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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autologous bone marrow transplantation (AuBMT) is an accepted treatment modality for patients with high-risk or relapsed hematological malignancies. Hepatotoxicity, in particular veno-occlusive disease (VOD), is a significant complication of this therapy. The purpose of this study was to determine the clinical relevance of abnormal liver function in the patients who received high-dose cytotoxic therapy and AuBMT for hematological malignancies at Memorial Sloan Kettering Cancer Center. Medical records of 180 consecutive patients between 1984 and 1991 treated with cytotoxic chemotherapy and AuBMT for acute myelogenous leukemia, non-Hodgkin's lymphoma, and Hodgkin's disease were reviewed. Forty-six patients (26%) developed jaundice with bilirubin > 4 mg/dl. These patients had a 43% toxic death rate compared to an 11% toxic death rate in patients with lower bilirubins (p < 0.001). The main etiology of hyperbilirubinemia was VOD of the liver noted in 22 of the 180 patients (12%). Other etiologies of jaundice included hepatitis, sepsis with multiorgan dysfunction, cholecystitis, and recurrent disease. Hyperbilirubinemia of various etiologies is a significant complication of AuBMT. Several new strategies are under investigation to decrease the toxicity of intensive therapy.
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PMID:Abnormal liver function in patients undergoing autologous bone marrow transplantation for hematological malignancies. 762 20

Hepatotoxicity is a rare complication of coumarin anticoagulants. We present the case of a 56-year-old woman who developed a viral-hepatitis-like picture 8 months after mitral valve replacement and oral anticoagulation. Phenprocoumon-induced hepatitis was diagnosed after positive reexposure and improvement following withdrawal of the drug. There appeared to be cross-reactivity to warfarin since this drug led to a similar increase in alkaline phosphatase and gamma-glutamyl transferase after a few days of administration. Liver biopsy showed an acute viral-hepatitis-like picture. Anticoagulation was changed to a subcutaneous low molecular weight heparin and low-dose aspirin. Because of the widespread use of coumarin anticoagulants, physicians should be aware of the hepatotoxic potential of these drugs, which most frequently mimics the clinical presentation of viral hepatitis.
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PMID:Drug-induced hepatitis: a rare complication of oral anticoagulants. 783 16

Valproic acid is a useful antiepileptic drug, with occasional gastrointestinal side effects. Hepatotoxicity is the most serious adverse reaction and, although rare, it can be fatal. Risk factors for hepatotoxicity are an age of less than two years, polytherapy and mental retardation; it has been rarely reported in adults. We report three mentally retarded adult patients receiving polytherapy, who developed valproic acid induced hepatotoxicity. Two patients had a symptomatic hepatitis with a concomitant paradoxical increase in seizure frequency and one an asymptomatic alteration of hepatic function tests. After discontinuing the drug, the hepatitis subsided. We conclude that hepatotoxicity must be considered as a possible side effect of valproic acid and we suggest some recommendations for its early detection.
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PMID:[Hepatotoxicity induced by valproic acid in adults. Report of 3 cases]. 808 69

Hepatotoxicity has been reported with most of the nonsteroidal antiinflammatory drugs (NSAID). We describe four patients who presented hepatic injury after of treatment with Droxicam, a new NSAID prodrug of piroxicam. Hepatitis was attributed to Droxicam because of the absence of other etiological factors, temporal relation with drug administration, clinical, laboratory and histological picture and evolution favorable after the drug suppression. The hepatic injury was manifested as cholestasis and withdrawal of the drug was followed by biochemical and clinical improvement until the complete normalization in three of the four patients. Postmarketing surveillance is necessary in new drugs with unknown hepatotoxicity.
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PMID:[Hepatotoxicity induced by Droxicam: presentation of 4 cases]. 848 15

The therapeutic effect of most immunosuppressive agents is unspecific and therefore often limited by an increased risk of infection by viral, bacterial or fungal organisms as well as by an increased incidence of malignant neoplasms. This short review includes the most commonly used immunosuppressants such as corticosteroids, azathioprine, methotrexate, cyclophosphamide and cyclosporine. The most common risks of long-term corticosteroid treatment are Cushing-like changes, decreased glucose tolerance and the usually benign steroid diabetes. Also clinically important is osteoporosis, since it can be prevented by physical training, calcium supplementation and treatment with vitamin D if necessary. Although there is still no proof of a significantly increased risk of peptic ulcer during steroid therapy, patients may develop gastrointestinal hemorrhage and even perforation without producing pain while being treated with corticosteroids. Mineralocorticoid effects, such as salt and water retention, are seen only with hydrocortisone and prednisone, whereas with synthetic steroids such as dexamethasone, sodium retention is absent despite their strong antiphlogistic activity. The most important side effect of the cytotoxic agents azathioprine, methotrexate and cyclophosphamide is marrow suppression. Due to the high turnover of neutrophils, patients most frequently suffer neutropenia rather than thrombocytopenia or anemia. Neutropenia, as well as impaired humoral and cellular immune mechanisms, are responsible for increased susceptibility to bacterial, viral or parasitic diseases during immunosuppressive therapy. Hepatotoxicity has been reported among patients receiving azathioprine (cholestatic hepatitis) and methotrexate (elevated AST levels and, rarely, liver fibrosis or cirrhosis). Cyclophosphamide causes hemorrhagic cystitis in a substantial proportion of patients, as well as an increased incidence of urothelial neoplasms. Both these side effects may be prevented by Mesna. The most important side effects of cyclosporine are acute and chronic nephrotoxicity usually associated with significantly elevated plasma levels of the drug. It must be borne in mind that severe nephrotoxicity may occur in patients receiving cyclosporine and ketoconazole together, since the latter may inappropriately increase the plasma cyclosporine level.
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PMID:[Immunosuppression--a tightrope walk between iatrogenic harm and therapy]. 892 65

We report two patients with toxic hepatitis due to the solvent dimethylformamide (DMF). Other causes of hepatitis such as viral, drug induced or alcoholic hepatitis, could be excluded or were considered to be unlikely. Hepatotoxicity due to professional exposure to solvents e.g. dimethylformamide should be considered in any patient with unexplained hepatitis. The fast improvement of the clinical symptoms and the progressive normalisation of the liver function tests once the exposure to the product has been stopped, supports the diagnosis. Yet, non-drug induced toxic hepatitis remains an exclusion diagnosis. Therapy consists of avoiding every contact with the causative agent. Table 3 (Addendum) gives an overview of some industrial agents able to cause hepatitis.
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PMID:[Toxic hepatitis due to dimethylformamide: case reports and literature review]. 898 23

Hepatotoxicity by antituberculous drugs is well known. Nonetheless, severe liver involvement is infrequent. Several series of fulminant hepatitis by antituberculous drugs have recently been reported with a much greater frequency than previously reported. The present study describes the authors' experience which, similar to other groups, has shown a marked increase with respect to previous experience. During 1994 5 patients with acute severe hepatitis associated to antituberculous drugs were admitted to the authors' unit. The mean age of the patients was 43 years (range: 25-62). Two patients were healthy HBsAg carriers, one undergoing enzymatic inducer treatment and was anti-HIV positive. Another patient presented compensated liver cirrhosis by HCV. The 5 cases received combined isoniazid and rifampicin and four had also received pyrazinamide. Four patients presented hepatic encephalopathy. Of these cases, three could not undergo emergency liver transplantation because of contraindications and died due to complications of acute severe liver failure. Another patient evolved favorably following emergency liver transplantation. The only patient who presented good evolution with conservative treatment and who did not present hepatic encephalopathy had discontinued isoniazid because of the finding of slight hypertransaminasemia during a routine analytical control. Several risk factors have been reported for the appearance of hepatotoxicity by antituberculous drugs. The factor of greatest clinical importance for the development of severe hepatotoxicity is probably continuation of the treatment once hepatic dysfunction has initiated. The important increase in cases of severe toxicity urges the need for strict analytical monitoring following initiation of treatment.
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PMID:[Severe hepatotoxicity of tuberculostatic agents. Increase in the incidence]. 899 67

Hepatotoxicity by macrolide antibiotics, particularly erythromycin and derivatives, is a side effect extensively described in the literature. Midecamycin is a semi-synthetic derivative of this family with a wide safety margin of which isolated references of possible secondary hepatobiliary effects have been referred. The present clinical observation describes a case of cholestatic hepatitis which, in our opinion, was related to the administration of diacetyl midecamycin which evolved favorably following discontinuation of the drug. Despite its exceptional frequency and based on the wide therapeutic diffusion of this group of antibiotics, we believe this case to be of interest.
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PMID:[Cholestatic hepatitis caused by midecamycin]. 899 70

Drug-induced hepatitis is uncommon and generally unpredictable. Hepatotoxicity may be related to the drug itself, or to chemically reactive metabolites which can bind covalently to hepatic macromolecules and may lead to either idiosyncratic, toxic hepatitis or to immunoallergic hepatitis. There is now evidence indicating that genetic variations in systems of biotransformation or detoxication may modulate either the toxic or sensitizing effects of some drugs. Thus, the genetic deficiency in a particular hepatic cytochrome P 450 isozyme (CYP 2D6) is involved in per-hexiline liver injury. The deficiency in CYP 2C19 might also contribute to Atrium hepatotoxicity. Slow acetylation related to N-acetyltransferase 2 deficiency contributes to sulfonamide hepatitis. The genetic deficiency in glutathione synthetase may increase the susceptibility to several drugs including acetaminophen. A constitutional deficiency in another cell defense mechanism, still not characterized, seems to increase significantly the risk of hepatotoxicity with halothane, phenytoin, carbamazepine, phenobarbital, sulfamides and amineptine.
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PMID:Genetic predisposition to drug-induced hepatotoxicity. 920 5

Two cases of toxic hepatitis from dimethylacetamide (DMAC) occurred among 25 employees on a new acrylic-fiber production line at a western U.S. manufacturing plant. Interesting features of these cases include: 1) inadequate personal protective equipment (PPE) for dermal exposures, resulting in skin penetration during maintenance and repair procedures; 2) the subjects of these case reports are female; all workers at the manufacturer's European plant were male, and DMAC-related liver dysfunction had not been encountered at that site; 3) the new American production line required more frequent maintenance and repair work than existing production lines at the European parent company, resulting in greater opportunities for DMAC exposure. Hepatotoxicity due to dermal absorption of DMAC and other amide-type solvents deserves special consideration in industrial settings.
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PMID:Toxic Hepatitis from Dimethylacetamide. 989 Oct 94


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