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)

Among 530 consecutive patients hospitalized for acute hepatitis cytomegalovirus infection was diagnosed in 5 (0.9%). In 2 cases the infection was due to blood transfusion. The course of the disease was Got essentially different from hepatitis A, B, or non-A, non-B, however, clinical and biochemical manifestations of cholestasis were common. All biochemical abnormalities returned to normal within few weeks. In conclusion, it seems that cytomegalovirus is a rare cause of clinically overt hepatitis and its course is often cholestatic.
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PMID:[Cytomegalovirus hepatitis]. 164 69

The work deals with a group of 212 patients suffering from various forms of precirrhotic alcoholic liver disease and includes a period of 8.5 years (January 1981-June 1989). At least two liver biopsies were performed in all patients. according to the histological diagnosis, the patients were distributed into 6 subgroups: simple hepatic steatosis--24 cases (11.3%), hepatic fibrosis--40 cases (18.8%), hepatic steatofibrosis--69 cases (32.5%), acute alcoholic hepatitis--18 cases (8.5%), chronic active hepatitis--43 cases (20.3%) and chronic persisting hepatitis--18 cases (8.5%). The assessed histological parameters included: fatty transformation, hepatic fibrosis, inflammatory infiltrate within the lobules and in the portal spaces, hepatocellular necrosis, cholestasis, proliferation of the bile ductules and modification of the lobular architectonic. The work is aimed at pointing out the precirrhotic hepatic histological lesions induced by alcohol and fraught with an increased risk of progression towards liver cirrhosis. The histological sequential examination of alcoholic hepatic lesions confirm the possibility of progression and installation of the cirrhotic stage for a number of these lesions. Liver cirrhosis developed in 44 patients (20.7%) within a period of 3-7 years, on an average 5.5 years. The progression toward cirrhosis occurred in 12 patients (5.7%) with steatofibrosis, in 11 (5.2%) with hepatic fibrosis, in 14 (6.6%) with an intralobular inflammatory infiltrate, in 17 (8%) with hepatocellular necrosis, in 3 (1.4%) with cholestasis, in 5 (2.3%) with proliferation of the bile ductules and in 10 patients (4.7%) with a modification of the lobular architectonic. In addition, cirrhosis was detected in 8 patients (3.8%) with alcoholic hepatitis and in 13 patients (6.1%) with chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The criteria of histological activity and the prognosis in precirrhotic alcoholic hepatopathies]. 167 Jan 14

Diphenylhydantoin-induced hepatitis and mononucleosis are uncommon in children. The occurrence of these two diseases in the same individual, with progression to hepatic failure is rare and has not been reported in infants. This report represents a 6-month-old male infant who developed an infectious mononucleosis-like syndrome and hepatic failure 16 days after diphenylhydantoin administration. He took this anticonvulsant for controlling seizures after a head injury. Fever, skin rash, hepatosplenomegaly, lymphadenopathy, and atypical lymphocytosis led to the initial diagnosis of infectious mononucleosis. However, negative heterophil antibody did not support the diagnosis. Jaundice ensued in the following course and became more and more profound. Meanwhile, physical examination showed shrinking in liver size. Negative virology studies, including Epstein-Barr virus, cytomegalovirus, and hepatitis B virus, excluded them as causative agents. The patient lapsed into a stage I hepatic coma, but gradually recovered clinically and biochemically after eight successive exchange transfusions and supportive care. Two liver biopsies were performed 20 and 50 days after the onset of disease, respectively. Remarkable hepatic parenchymal loss, cholestasis, and fatty change were found on histologic examination of the first biopsy specimen, and portal fibrosis was noted on the second.
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PMID:Mononucleosis and hepatic failure associated with diphenylhydantoin treatment in an infant. 167 17

Non-sulfated bile acid levels including cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), lithocholic acid (LCA), ursodeoxycholic acid (UDCA), five taurine conjugates, and five glycine conjugates in duodenal juice were measured in 50 Chinese infants with cholestasis to test their diagnostic value. All 17 with biliary atresia (BA) cases, 11 out of 26 neonatal hepatitis (NH) cases and one case with paucity of the interlobular bile duct were without detectable bile acids. In those NH patients with detectable bile acids, the major components were conjugated forms of CA and CDCA, which was similar to all 6 cases of the comparison group with other diseases. The minor bile acid components identified in them were glycine conjugated UDCA, free CDCA, free CA, and free and conjugated DCA. Only one patient with NH had taurine conjugated LCA. The mean total duodenal bile acid level in 15 patients with NH was significantly lower than that in the 6 patients of the comparison group. Most patients with NH had a CDCA/CA ratio of less than one, indicating that cholic acid is the predominant form in their bile. Glycine conjugated bile acids were the predominant bile acids present in 11 out of 15 patients with NH and 4 out of 6 of the comparison group patients. The results suggest that the detection of duodenal bile acids by a sensitive HPLC method is of limited value in making a differential diagnosis between BA and NH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of duodenal bile acids by high performance liquid chromatography in infants with cholestasis. 168 Sep 88

Low gamma-glutamyl transpeptidase (gamma-GTP) activity in serum was observed in 11 patients with acute intrahepatic cholestasis (cholestatic hepatitis and fulminant hepatitis), despite a marked increase in bilirubin levels. Inhibitors of gamma-GTP were not detected in sera of these patients. Their gamma-GTP levels in the liver were significantly higher than those in chronic liver diseases. An electrophoretic study of liver gamma-GTP in acute intrahepatic cholestasis showed the same mobility as in chronic liver diseases. These results suggest that the low serum gamma-GTP activity in acute intrahepatic cholestasis is due to factors inhibiting the release of the enzyme from the liver.
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PMID:Low activity of gamma-glutamyl transpeptidase in serum of acute intrahepatic cholestasis. 168 17

The clinical specifity of an intraparticular virus-DNA of 5001 Bp associated with non-A, non-B hepatitis (HNANB) was evaluated. Investigations were done in liver biopsies and lymphocytes in 173 patients having acute or chronic HNANB (n = 107) or liver diseases of other etiology (n = 66). The sensitivity of the test system (polymerase chain reaction, southern-transfer, DNA-hybridisation with synthetic oligonucleotides) was less than 100 virus particles per probe. In all patients with acute HNANB (n = 5) (parenteral mode of infection) the DNA was found in 100% in liver and lymphocytes, and in 22 of 27 patients with acute sporadic HNANB. HNANB associated substance (HNANB-AS) (1.3 g/ml CsCl) excreted with feces was found in 50%, and 29.6%, respectively. In chronic HNANB the DNA was found in 83.3% in the liver (n = 42) and in 56.7% in lymphocytes (n = 30). The HNANB-AS was found in 45.6% (n = 68). In liver diseases with other etiologies as HNANB-infection (e.g. HBV, HAV, cholestasis, HBsAg pos.-liver cirrhosis) (n = 33) the DNA was found neither in liver biopsies nor in lymphocytes. In liver diseases of uncertain etiology, but with NANB-infection under discussion (e.g. nonspecific reactive hepatitis, fatty liver, HBV neg liver cirrhosis) the DNA was found in the liver in 24% (n = 25) and in lymphocytes in 40% (n = 5). In patients with clinically resolved HNANB no DNA was found in liver and lymphocytes (n = 5). All stools were negative for HNANB-AS in the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of the specificity of detecting viral DNA in non-A, non-B hepatitis in liver tissue and lymphocytes]. 170 May 57

It has become apparent that with sophisticated technology we are now able to recognize defective bile acid metabolism in a wide variety of disease states. Recognition of specific aberrations, such as inborn errors in bile acid metabolism manifesting as neonatal cholestasis, offers new opportunities for therapeutic intervention. Future studies should determine the incidence of inborn errors in patients with enigmatic and unexplained liver diseases such as idiopathic neonatal hepatitis.
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PMID:Fetal and neonatal bile acid synthesis and metabolism--clinical implications. 174 13

The alpha 1-antitrypsin deficient subject (protease inhibitor (PI) phenotype ZZ) has an increased susceptibility to liver disease. The condition is most commonly identified in early infancy as a conjugated hyperbilirubinaemia with hepatitis (11%) or a bleeding state due to vitamin K malabsorption (2%). 50% of cases have cirrhosis and 25% die in the first decade of life. A further 2% present with cirrhosis in later childhood. Adult males are at risk of hepatoma development with or without cirrhosis. Diagnosis is by isoelectric focussing or allele-specific oligonucleotide hybridization. The treatment is that of cholestasis and cirrhosis including transplantation. The pathobiology of the deficiency state, the mechanism of liver damage and the vulnerability of the newborn liver are discussed in this review. A plea is made for a trial of infusions of alpha 1-antitrypsin in early infancy, as is used safely but without proven efficacy in the emphysematous PIZZ subject. Prospects of therapy by gene modification are also reviewed.
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PMID:Alpha 1-antitrypsin deficiency and liver disease: clinical presentation, diagnosis and treatment. 174 15

The value of transcutaneous biopsy of the liver was assessed in a series of 110 cases of fever of unknown origin or of unexplained inflammatory syndrome. Liver histology was useful to the ultimate etiological diagnosis in 12 cases (11 per cent). The result of a transcutaneous biopsy of the liver was considered an essential aid to the ultimate diagnosis in 7 of these 12 cases. A hepatic lesion regarded as useless for the ultimate diagnosis was present in 16 cases (14.5 per cent). In the other cases, hepatic histology was normal or showed a non-specific reactive hepatitis. Unicteric cholestasis was present in 73 per cent of the cases but was of no predictive value for the detection of a useful hepatic lesion. On the other hand, serum transaminase levels were significantly higher when a useful lesion of the liver was observed.
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PMID:[Unexplained fever or inflammatory syndrome. Diagnostic value of liver puncture-biopsy]. 182 78

The aim of this study was to assess the diagnostic sensitivity and specificity of hepatobiliary scintigraphy using a 99mTc-HIDA compound to differentiate intrahepatic cholestasis from extrahepatic forms during the first months of life. The tracer used was acid N-(2,6)-diethylacetanylido-iminodiacetic (diethyl-HIDA) with almost exclusively biliary excretion and a high concentration of radioactivity in the bile. Each neonate was injected with 0.5 mg/kg i.v. of the compound marked with a dose of 99mTc equivalent to 80-100 microCi/kg. Scintigraphic recordings were carried out every 10' for the first hour and further controls were performed at 2, 3, 4, 8 and 24 hours. Scintiphotos were obtained using a Polaroid scintillation camera, PHO Gamma V. Fifty-four patients were included in the study (34 males and 20 females) aged between 4 days and 3 months old. All patients were clinically suspected of pathologies involving the hepatobiliary tract. All cases were affected by persistent jaundice (total bilirubin between 1.8 and 39.6 mg%) with predominantly direct bilirubin (range 1.5-26.2 mg%), acholic feces and hyperchromic urine. Hepato-biliary scintigraphy revealed an intestinal excretion of tracer in 31 out of the 54 neonates examined, excluding the presence of an extrahepatic obstruction of the biliary tract. On the other hand, only 13 out of 23 cases in which no enteric excretion of the tracer was observed, was the final diagnosis one extrahepatic cholestasis. Scintigraphic tests therefore showed a 100% sensitivity associated with a specificity of only 56.52%. This demonstrates that the finding of tracer in the intestine is pathognomonic of the permeability of extrahepatic biliary ducts and that biliary atresia can be ruled out. On the contrary, the absence of the intestinal excretion of the tracer is nor constantly associated with biliary atresia. This study has confirmed this finding in 10 cases of intrahepatic cholestasis (4 hypoplasias of the intrahepatic biliary tract, 3 thick bile syndromes, 3 cases of hepatitis due to cytomegalovirus). In conclusion, the Authors state that hepato-biliary scintigraphy represents a straightforward and non-invasive diagnostic method which enables the permeability of the biliary tract to be assessed in subjects with jaundice.
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PMID:[Neonatal hepatic cholestasis with particular regard for the use of radioisotopes in its diagnosis]. 184 29


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