-nine Chinese patients with aplastic anaemia, were studied. In ten it was induced by drugs, one followed hepatitis and the remainder were of unkown cause. Mortality within the first six months was 47.3 per cent. Features associated with poor prognosis included a short duration of symptoms of three months or less, neutropenia of less than 0.5 x 10(9)/l and severe thrombocytopenia. On the other hand, some preservation of erythroid activity of the bone marrow was associated with long survival. Remission occurred in 47 patients and this was associated with androgen therapy in 33. Remission was complete in 18 and partial in 29. In the latter group, persistent thrombocytopenia was the main abnormality and treatment with calusterone led to an increase in platelets although the effect was not sustained after its withdrawal. Hepatotoxicity was seen in 16.0 per cent of patients treated with androgens and this occurred even with non-17alpha-alkylated compounds. It is concluded that androgen therapy was useful and should be started as early as possible after diagnosis. Hepatic intolerance to androgens may be an indication for bone marrow transplantation.
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PMID:Aplastic anaemia: a study of prognosis and the effect of androgen therapy. 59

Hepatotoxicity associated with intravenous sodium oxacillin therapy is reported in two drug abusers cured of staphylococcal endocarditis. Coincident with the administration of oxacillin, marked increases in hepatic transaminase were observed and liver biopsy showed nonspecific hepatitis. Upon cessation of oxacillin therapy, liver enzyme values returned to(ward) normal. Reports of oxacillin-associated changes in hepatic enzyme levels are reviewed; further observation of oxacillin-associated hepatotoxicity is warranted.
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PMID:Oxacillin hepatitis. Two patients with liver biopsy, and review of the literature. 63 61

Hepatotoxicity to different combinations of anti-tuberculosis drugs containing, Rifampicin (R), Streptomycin (S), Isoniazid (H), Pyrazinamide (Z) and Myambutol (E) is described in 47 patients who completed 6 to 9 months therapy. Seven cases (15%) showed signs of toxicity and in 4 patients (8.5%) the drugs had to be withdrawn. Two patients developed hepatitis, one with jaundice and the other with fever and deranged liver functions, while others 2 developed severe hypersensitivity reactions. Burning palms, difficulty in micturition, itching and giddiness were complained of by one patient each, which settled in due course without recourse to withdrawal of drugs.
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PMID:Hepatotoxicity to different antituberculosis drug combinations. 212 69

Diclofenac is a widely used non-steroidal anti-inflammatory drug, being the most commonly prescribed of its kind in the world. This paper describes five cases of hepatitis with clinical features indicating a direct link with diclofenac. All the patients presented with an acute hepatitis, three being jaundiced. They gave a history of taking diclofenac up to the time of presentation, four of the five having started the drug within the previous 3 months. There were no other features in the histories to suggest alternative causes for the liver dysfunction. Liver function tests were grossly abnormal in all cases, showing a hepatitic picture. A liver biopsy was performed in 4 cases, and showed features of an acute hepatitis with inflammation and hepatocyte damage dominating. The liver dysfunction returned to normal on drug withdrawal in four of the five cases, with full recovery by 3 months. One patient developed steroid-responsive chronic active hepatitis. Hepatotoxicity associated with diclofenac is documented, but previously only a few isolated cases have been described. The occurrence of five cases in one gastroenterology unit over a 12-month period suggests that hepatitis associated with diclofenac may be commoner than previously supposed.
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PMID:Diclofenac associated hepatitis. 230 31

The extended prescription of non-steroidal anti-inflammatory drugs in medical practice involve numerous adverse effects. Among them, hepatic injuries, rather uncommon, are very diverse with regard to clinical type and evolution scheme, according to the derivatives used. Salicylates, when taken at high doses, increase serum transaminases, mostly without overt clinical symptoms. Phenylbutazone is obviously hepatotoxic: it induces cytolytic hepatitis, in some cases with fatal issue. Among the indole derivatives, indometacine was involved, especially in children; mixed hepatitis have been noted during sulindac therapy, mostly with favourable outcome. In the group of propionic acid derivatives, ibuprofen, pirprofen and naproxen have been implicated in hepatitis of various types; ibufenac and benoxaprofen were quickly retired after occasioning several deaths. Concerning others non-steroidal anti-inflammatory drugs, some cases have been reported with piroxicam and diclofenac. Hepatotoxicity mechanisms are often unknown; they appear different according to each drug. Besides, the rheumatic disease under treatment and pharmacokinetic particularities (sulindac, diclofenac) might be important in this view. Monitoring of serum hepatic-enzyme concentrations seems recommended for patients receiving non-steroidal anti-inflammatory for long time therapy.
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PMID:[Hepatitis due to nonsteroidal anti-inflammatory agents]. 332 27

Hepatotoxicity has been recently described as a rare complication of sulfasalazine therapy. Two patients with hepatic damage after sulfasalazine treatment are reported. Liver biopsy performed in one patient revealed granulomatous hepatitis. On rechallenge with 5 aminosalicylic acid enema the second patient developed a hypersensitivity reaction without hepatic involvement.
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PMID:Sulfasalazine hepatotoxicity. 614 68

A 13% incidence of hepatitis was observed among 54 cases of multibacillary leprosy treated daily with the three-drug combination of dapsone, rifampin, and a thioamide (ethionamide or prothionamide). No hepatitis was observed among 109 cases of paucibacillary leprosy treated daily with the two-drug combination of dapsone and rifampin. Symptoms were jaundice in five cases and nausea plus vomiting associated with a significant increase of transaminase levels in two cases. In five cases, the symptoms appeared during the first two months of therapy and in two cases, later. Discontinuing treatment with rifampin and the thioamide but not dapsone resulted in recovery. When rifampin was resumed without the thioamide, the hepatitis did not recur. Viral etiology could be eliminated in six cases. Neither sex, age, weight nor the fact that the patient was a new case or a relapse case appeared to be a contributing factor. Hepatotoxicity caused by administration of a thioamide might have been potentiated by the concurrent administration of rifampin.
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PMID:Hepatitis in leprosy patients treated by a daily combination of dapsone, rifampin, and a thioamide. 668 70

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

Liver function was studied primarily by determination of serum gamma glutamyl transferase and alkaline phosphatase. In subsamples of patients the investigation was extended by determination of serum amino-transferases, isoenzyme analysis of alkaline phosphatase, 99mtechnetium scintigraphy, and liver biopsy. In 183 in-patients with rheumatoid arthritis, the serum gamma glutamyl transferase level was elevated in 47% and serum alkaline phosphatase (of liver origin) in 24%. A concomitant increase in serum aminotransferases was found in 15% of patients with elevated gamma glutamyl transferase level. A closely similar pattern was found in 45 patients with non-rheumatoid arthritis (ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and undefined arthritis), and in 5 patients with polymyalgia rheumatica. In 23 patients with non-rheumatic inflammation (pneumonia), liver dysfunction was common, though the pattern of serum enzyme changes was different. In rheumatoid arthritis, liver scanning showed irregular or low uptake, but biopsy only indicated reactive hepatitis. Hepatotoxicity could not be traced to any single drug or combination of drugs given. On the contrary, chloroquine appeared to reduce serum gamma glutamyl transferase, and corticosteroids had a similar effect on serum alkaline phosphatase. In patients not treated with corticosteroids, both serum gamma glutamyl transferase and alkaline phosphatase were weakly to moderately correlated with laboratory indices of disease activity (ESR and serum orosomucoid). The frequently occurring isolated increase of serum gamma glutamyl transferase and/or serum alkaline phosphatase in arthritis may be an unspecific reaction to inflammation.
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PMID:Liver function in some common rheumatic disorders. 743 28


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