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 rate of hepatic metabolism of dimethylaminoantipyrine (aminopyrine), which occurs primarily through N-demethylation, was assessed by measurement of the specific activity of 14CO2 excreted in breath samples obtained 2 hours after oral administration of a trace dose of [14C]aminopyrine. The percentage of administered 14C excreted in 14CO2 in 2 hours was 7.0 +/- 1.3 (SD)% in control patients, and significantly less (P less than 0.01) in patients with portal cirrhosis (2.6 +/- 1.2%), fatty liver (4.7 +/- 1.1%), hepatitis (2.6 +/- 1.4%), and hepatic malignancy (3.5 +/- 1.8%). In 16 of 24 subjects with cholestasis not caused by malignant disease the mean 14CO2 excretion was normal. The 14CO2 excretion in patients with portal cirrhosis correlated highly with aminopyrine metabolic clearance rate (r equals 0.92), serum albumin (r equals 0.75), and retention of bromsulphalein (r equals 0.73). Abnormal 14CO2 excretion returned to normal in patients with hepatitis, when the hepatitis resolved. The data suggest that the aminopyrine breath test is a safe, simple, qualitative and quantitative liver function test.
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PMID:Quantitative assessment of hepatic function by breath analysis after oral administration of (14C)aminopyrine. 120 Apr 95

The morphological and functional alterations of the smooth endoplasmic reticulum of the liver cell related to biliary stasis have brought attention to drug biotransformation during cholestasis. The metabolism of meprobamate, pentobarbital and tolbutamide was assessed in subjects with intrahepatic recurrent cholestasis (3), cholestatic hepatitis (6), extrahepatic biliary obstruction (7) and normal controls (16). In the patients with recurrent intrahepatic cholestasis no differences in drug metabolism were noted as compared to the control group. In cholestatic hepatitis the plasma half-lives of meprobamate (828 +/- 422 min.) and pentobarbital (39+-65) were significantly longer than in in controls (444 +/- 37 and 25.4 +/- 1.1 respectively). Tolbutamide plasma half-life appeared unchanged. The most striking variations were observed in the patients with extrahepatic biliary obstruction. In such cases while meprobamate half-life was unchanged, pentobarbital half-life was significantly prolonged (31.2 +/- 2.5) and the in vitro metabolism of the drug, using liver preparations, was decreased to less than 50% of the control value. In contrast the metabolism of tolbutamide was accelerated as evidenced by a significant decrease of plasma half-life (165 +/- 48 min. versus 384 +/- 76 of the controls) and an enhanced urinary excretion of the drug's metabolites. However the metabolism of tolbutamide in vitro did not show any difference between normal and cholestatic liver. Whatever the mechanism of the peculiar behaviour of tolbutamide in extrahepatic biliary obstruction it seems to be related to the increased bile dalt concentration during cholestasis. In fact the low values of plasma half-life increase significantly either relieving the biliary obstruction or producing a bile salt depletion with cholestyramine. Preliminary results in vitro suggest the bile salt could displace tolbutamide from albumin binding thus increasing the amount of free drug available for biotransformation by the liver. In conclusion cholestasis may affect drug metabolism depending on the degree of biliary stasis, liver cell injury and the type of drug tested. The mechanism could be that of an impaired biotransformation in the smooth endoplasmic reticulum or could involve extrahepatic factors.
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PMID:Alteration of drug metabolism during cholestasis in man. 120 63

The isoenzymes of alkaline phosphatase were measured on admission to hospital, and then weekly over a 2 to 3 month period, in 40 patients presenting with uncomplicated acute hepatitis, 12 patients with cholestatic hepatitis, and 10 patients with histologically confirmed chronic persistent hepatitis. In acute uncomplicated hepatitis the increase in total alkaline phosphatase is not due to a cholestatic reaction of the damaged liver, but reflects the impaired catabolic capacity of the liver cells to degrade alkaline phosphatases from intestine and bone, as well as that of hepato-biliary origin. The isoenzyme distribution pattern is the same as found in normal healthy subjects. The increase in total alkaline phosphatase in patients with cholestatic hepatitis results from this impaired catabolic capacity for degradation of all isoenzymes, together with an increase in cholestatic reflux of hepato-biliary enzymes. In patients with chronic persistent hepatitis the raised total alkaline phosphatase activity at each point during the illness is due to this catabolic impairment of degradation of all isoenzymes. A cholestasis is not seen. The isoenzyme distribution pattern remains normal; only the enzyme activity due to the intestinal fraction, when compared with the acute hepatitis, is slightly, but significantly, raised.
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PMID:[Distribution pattern of isoenzymes of alkaline phosphatase in patients with various forms of hepatitis (author's transl)]. 125 32

Cholestatic hepatitis, whilst having a longer course than cytolytic forms, in general regresses in a few months. The authors report here seven cases of cholestatic hepatitis lasting for more than 18 months. These chronic forms have certain characteristic features: - female predominance (6 cases out of 7). - a severe degree of cholestasis with, in particular, marked elevation of lipids, cholesterol and alkaline phosphatase. - the absence of Australia antibody and antigen, together with the absence of anti-smooth muscle antibody and anti-mitochondrial natibody. - a decrease in the number of permeable biliary canaliculi in the portal spaces. - a decrease in the number of permeable biliary canaliculi in the portal spaces. - a course which appears to be little influenced by various therapeutic measures. Although the final course seems satisfactory on the majority of cases, the possibility of a slow cirrhogenic transformation cannot be excluded in certain instances.
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PMID:[Cholestatic hepatitis with a chronic course. 7 cases]. 125 18

The serum non-caeruloplasmin copper concentrations were measured in normal subjects and patients with various types of liver disease by a sensitive direct method involving complexing the copper and measurement by atomic absorption spectrophotometry. In normal subjects the mean concentration (+/- S.D.) was 10.1 +/- 1.6 mug/100 ml, males having a slightly higher value (10.7 +/- 1.3 mug/100 ml) than females (9.2 +/- 1.8 mug/100 ml). In patients with various non-hepatic diseases concentrations were raised (15.8 +/- 8.9 mug/100 ml), as also in hepatitis (14.7 +/- 4.3 mug/100 ml), cholestasis (16.1 +/- 6.4 mug/100 ml) and cirrhosis (16.3 +/- 8.7 mug/100 ml). Heterozygotes for Wilson's disease and patients treated for Wilson's disease had concentrations (12.9 +/- 5.9 and 9.8 +/- 3.7 mug/100 ml, respectively) which did not differ significantly from normal whereas untreated patients had very significantly raised concentrations (22.9 +/- 4.5 mug/100 ml). Direct measurement of serum non-caeruloplasmin copper is more accurate than indirect measurement and may help in assessing the effect of treatment but it is concluded that measurement of this fraction of serum copper will not enable Wilson's disease to be differentiated from other forms of liver disease.
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PMID:Direct measurement of serum non-caeruloplasmin copper in liver disease. 127 46

The authors performed 20 liver transplantations from living related donors between June 1990 and July 1991. The 20 pediatric patients (14 biliary atresia, two Budd-Chiari syndrome, one liver cirrhosis after hepatitis C viral infection (HCV hepatitis), 1 progressive intrahepatic cholestasis, 1 liver cirrhosis, 1 protoporphyria) were transplanted with 11 left lobes, eight left lateral segments, and one right lobe. The choice of donors was restricted to the parents of the recipients. The immunosuppressive treatment consisted of FK 506 and steroids. Seventeen recipients are alive, 15 of whom are well and at home. Two recipients, who underwent emergency transplantation, died of postoperative complications. Another recipient died of accidental asphyxia at 6 months after the transplantation. All 20 donors had uneventful postoperative courses and were able to resume their normal social lives. The arterial ketone body ratio (AKBR) increased to above 1.0 within 2 days after the transplantation in all cases. Relatively mild rejection episodes were encountered in only two cases transplanted with ABO-compatible grafts, and these were treated successfully with steroids and FK 506.
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PMID:An appraisal of pediatric liver transplantation from living relatives. Initial clinical experiences in 20 pediatric liver transplantations from living relatives as donors. 128 74

Ninety-seven cases of liver disease in pregnancy confirmed by pathological examination were studied. The results showed that in addition to virus hepatitis (58.8%), which was the leading cause, there were quite a proportion of other liver diseases. Among these acute fatty liver of pregnancy accounted for 18.6%, intrahepatic cholestasis of pregnancy were 16.5%. The causes of misdiagnosis and the bases for differential diagnosis were discussed. It was considered that early pathological examination of liver and other morphological study were important in diagnosis of liver diseases in pregnancy.
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PMID:[Pathological and clinical study on 80 cases of liver disease in pregnancy]. 129 Dec 16

Fifty infants with obstructive jaundice were reviewed. Other than jaundice, hepatomegaly and splenomegaly were the other common presentations. The mean age of referral was 9.4 weeks. This was unsatisfactory as the prognosis depends on the age of corrective surgery. Majority of the non surgical cholestasis were due to idiopathic hepatitis. These patients did well as all of them were asymptomic and had no evidence of liver disease at 2 years of age.
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PMID:A clinical study of obstructive jaundice among Singapore infants. 130 62

Neonatal hepatitis is closely related to human cytomegalovirus infection in Taiwan, a conclusion based on serological and urine culture studies. To obtain more direct evidence further relating cytomegalovirus to the pathogenesis of neonatal hepatitis, the cytomegalovirus genome was studied in the liver tissues of 50 infants with neonatal hepatitis using the polymerase chain reaction (PCR). Liver tissues from 26 infants with biliary atresia and another 30 infants and children with diagnoses other than neonatal hepatitis, cholestasis, or hepatitis were also studied for comparison. Sequences from the immediate early gene 1 and 2 regions were used as primers. The liver tissues from 23 (46%) of the 50 infants with neonatal hepatitis were positive for cytomegalovirus genome, whereas those of 2 of the 26 infants with biliary atresia and none of the liver tissues from 30 infants and children without neonatal hepatitis were positive for cytomegalovirus genome, by PCR. The results of PCR correlated well with that of serology and urine culture. This study provides further evidence of cytomegalovirus in the pathogenesis of neonatal hepatitis.
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PMID:Polymerase chain reaction to detect human cytomegalovirus in livers of infants with neonatal hepatitis. 132 96

Hepatitis A is an acute, necroinflammatory disease of the liver which results from infection by the hepatitis A virus (HAV). The mean incubation period is approximately 30 days. Although the disease is usually self-limited, the severity of illness is age-dependent. In children, hepatitis A is usually asymptomatic, while in adults, symptomatic infection is characteristic and jaundice is common. Fulminant hepatitis A is rare and is also age-dependent. The onset of hepatitis A is often abrupt and characteristic prodromal symptoms are followed, within a few days to a week, by dark urine and jaundice. Mild to moderate tenderness over an enlarged liver is usually detected. Serum alanine and aspartate aminotransferase levels usually both rise rapidly during the prodromal period, reach peak levels and then decrease by approximately 75% per week. Serum bilirubin concentrations reach peak levels later and decline less rapidly than serum aminotransferases. Nonetheless, the period of jaundice persists for < 2 weeks in approximately 85% of cases. Nearly all adult patients with clinically apparent disease experience complete clinical recovery with restoration of normal serum bilirubin and aminotransferase values by 6 months. Relapses and prolonged cholestasis are unusual manifestations of hepatitis A, and even in these circumstances, recovery is the rule and chronic hepatitis is not seen. The diagnosis of hepatitis A requires the detection of immunoglobulin M antibody to HAV in a patient who presents with, or has recently had, clinical features of hepatitis (icteric or anicteric disease) or in an individual with inapparent, asymptomatic infection in whom serum aminotransferase elevations may be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical manifestations and diagnosis of hepatitis A virus infection. 133 49


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