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)

A 57-yr-old female with no previous history of liver disease was exposed to enflurane during three separate surgeries over a 12-mo period. After the second and third exposures, she developed systemic symptoms and abnormal liver tests similar to those seen in halothane hepatitis. A liver biopsy obtained after the third exposure was compatible with drug-induced hepatitis. This is the first reported case of enflurane-associated hepatitis.
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PMID:Enflurane-associated hepatitis. 738 Feb 8

Circulating immune complexes have been described in viral hepatitis and primary biliary cirrhosis but their significance is unclear. Seventy-three patients with acute and chronic liver diseases were evaluated to determine the specificity of immune complex detection for a given liver disease. Immune complexes were measured by the fluid- and solid-phase Clq-binding assays. They were demonstrated frequently in all patients with liver disease, including those with viral hepatitis, alcoholic cirrhosis, chronic active and persistent hepatitis, drug-induced hepatitis and hepatic metastases. The presence of immune complexes was not specific for a given type of liver disease and did not correlate with hepatic dysfunction. We conclude that the detection of immune complexes is of no apparent diagnostic use in liver disease. Further evaluation of the antigen-antibody composition would be required to determine any pathogenic significance of the detected circulating immune complexes.
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PMID:Non-specificity of circulating immune complexes in patients with acute and chronic liver disease. 743 39

In the light of three deaths due to liver failure secondary to anti-tuberculosis therapy at the Royal Free Hospital, we have reviewed the current literature, and asked--How common is liver dysfunction with anti-tuberculosis medications and how might it be prevented? Anti-tuberculosis chemotherapy is associated with abnormalities in liver function tests in 10-25% of patients. Clinical hepatitis develops in about 3%, though estimates vary, and in these patients there is likely to be significant morbidity and mortality. On the basis of reported cases of tuberculosis, 160 patients in England and Wales can be expected to develop drug-induced hepatitis due to anti-tuberculosis therapy each year. There are published guidelines from the British and American Thoracic Societies regarding the choice of drug therapy for tuberculosis. Current recommendations with regard to monitoring liver function, and what to do when these tests become abnormal, vary considerably. We suggest a protocol for using liver function tests to monitor for liver damage, and give recommendations on what action to take when these become abnormal.
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PMID:Anti-tuberculosis medication and the liver: dangers and recommendations in management. 877 84

In three alcoholic patients, two men aged 30 and 42, and a woman aged 52, hepatitis was diagnosed after the use of disulfiram. In all cases, there was a close temporal relationship between the occurrence of symptoms and disulfiram intake. Other possible causes were excluded. The 30-year-old man died from liver damage. Biopsy showed massive hepatic necrosis without signs of alcoholic hepatitis. In the other patients, symptoms subsided quickly and liver function returned to normal after discontinuation of disulfiram, but there was no confirmation by biopsy. The possibility of drug-induced hepatitis should always be considered in an alcoholic patient treated with disulfiram.
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PMID:[Liver damage attributed to the use of disulfiram]. 750 Oct 79

Drug hepatotoxicity is partially determined by genetic factors involved in drug metabolism, which may involve the debrisoquine oxidation polymorphism mediated by cytochrome (CYP) 2D6. The purpose of this study was to assess the relationship between drug hepatotoxicity and another genetic polymorphism of drug oxidation, namely that of S-mephenytoin metabolism mediated by CYP2CMP. Mephenytoin hydroxylation capacity was assessed by a hydroxylation index in 24 patients with drug-induced hepatitis and in 23 healthy controls. Hydroxylation index was calculated as the ratio of S-mephenytoin dose to the (0-10 h) urinary excretion of 4-hydroxymephenytoin after oral administration of 100 mg racemic mephenytoin. The test was performed following the patient's recovery. In three patients, hepatitis was related to Atrium, a drug containing phenobarbital, febarbamate and difebarbamate. The mean hydroxylation index (+/- SD) value in patients with Atrium hepatitis (12.4 +/- 8.3) was markedly higher than that found in healthy controls (1.8 +/- 0.4) or in patients with other drug-induced hepatitis (2.5 +/- 3.3). Mean hydroxylation index values were similar in the two latter groups. Considered individually, oxidation capacity was low (hydroxylation index > 9) in two of the three patients with Atrium hepatitis and intermediate (hydroxylation index between 4 and 9) in the third patient. In contrast, all 23 healthy subjects exhibited a high oxidation capacity (hydroxylation index < 4). In the 21 patients with other drug-induced hepatitis, oxidation capacity was high in 19 subjects, intermediate in one subject with chlorpromazine hepatitis, and low in one subject with dapsone hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible association between poor metabolism of mephenytoin and hepatotoxicity caused by Atrium, a fixed combination preparation containing phenobarbital, febarbamate and difebarbamate. 769 30

Possible associations between particular human leucocyte antigen molecules and immunoallergic hepatitis have been suggested previously (HLA-A11 in halothane hepatitis, HLA-DR6 and DR2 in nitrofurantoin hepatitis, HLA-B8 in clometacin hepatitis). In this study the HLA haplotype was determined in 71 patients with idiosyncratic hepatitis due to different drugs. The prevalence of HLA-A11 was twice as high in the 71 patients in the study (23%) as in controls (12%), but p-values were not significant when corrections were made for the large number of comparisons (n = 39). The prevalences of HLA-DR2, DR6, and B8 were similar in the 71 patients and in controls. When hepatitis due to particular drugs was considered, HLA-A11 was found to be present in six of 12 patients (50%) with hepatitis caused by tricyclic antidepressants, and three of four patients (75%) with diclofenac hepatitis, compared to 12% in controls. HLA-DR6 was present in four of five patients (80%) with chlorpromazine hepatitis, compared to 22% in controls. In conclusion, the HLA phenotype does not contribute significantly to idiosyncratic drug-induced hepatitis considered collectively. Possible associations between some HLA molecules and the hepatotoxicity of certain drugs require further confirmation.
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PMID:Possible role of HLA in hepatotoxicity. An exploratory study in 71 patients with drug-induced idiosyncratic hepatitis. 801 43

A 52-year-old female was hospitalized with malaise, pruritus, jaundice, abdominal discomfort and vomiting. For 20 weeks she had been taking enalapril (Reniten) for hypertension. Serum aminotransferases and bilirubin were highly elevated with prolonged thromboplastin time. There was no evidence for extrahepatic cholestasis in ultrasonography. Serological investigations for a viral etiology of the liver failure were negative and the patient had no risk factors for viral hepatitis or exposure to hepatotoxic substances. Liver puncture revealed hepatitis of the fulminant viral hepatitis type, a picture that can be seen in a drug-induced hepatitis. The complete recovery of liver function after cessation of enalapril administration suggests acute toxic hepatitis due to enalapril. A metabolically mediated idiosyncratic reaction is the most plausible. Potential mechanisms of enalapril-induced hepatotoxicity are discussed and the current literature is surveyed.
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PMID:[Enalapril (Reniten)-associated toxic hepatitis]. 806 14

Drug-induced hepatitis can be caused by an abnormal immunological response. In the case of tienilic acid- and dihydralazine-induced hepatitis, we postulated a scheme in which a P450 produced a reactive metabolite (step 1); this reactive metabolite bound to the P450 producing it (step 2) leading to a neoantigen triggering the immune response (step 3); the autoantibodies produced during the immune response recognized the P450 producing the reactive metabolite (step 4). The use of microorganisms (yeast or bacteria) expressing cloned human P450 helped in proving some steps of this postulated scheme, particularly steps 1 and 4.
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PMID:Immunotoxicology and expression of human cytochrome P450 in microorganisms. 823 81

Anti-mitochondria (anti-M6) autoantibodies have been found in the serum of patients with immunoallergic iproniazid (Marsilid)-induced hepatitis, but to date the identity of the protein antigen has not been determined. Here we show, using immunoprecipitation of pargyline-labelled proteins, that among the mitochondrial proteins, liver MAO-B is specifically recognized by the sera containing anti-M6 antibodies. Moreover the enzymatic activity of MAO-B towards phenylethylamine and tyramine is also suppressed after this immunoprecipitation, contrary to the MAO-A activity towards 5-hydroxy-tryptamine. As MAO is irreversibly inhibited by iproniazid, these results suggest that the mechanism of iproniazid-induced appearance of anti-M6 antibodies could be another example of the reactive metabolite/enzyme haptenization mechanism already proposed in the case of tienilic acid for the appearance of anti-organelle antibodies in a drug-induced hepatitis.
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PMID:Human anti-mitochondria autoantibodies appearing in iproniazid-induced immunoallergic hepatitis recognize human liver monoamine oxidase B. 857 15

Two cases of unusual extrapulmonary tuberculosis are presented. One patient was suffering of a pulmonary tuberculosis involving the brain, liver, spleen and peritoneum, with headaches, ascites, weight loss and night sweats. The other patient had lymph nodes and nodular liver tuberculosis and complained of fever, right upper quadrant pain, anorexia and weight loss. This tuberculosis form is extremely rare; only 23 cases were reported between 1950 and 1990. Furthermore, a drug-induced hepatitis developed in a liver already damaged by the tuberculosis and a chronic active C hepatitis. These two cases remind us that the diagnosis of extrapulmonary tuberculosis may be extremely difficult. It must be suspected mostly in patients that are immuno-depressed or whose origins are not caucasian. Other diagnoses are often wrongly suggested, such as tumors, inflammatory diseases or other infectious diseases. As a result, the correct diagnosis or other infectious diseases. As a result, the correct diagnosis is often delayed. If cultures are negative and the chest roentgenogram is normal, procedures such as transbronchial, liver, bone marrow or lymph node biopsies may help to properly identify the disease.
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PMID:[Extrapulmonary tuberculosis: 2 cases with hepatic, splenic, peritoneal and cerebral involvement]. 869 77


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