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)

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
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PMID:Patterns of hepatic injury induced by methyldopa. 42 37

Liver biopsies of 155 oral contraceptives users (ages 16-45) showed that 106 (68.4%) had histologically observable hepatic damage. Sinusoidal ectasia was observed in 73 cases. 53 women had transaminase levels between 50 and 100 E/1, 34 over 100 E/1; such elevated transaminase levels often indicate lesions of the hepatic parenchyma. In 20 cases evidence of hepatitis was found, but it could not be determined whether it was viral in nature or caused by medication use. 5 cases of intrahepatic cholestasis were observed.
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PMID:[Morphological and clinical liver changes after taking oral contraceptives]. 42 84

The behaviour of LCAT was examined in acute viral hepatitis and post-hepatic cirrhosis. In the former case, the enzyme was also investigated during remissions. The influence of cholestasis on LCAT activity was evaluated. Depression was noted in cirrhosis and the acute stage of hepatitis, whereas enhanced values were observed during remissions. Depression of the enzyme by cholestasis is explained in a variety of ways.
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PMID:[The behavior of lecithin cholesterol acyltransferase (LCAT) in acute viral hepatitis and post-hepatitis cirrhosis]. 44 Jun 18

Measurements of serum bile acids (glycine conjugates of cholic, chenodeoxycholic, deoxycholic, and lithocholic acids) by radioimmunoassay in a variety of pediatric hepatobiliary disorders showed elevations in neonatal hepatitis syndromes, cholestasis, and hepatitis of extrahepatic or intrahepatic origin. Measurements of individual serum bile acids failed to differentiate between the various neonatal hepatitis syndromes. In one patient with cholestasis, the increased levels of bile acids observed returned to normal following therapy with cholestyramine and phenobarbital. In chronic active hepatitis the serum bile acid values correlated well with the bilirubin and SGOT in response to therapy with corticosteroids. These data confirm suggestions that serum cholylglycine and chenodeoxycholylglycine levels are a sensitive indicator of disturbed hepatic function and can be used in monitoring the course, activity, and therapeutic response in various hepatitis syndromes. In Reye's syndrome and protracted diarrhea of infancy, elevations in serum bile acids were detected without associated hyperbilirubinemia and provided additional evidence of disturbed hepatic function.
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PMID:Serum glycine-conjugated bile acids in pediatric hepatobiliary disorders. 44 3

Cholestasis in early infancy produces reactive alterations of liver parenchyma within the first weeks of life; histological examination of liver biopsy specimens may give hints as to the underlying disease. Differentiation of bile duct atresia and giant cell hepatitis at an early stage is especially important. Hyperplasia of the intrahepatic bile duct system can be due to rather different diseases. Congenital abnormalities of the duct system can be distinguished from reactive alterations only by early liver biopsy. Certain histological changes may give evidence of congenital or other metabolic disorders. Hemochromatosis of the neonatal period has been characterized morphologically but not as yet biochemically.
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PMID:[Cholestasis in early infancy - histological findings (author's transl)]. 44 71

Three cases of chronic nonhaemolytic jaundice with conjugated bilirubin in the serum are described in a Chinese family. Bromsulphthalein excretion tests gave results typical of the Dubin-Johnson syndrome. Liver histology in the proband showed cytoplasmic pigment of the lipofuscinmelanin variety, and intravenous cholecystography failed to show visualisation of the gallbladder. Unusual findings included onset during the neonatal period in the proband and the presence of some iron pigment in the hepatic cells with a little canalicular cholestasis. It is suggested that the infant may have had a concomitant nonspecific hepatitis. These cases are regarded as belonging to a disease group in which the Dubin-Johnson syndrome is at one end of a spectrum. The mode of inheritance is discussed.
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PMID:Dublin-Johnson syndrome with some unusual features in a Chinese family. 48 95

It is generally accepted that hepatitis occurring during treatment with INH and rifampicine results from the hepatotoxicity of INH metabolites. A case is reported of cholestatic hepatitis occurring during such treatment, in which there was a previous history of an isolated hepatic affection. The administration of INH and rifampicin caused cholestasis alone, which reoccurred after rifampicin administration only. No immuno-allergic phenomenon has been shown to be involved in rifampicin toxicity. This observation suggests that rifampicin may be hepatotoxic itself, especially in patients with previous hepatic affections.
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PMID:[Cholestatic hepatitis during treatment with I.N.H. and rifampicin: arguments in favour of the hepatotoxicity of rifampicin (author's transl)]. 49 38

Different groups of rats suffering from galactosamine hepatitis or ANIT-cholestasis received 200 mg galactose either by 5 minutes intravenous infusion or via a gastric tube. Blood galactose concentrations were measured for a time period of 1.5 hrs. after intravenous administration and the galactose elimination capacity (GEC) was calculated. After oral administration the galactose blood concentrations were determined for a period of 3.5 hrs. and the oral galactose clearance was estimated. After termination of both types of galactose loading the activity of the galactokinase (EC 2.7.1.6.) was determined in total liver homogenate and compared either to the GEC or to the oral galactose clearance in vivo. Galactokinase activity in the liver increased in the group of animals with experimental cholestasis and was significantly reduced in the galactosamine treated group. In vivo these changes could be estimated much better by the GEC than by determination of the oral galactose clearance.
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PMID:[Intravenous and oral galactose loading of rats suffering from galactosamine hepatitis and ANIT-cholestasis; comparison of the kinetics in vivo and the galactose metabolism in the liver in vitro (author's transl)]. 52 47

In the course of 4 years, among 11,738 admissions there were 245 (2.08%) patients with cholestasis (106 women and 139 men). Intrahepatic cholestasis (i.c.) was detected in 46.5%, and extrahepatic (e.c.) in 53.5%. The most frequent cause of i.c. were alcoholic and nonalcoholic chr. liver disease (fatty liver, chr. hepatitis, cirrhosis) (37% and 30%), acute viral hepatitis (15%) and toxic liver injury (14%) respectively. The causes of e.c. were: choledocholithiasis (44%), cancer of the pancreatic head (15%), cancer of gallbladder and extrahepatic ducts (12%) and cancer of liver (10%). The causes of c. were benigne, in 78.2%, while malignant neoplasms were present in 21.8%. Out of the multitude of laboratory tests two appeared particularly significant: glut, transpeptidase was pathologic in 81% of alcoholic liver disease, in 62% of the cases with obstructive jaundice and in 27.7% of malignant neoplasms. LX-lipoprotein examined in 52 patients was positive in 24% of i.c., and 60% of e.c. Proliferation of bile ducts was the most frequent finding in surgical liver biopsies in choledocholithiasis cases.
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PMID:Differential diagnosis, laboratory tests and histology in 245 patients with cholestasis. 52 15

Object of the investigation was to find out whether otherwise cholephilic metabolites are excreted via an alternative pathway into urine in experimental liver disease. Intraduodenal application of 14C-labelled hexobarbital in rats is followed by an immediate biliary excretion of metabolites in the range of 400 microgram/100 g bw/h. Using TLC these metabolites can be separated into a polar fraction (about 80% of total) and a non-polar fraction. Phenobarbital treatment leads to a decrease of the total biliary excretion of metabolites to about 200 microgram/100 g bw/h, the metabolite pattern remaining unchanged. Animals with a mild form of GalN-hepatitis had a moderate reduction of bile flow and a total metabolite output of 40 microgram/100/gbw/h. The metabolite pattern showed a decrease mainly of the polar fraction. In animals with an early stage of ANIT cholestasis a 50% reduction of bile flow was associated with a total metabolite excretion of only 20 microgram/100 g bw/h and polar metabolites were nearly absent. In both types of experimental liver disease in corresponding urine samples otherwise cholephilic metabolites appeared. The results obtained show that clinically moderate stages of experimental liver disease lead to a significantly diminished output especially of polar 14C-hexobarbital-metabolites into the bile, which can, therefore, appear in the urine instead.
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PMID:Alternative transport pathways of cholephilic 14C-hexobarbital metabolites in rats with experimental hepatitis and cholestasis. 54 23


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