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)

Simvastatin, recently introduced in clinical practice for pharmacological treatment of hypercholesterolemia, has been found to cause minor and reversible elevations of serum transaminases. We report a case of acute cholestatic hepatitis during simvastatin therapy. Clinical, biochemical, immunological, and histological findings were consistent with a simvastatin-induced liver damage through an immunological-mediated mechanism. This case suggests a careful monitoring of liver function tests during simvastatin therapy, and caution in continuing simvastatin administration when elevations of serum transaminases take place.
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PMID:Acute cholestatic hepatitis during simvastatin administration. 185 44

Simvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, has been administered to approximately 2,400 patients with primary hypercholesterolemia with a mean follow-up of 1 year in controlled clinical studies and their open extensions. Approximately 10% of this population received simvastatin for a period of greater than or equal to 2 years. The population on whom this safety analysis is based had a mean age of 50 years; 62% were men and approximately 27% had preexisting coronary artery disease. Simvastatin was titrated to the maximal daily dose of 40 mg each evening in 56% of the study population (last recorded dose). The most frequently reported drug-related clinical adverse experiences were constipation (2.5%), abdominal pain (2.2%), flatulence (2.0%) and headaches (1%). Persistent elevations of serum transaminase levels greater than 3 times the upper limit of normal were observed in only 1% of this cohort with only 0.1% of the total population requiring discontinuation of therapy. There were no clinically apparent episodes of hepatitis. Discontinuation of therapy due to myopathy was extremely rare (0.08%). Only minimal increases in the frequency of lens opacities (1%) were observed from baseline to the last lens examination during follow-up, consistent with the expected increase in lens opacity development due to normal aging. Patients who were greater than or equal to 65 years old had a clinical and laboratory safety profile comparable to the nonelderly population.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term safety and efficacy profile of simvastatin. 195 Oct 69

Plethoryl is a combination of triatricol, cyclovalone and vitamin A normally prescribed in the treatment of hypercholesterolaemia. Four cases of side-effects most probably caused by this product are reported. They include: 1) a case of common acute hepatitis, 23 cases of which have already been published, with aggravation and reduced time-lapse after reintroduction; 2) a case of clinically silent but biochemically classical hepatitis; 3) a case of cirrhosis due to vitamin A toxicity; 4) a case of inflammatory arthralgias recurring after the same time-lag when the drug was reintroduced despite double doses and without clinical evidence of hepatitis. The last three side-effects have never been previously reported. The adverse reactions to Plethoryl almost always occur in the unofficial indications of the product, notably in the "treatment" of obesity.
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PMID:[Probable side effects caused by plethoryl. Common acute hepatitis, anicteric hepatitis, cirrhosis due to hypervitaminosis A, inflammatory arthralgias]. 252 55

Nicotinic acid has a proven efficacy in the treatment of hypercholesterolemia. Therapeutic use of this water-soluble B vitamin has resulted in a survival benefit among patients enrolled in the Coronary Drug Project. Conversely, nicotinic acid has been associated with a high side-effect profile when used at therapeutic doses. Nevertheless, there are no previously reported cases of hematemesis temporally associated with nicotinic acid use. The authors report the case of a previously healthy 20-year-old man who developed hematemesis and hepatitis 1 week after self-initiating the daily consumption of 6 g of nicotinic acid. Supportive therapy and discontinuing nicotinic acid resulted in rapid clinical improvement in this patient. The clinical circumstances suggest a possible causal relationship between nicotinic acid consumption and his presenting problems. The use of large doses of nicotinic acid may be rapidly complicated by hematemesis and hepatitis.
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PMID:Hepatitis and hematemesis complicating nicotinic acid use. 280 56

Nutritionally induced hypercholesterolemia in A/J mice causes susceptibility to Mouse Hepatitis type 3 (MHV 3), whereas normal A/J mice are fully resistant. A/J mice fed with a hypercholesterolemic diet for 15 to 60 days develop 5 to 7 days after MHV 3 infection an acute hepatitis which led to high levels of mortality. A direct relationship was found between the high levels of plasma and hepatic cholesterol and the mortality. In attempting to define the dietary-induced physiological changes which led to the loss of resistance, the Kupffer cells were shown to exhibit an impairment of functions in their ability to become activated by LPS in order to take up C3-coated IgM opsonized sheep red blood cells, C3(IgM)SRBC, or 3H-thymidine Escherichia coli, and the susceptibility to interferon (IFN) for the induction of an antiviral state. Peritoneal macrophages which were studied in comparison with the Kupffer cells showed no impaired functions. The findings presented here indicate an inhibition of host resistance, by nutritional hypercholesterolemia, of A/J mice to MHV 3 infection and that, at least one site of impairment occurs specifically at the stage of Kupffer cells function.
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PMID:Increased susceptibility of mice to MHV 3 infection induced by hypercholesterolemic diet: impairment of Kupffer cell function. 362 5

In most cases, primary liver carcinoma in tropical areas remains an hepatoma. The high incidence of this malignant tumor of the liver in some regions, and especially in black Africa, is still unexplained. As compared with the form found either in the European or in the North-African, this hepatoma shows special features since it occurs in younger people (35 years), follows a bursting-out course and is precipitously associated not to an alcoholic cirrhosis but to a post-hepatitic one. An humoral syndrome leading to a presomptive diagnosis consists of hypoglycemia, hypercholesterolemia, hyperlipemia, and high blood level of alcaline phosphatases. In 85% of the cases, these tumors secrete an alpha fetoprotein determined by radioimmunoassay. A major etiologic factor is the oncogenous activity of hepatitis virus B which could be either an induction factor or a "co-factor" which would initiate, facilitate or increase the activity of the carcinogen. In this respect, aflatoxin has to be regarded as a "co-factor" too. The best treatment, when it is possible, is an exeresis carried out through a partial hepatectomy. If such a surgical intervention is unadvisable, chemotherapy is the only possibility. Immunization against viral hepatitis has raised hope for the prophylaxis of hepatoma. But it will not be possible to evaluate it before the year 2.000.
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PMID:[Primary liver cancer in the tropical environment. Classical and current data]. 619 92

A 37-yr-old woman with RF-positive RA developed cholestatic hepatitis after 10 days of D-penicillamine therapy. This was discontinued immediately. The cholestasis persisted for the remaining 14 months of her life. Severe hypercholesterolemia developed with xanthelasmata and eventually pancytopenia, which was caused by a massive infiltration of the bone marrow by lipid-containing foam cells. The patient died of sepsis. Review of the literature shows intrahepatic cholestasis to be a rare and idiosyncratic complication of D-penicillamine therapy. To our knowledge, ours is the first documented case of persistent cholestatic icterus.
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PMID:Fatal cholestatic hepatitis caused by D-penicillamine. 805 7

Liver directed gene transfer with adenoviral vectors is being considered for the treatment of several metabolic diseases, including familial hypercholesterolaemia (FH). Gene replacement therapy of human low density lipoprotein (LDL) receptor gene into the murine model of FH transiently corrected the dyslipidaemia; however, humoral and cellular immune responses to LDL receptor developed--possibly contributing to the associated hepatitis and extinguishing of transgene expression. We evaluated an alternative strategy of ectopic expression in the liver of the very low density lipoprotein (VLDL) receptor, which is homologous to the LDL receptor but has a different pattern of expression. Infusion of recombinant adenoviruses containing the VLDL receptor gene corrected the dsylipidaemia in the FH mouse and circumvented immune responses to the transgene leading to a more prolonged metabolic correction.
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PMID:Effective treatment of familial hypercholesterolaemia in the mouse model using adenovirus-mediated transfer of the VLDL receptor gene. 867 4

Two women of 57 and 59 years of age, presented anicteric hepatitis at 9 months and 3 years, respectively, of the initiation of treatment with lovastatin (20 mg/day) for hypercholesterolemia. In both cases other causes of liver damage were excluded and the analytical alterations normalized within a few weeks following discontinuation of the medication.
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PMID:[Hepatitis associated with treatment with lovastatin. Presentation of 2 cases]. 960 93

Hepatocytes are rich in mitochondria, which play an important role in hepatic metabolism. In certain pathologic conditions (most often alcoholic liver disease) mitochondria became enlarged; nevertheless, even in these conditions they are hardly detectable on light microscopy. Recently an antimitochondrial antibody (mAM), which recognizes a 60-kDa protein, has been characterized. The purpose of the present study was to study immunoreactivity of this antibody in a series of liver biopsies. We studied 146 liver biopsies using an mAM. In 8 cases an ultrastructural study was also done, and in 2 cases Western blot analysis was performed. Cases were divided as follows: alcoholic liver disease (ALD, 31); steatosis (8); nonalcoholic steatohepatitis (NASH, 1); hepatitis C virus (HCV)-related hepatitis (83); hepatitis B virus (HBV)-related hepatitis (6); primary biliary cirrhosis (1); sclerosing cholangitis (1); haemosiderosis (1); sarcoidosis (1); alpha-1-antitrypsin deficiency (1); nonspecific findings (12). All the patients were investigated for alcohol or drug abuse, pharmacological treatment, hyperlipidaemia, hypercholesterolaemia and diabetes. Immunoreactivity was diffuse in cases of ALD, NASH and steatosis, and in patients with drug abuse. Electron microscopic immunogold and Western blot analysis confirmed that in the conditions examined the protein recognized by the mAM showed greater expression. Immunohistochemical staining was helpful in demonstrating a toxic or a metabolic insult even in cases in which the histological picture was blurred by viral infection.
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PMID:Identification of mitochondria in liver biopsies. A study by immunohistochemistry, immunogold and Western blot analysis. 976 31


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