1/13. Acute cholestatic hepatitis associated with pravastatin.A 57-yr-old man presented with clinical and laboratory signs of acute cholestatic hepatitis. Symptoms had appeared 7 wk after he was started on pravastatin 20 mg/day for hypercholesterolemia. A full evaluation including ultrasound, computed tomography, endoscopic cholangiography, and liver biopsy confirmed the diagnosis of intrahepatic nonobstructive jaundice. The liver function abnormalities normalized 7 wk after cessation of therapy. pravastatin should be considered as a potential cause of cholestatic hepatitis with favorable clinical outcome after drug withdrawal.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
2/13. myositis, microvesicular hepatitis, and progression to cirrhosis from troglitazone added to simvastatin.A 68-year-old woman, with type 2 diabetes mellitus, hypercholesterolemia, and prior long-term simvastatin therapy, self-resumed troglitazone after running out of metformin. She developed an acute severe hepatitis with microvesicular steatosis and mysositis. There was subsequent resolution of the myositis but progression of the hepatitis to symptomatic cirrhosis over a period of 12 weeks. Both troglitazone and simvastatin are metabolized by cytochrome P-450 3A4. Troglitazone typically induces metabolism of drugs metabolized by this cytochrome so that simple simvastatin toxicity seems less likely to have been involved. The association with myositis, the severity of the hepatitis with progression to cirrhosis, and the presence of microvesicular steatosis suggests altered mitochondrial metabolism, which has been described with each agent, as the underlying pathogenic mechanism. Although troglitazone (Rezulin) has been withdrawn from the market, other similar agents are available for therapy of type 2 diabetes mellitus. Increased awareness of a potential interaction between these two classes of drugs is warranted.- - - - - - - - - - ranking = 1.1666666666667keywords = hepatitis (Clic here for more details about this article) |
3/13. Evaluation and treatment of the hiv/HCV coinfected patient: a case history and discussion.Declining rates of morbidity and mortality related to opportunistic infections in the era of highly active antiretroviral therapy (HAART) have led to a new focus on hepatitis c (HCV). Several studies suggest that the natural history of HCV is accelerated in patients with hiv infection. Recent literature highlights higher rates of fibrosis progression and increasing rates of morbidity and mortality related to end-stage liver disease. As a result, more and more clinicians are turning their attention to the evaluation and management of hepatitis c in an effort to prevent or slow down the progression to advanced liver disease. The following case history illustrates many of the complicated steps in the evaluation process of these patients. Several important issues are discussed, such as the rationale in performing a liver biopsy, when to initiate treatment, drug interactions, and adverse effects of therapy.- - - - - - - - - - ranking = 0.33333333333333keywords = hepatitis (Clic here for more details about this article) |
4/13. simvastatin-induced lactic acidosis: a rare adverse reaction?simvastatin, a hydroxymethylglutaryl coenzyme a (HMG-CoA) reductase inhibitor, is a commonly used cholesterol-lowering agent. The long-term safety profile of simvastatin, established over 10 years of clinical use, is excellent. HMG-CoA reductase inhibitors block 3-hydroxy-3-methylglutaryl coenzyme a reductase, the rate-limiting enzyme in cholesterol synthesis. However, other important nonsterol compounds, such as coenzyme Q10 (CoQ10), are also derived from the same synthetic pathway. CoQ10 is an essential carrier in the mitochondrial respiratory chain that participates in oxidative phosphorylation. simvastatin and other HMG-CoA reductase inhibitors have been documented to lower serum concentrations of CoQ10. It has been suggested that the adverse effect of myopathy caused by HMG-CoA reductase inhibitors is due to CoQ10 deficiency in the tissue mitochondria. documentation of this cause-and-effect phenomenon, however, has been lacking. We offer evidence that lactic acidosis may develop as a complication of simvastatin therapy. Our patient also manifested the well-known HMG-CoA reductase inhibitor drug toxicities of rhabdomyolysis and hepatitis. The occurrence of these known adverse events with lactic acidosis in our patient suggests that interference of the mitochondrial respiratory chain may play a role in the toxicity of this class of drugs.- - - - - - - - - - ranking = 0.16666666666667keywords = hepatitis (Clic here for more details about this article) |
5/13. Granulomatous hepatitis, increased platelet aggregation, and hypercholesterolemia.Two young patients presented with an unusual liver disease, granulomatous hepatitis with postnecrotic cirrhosis, and both underwent a splenorenal shunt procedure. Each developed an arterial embolic episode probably related to increased platelet aggregation. This represents the first report of a liver disease associated with increased platelet aggregation that was clinically significant, a myocardial infarction in one and a posterior cerebral infarction in the other. Also, unexpectedly, both patients became hypercholesterolemic after the splenorenal shunt was established.- - - - - - - - - - ranking = 0.83333333333333keywords = hepatitis (Clic here for more details about this article) |
6/13. Drug-induced acute autoimmune hepatitis during combination therapy with atorvastatin and ezetimibe.A case is presented of a patient who developed acute hepatitis during cholesterol-lowering treatment with atorvastatin and ezetimibe. Further investigations reveal a probable drug-induced autoimmune hepatitis, and ezetimibe is considered to be the most likely causal agent. This case is the first report of an autoimmune hepatitis associated with ezetimibe therapy.- - - - - - - - - - ranking = 1.1666666666667keywords = hepatitis (Clic here for more details about this article) |
7/13. Severe hepatic side effects of ezetimibe.BACKGROUND AND AIMS: Ezetimibe was introduced recently as a new class of cholesterol-lowering drugs. Until now only limited increases of transaminase levels were reported. methods: We studied 2 patients with severe hepatic side effects of ezetimibe in a general community hospital. RESULTS: Ezetimibe may lead to 2 distinct types of severe hepatic side effects. CONCLUSIONS: Ezetimibe may rarely cause hepatotoxicity, severe cholestatic hepatitis, or acute autoimmune hepatitis.- - - - - - - - - - ranking = 0.33333333333333keywords = hepatitis (Clic here for more details about this article) |
8/13. Autoimmune hepatitis triggered by statins.Although the cause of autoimmune hepatitis (AIH) is unknown, drugs are believed to be potential triggers in some patients. In isolated case reports, statins have been considered such triggers. Here we describe 3 patients in whom it is probable that statins initiated the development of AIH. Two men (aged 47 and 51) and one woman (aged 57) developed AIH after the initiation of statin therapy. They developed positive titers of antinuclear antibodies, antismooth muscle antibodies (1/40 to 1/160), and hypergammaglobulinemia. Features of all 3 patients met the criteria for AIH according to the International Autoimmune Hepatitis Panel. Liver biopsies in all 3 showed varying stages of fibrosis and plasma cell infiltration, compatible with AIH. The woman developed hepatitis due to statins on 2 separate occasions: the first in 1999, due to simvastatin, and the second in 2001 to 2002, due to atorvastatin, which was severe and persisted even after discontinuing medication. Similarly, in the 2 other cases, exposure to statins preceded development of AIH, which persisted despite discontinuing medications. All 3 patients responded well to prednisone and azathioprine or mycophenolate therapy. 3 similar previously reported cases are reviewed. We conclude that the 3 cases reported here and 3 similar previously reported cases, indicate that severe, ongoing AIH on rare occasions can be triggered by statins.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
9/13. A case of alcoholic liver injury with an unusual polyacrylamide-gel disc-electrophoretic pattern of serum lipoproteins.An unusual lipoprotein pattern on polyacrylamide-gel disc-electrophoresis was observed in 37 year-old male diagnosed as alcoholic liver injury. The electrophoretic lipoprotein pattern consisted of a major band of pre-beta mobility and minor intermediate, fast-beta and slow-alpha bands. The normal beta band was virtually absent and the alpha band was diminished. The abnormal lipoprotein pattern was observed one week after discontinuing alcohol consumption when marked hypertriglyceridemia demonstrated earlier had already normalized leaving a moderate hypercholesterolemia with reduced esterified cholesterol and abnormal liver function tests. The lipoprotein abnormalities were completely normal one month later. The appearance of a major pre-beta band with normal triglyceride and high cholesterol levels is discussed in relation to the formation of larger triglyceride-rich LDL particles in recovery from alcoholic hepatitis.- - - - - - - - - - ranking = 0.16666666666667keywords = hepatitis (Clic here for more details about this article) |
10/13. hypercholesterolemia associated with alpha-1 antitrypsin deficiency and hepatitis: lipoprotein and apoprotein determinations, sterol balance and treatment.lipid metabolism was investigated in a 4-year-old boy with alpha-1 antitrypsin deficiency (ZZ phenotype) and liver disease. plasma cholesterol and triglyceride levels were 604 mg/dl and 336 mg/dl respectively. Both parents had normal plasma lipids. Lipoprotein X was present at a concentration of 855 mg/dl and levels of apoproteins A-I, A-II, B and C-III were elevated. The plasma free fatty acid pattern was normal. plasma cholesterol esterification was greatly depressed. Cholesterol absorption on two occasions was reduced about 13% compared with adult controls. Neutral and total steroid excretion was normal with increased excretion of bile acids. A low-cholesterol, low-fat diet reduced plasma cholesterol to 374 mg/dl and triglyceride to 236 mg/dl in two months. Cholesterol and lipoprotein X concentrations were elevated far out of proportion to the severity of the liver disease (total bilirubin 3.7 mg/dl, SGOT 280 IU/L). This suggests that lipoprotein metabolism in patients with this disorder is unusual and may differ from the derangements seen in other forms of liver disease.- - - - - - - - - - ranking = 0.66666666666667keywords = hepatitis (Clic here for more details about this article) |
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