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)

The patient we describe developed a cholestatic hepatitis and an unusual threshold elevation of about 425%, coincidently, 5 weeks after pacemaker implantation. Lead dislocation, myocardial infarction or metabolic disorder could be excluded as a reason for the pacemaker complication. Neither a biliary obstruction nor an infection of the liver could be found to explain the liver injury. Most probably, both disorders were caused by propafenone (450 mg day-1), withdrawal of the drug resulted in normalization of elevated enzyme and threshold levels.
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PMID:Acute cholestatic hepatitis and the sudden rise of the pacing threshold 5 weeks after VVI-pacemaker implantation. 807 95

Drug-induced hepatotoxicity is a major cause of iatrogenic diseases. More than 900 compounds, including herbal medicines are involved and can reproduce the full spectrum of liver injuries. Acute hepatitis are the most frequently observed. Three types are described: acute hepatocellular hepatitis which are frequently similar to viral hepatitis, and can lead to fulminant liver failure and death within a few days, or, more insidiously, to cirrhosis; acute cholestatic hepatitis, which exhibits a better prognosis, may be misleading by mimicking biliary obstruction; mixed-pattern hepatitis, which associates features of hepatocellular and cholestatic hepatitis. Acute hepatitis generally exhibits no specific patterns. Then, the diagnosis is difficult and relies upon the elimination of other causes and a compatible or a suggestive time-relationship between drug ingestion and the onset of hepatitis as well as between drug withdrawal and recovery. Sometimes, drug hepatotoxicity is suggested by the association of hepatitis to hypersensitivity manifestations (hypereosinophilia), to some histopathological features (eosinophilic infiltration, microvesicular steatosis, giant hepatocytes) or, more uncommonly, to specific autoantibodies (anti-mitochondrial type 6, anti-LKM2, anti-LM antibodies). Cross hepatotoxicity may occur between drugs having related chemical structures.
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PMID:[Drug-induced hepatitis: epidemiologic, clinical, diagnostic and physiopathologic aspects in 1995]. 852 55

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

For the past few years, we have been investigating polysaccharides from Ganoderma lucidum as antifibrotic agents. In a previous study, we discovered that polysaccharides extracted from G. Iucidum lowered the collagen content in liver but had no effect on serum biochemical parameters in rats subjected to bile duct ligation and scission-induced fibrosis. In this study, we changed the extraction method and obtained polysaccharides extracted from G. Iucidum. The polysaccharide from G. Iucidum reduced the serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and total bilirubin and also reduced the collagen content in liver and improved the morphology. Pentoxifylline, which is reported to exhibit an antifibrotic effect in pigs with fibrosis induced by yellow phosphorus, did not have any antifibrotic effects in fibrosis induced by biliary obstruction. Glycyrrhizin, which is used in the treatment of hepatitis, reduced serum ALT and AST values but there was no significance. It had no effect on liver hydroxyproline content which implies that glycyrrhizin has no antifibrotic effect in the rats with fibrosis induced by bile duct ligation and scission. These data suggest that the polysaccharide from Ganoderma lucidum could be a promising antifibrotic agent. However, further study is needed to understand the inhibition mechanism of collagen deposition of polysaccharides from Ganoderma Iucidum and its clinical applicability remains to be established.
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PMID:Antifibrotic effects of a polysaccharide extracted from Ganoderma lucidum, glycyrrhizin, and pentoxifylline in rats with cirrhosis induced by biliary obstruction. 914 21

We determined the Guanine Deaminase (GD) activity of 200 patients with different diseases. It was found that GD activity of hepatic patients is higher than that of health adults, while the GD activity of other patients is in the normal range. There is a linear correlation between GD activity and ALT in patients with chronic hepatitis, billiary obstruction, and between GD activity and total bilirubin in patients with chronic active hepatitis, biliary obstruction and liver cirrhosis. Moreover, the GD activity of patients positive for anti-HCV is significantly increased. So GD activity in serum is a specific and sensitive index to estimating hepatic functions and can be used in the diagnosis of acute and chronic hepatitis, cirrhosis of liver, and C virus hepatitis.
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PMID:[The value of determining guanine deaminase in diagnosis of hepatic diseases]. 938 40

Some liver allograft recipients with hepatitis C virus (HCV) infection develop hyperbilirubinemia, which might be the result of a cholestatic variant of hepatitis C. We evaluated all liver biopsy samples from 6 liver transplant recipients who had polymerase chain reaction-positive HCV infection and histologic evidence of hepatitis and jaundice and compared them with liver biopsy samples from a control group of transplant recipients with HCV hepatitis without jaundice. Patients with known ductopenic rejection, biliary obstruction, or co-infection with hepatitis A or B were excluded from the study. Measurement of viral titers and genomic typing were performed when possible. Six patients developed hepatitis and jaundice, with maximum bilirubin levels ranging from 5.8 to 47.6 mg/dL. In this group, 5 (83%) had moderate interface hepatitis (control group, 15%), 6 (100%) had confluent necrosis (control group, 12%), 5 (83%) had bridging fibrosis (control group, 18%), 4 (67%) had significant hepatocyte swelling (control group, 9%), 4 (67%) had prominent ductular proliferation (control group, 3%), and 6 (100%) had mild duct damage and inflammation (control group, 53%). All 6 of the patients with cholestasis had allograft failure. Of these, three allografts were available for review, which did not reveal occult obstruction, rejection, or duct loss. All patients in the control group have retained their allografts. In 4 patients with cholestasis, the median HCV RNA titer was 93.97 mEq/mL, with a mean of 54.19 mEq/mL (control mean = 5.2 mEq/mL). Five patients also underwent viral genomic typing: 2 with type 1a, 2 with type 1b, and 1 with mixed type 1a and 1b. Cholestasis in patients with posttransplantation hepatitis C may be caused by an aggressive HCV infection that exhibits histologic features of confluent necrosis, hepatocyte swelling, and/or ductular proliferation. Viral titers are often increased in such patients.
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PMID:Cholestatic hepatitis C in liver allografts. 964 45

Infectious mononucleosis due to Epstein-Barr virus (EBV) is almost always a self-limited disease, most commonly seen in young adults. Hepatitis is a well-recognized complication of EBV infection that usually resolves spontaneously. Jaundice occasionally results from the unusual complication of autoimmune haemolytic anaemia rather than hepatitis. We report a 60-year-old man with severe cholestatic jaundice whose history, liver histology and laboratory findings suggested EBV infection. He also developed significant jaundice related to his hepatitis, but not to autoimmune haemolysis, a situation that led to diagnostic delay. Costly diagnostic laboratory tests and invasive procedures were performed to rule out a malignant extrahepatic biliary obstruction. Physicians need to be aware of this complication and EBV infection should be included in the differential diagnosis of cholestatic jaundice in the elderly.
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PMID:Severe cholestatic jaundice induced by Epstein-Barr virus infection in the elderly. 973 76

We determined the diseases associated with extremely high levels of alkaline phosphatase in hospitalized patients. Computerized laboratory records of the Hospital of Saint Raphael identified all inpatients who had elevations of alkaline phosphatase above 1,000 U/l from April 1994 to September 1995. Thirty-seven inpatients with alkaline phosphatase levels above 1,000 U/l were identified. Six had bone involvement from malignancy or Paget's disease and were eliminated from further analysis, and 31 patients were included in the study. Levels of alkaline phosphatase ranged from 1,014 to 3,360 U/l. Ten patients had sepsis as the cause of the elevated alkaline phosphatase. These included gram-negative organisms, gram-positive organisms, and two patients with fungal sepsis. Seven of 10 patients with sepsis had an extremely high alkaline phosphatase level and a normal bilirubin, 3 of 10 patients with sepsis also had acquired immunodeficiency syndrome (AIDS). Eight patients had biliary obstruction, 7 with malignant obstruction and 1 with a common bile duct stone. Nine patients had AIDS. The cause of the elevated alkaline phosphatase in these included three with sepsis, three with mycobacterium avium intracellulare (MAI) infection, two with cytomegalovirus infection, and one with Dilantin toxicity. Three patients had diffuse liver metastases. Finally, four patients had benign intrahepatic disease, including one patient with liver hemangiomas, one patient with sarcoid hepatitis, one patient with lead toxicity, and one patient with drug-induced cholestasis. Extremely high elevations of alkaline phosphatase are most frequently seen in patients with sepsis, malignant obstruction, and AIDS. Patients with sepsis can have an extremely high alkaline phosphatase level and a normal bilirubin. A variety of other causes were also noted.
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PMID:Extremely high levels of alkaline phosphatase in hospitalized patients. 985 66

We report a case of ticlopidine-induced prolonged cholestasis in a 60-year-old man with no previous hepatobiliary disease who presented with sudden right upper abdominal pain, jaundice and pruritus three months after starting ticlopidine therapy. Other drugs taken by the patient were not considered probable causes. The diagnostic evaluation showed no biliary obstruction and other possible causes of intra-hepatic cholestasis were excluded. The liver biopsy showed a cholestatic hepatitis with bile duct damage. The disease ran a severe and protracted course, but symptoms and jaundice eventually subsided five months after drug withdrawal. More than a year later, relevant abnormalities of liver function tests consistent with anicteric cholestasis still persist, fulfilling criteria for a minor form of drug-induced prolonged cholestasis. This syndrome has been reported infrequently in relation to several drugs, mainly chlorpromazine, and only once with ticlopidine.
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PMID:Ticlopidine-induced prolonged cholestasis: a case report. 1041 41

In primary biliary cirrhosis, biliary epithelial cell death by apoptosis results in progressive bile duct loss. We examined immunohistochemically 4 apoptosis-regulating bcl-2 familial proteins (bcl-2, mcl-1, bcl-X, and bax) in the biliary epithelium in 19 cases of primary biliary cirrhosis. Ten cases of chronic hepatitis C, 9 cases of extrahepatic biliary obstruction, and 10 cases of normal liver were used as a control. Bcl-2 and mcl-1 are inhibitors of apoptosis, bcl-X, probably bcl-XL in biliary epithelial cells, an inhibitor, and bax, a promoter of apoptosis. First, we clarified the distribution of bcl-2 familial proteins on the intrahepatic biliary tree in normal livers. Bcl-2 was detected in the interlobular bile ducts and bile ductules, but not in the large and septal bile ducts in all cases examined. Mcl-1, bcl-X, and bax were diffusely detectable at the any level of the intrahepatic biliary tree, with a staining pattern that was diffuse and cytoplasmic. This distribution pattern was preserved in extrahepatic biliary obstruction. Bcl-2 expression was lost or markedly reduced in the damaged interlobular bile ducts in primary biliary cirrhosis, whereas the reduction was only focal or mild in the bile ducts with hepatitis-associated damage in chronic hepatitis C. Expression levels of mcl-1, bcl-X, and bax were similarly reduced to that of bcl-2 in these 2 diseases. These findings suggest that bax is not important as a proapoptotic factor in the damaged bile ducts and that downregulation of bcl-2 and mcl-1, and probably that of bcl-XL, leads to a decrease in the threshold of apoptosis and increase in the vulnerability to apoptotic stimuli in these bile ducts, followed by the progressive apoptotic loss of interlobular bile ducts, in primary biliary cirrhosis.
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PMID:Expression of Bcl-2 familial proteins is reduced in small bile duct lesions of primary biliary cirrhosis. 1068 31


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