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)

Between July 1987 and May 1989, 11 liver transplants were performed on 10 patients at the University Hospital of Geneva. Of 15 patients evaluated for elective transplantation, 10 were accepted and put on the waiting list. 5 patients were rejected because of a contraindication or because another treatment seemed preferable. 8 transplantations were eventually performed. Emergency transplantation was considered for 6 patients, but could be performed in only 3. Indications for transplantation were as follows: one hepatocellular carcinoma in a non-cirrhotic patient, 2 post-hepatitis cirrhoses (one B and one non-A-, non-B), 3 primary biliary cirrhoses, one autoimmune cirrhosis, one primary sclerosing cholangitis, one cirrhosis on alpha-1-antitrypsin deficiency, and one fulminant B-Delta hepatitis. Most of these patients had advanced liver disease and a limited life expectancy. 8 of the 10 patients transplanted are nevertheless alive and none is hospitalized at the present time. More than mere survival, however, quality of life regained after transplantation prompts us to consider transplantation early in the progress of the disease. Earlier evaluation of patients would make transplantation feasible soon after the first complication of the disease. This attitude would probably prevent patients from dying while on a waiting list and decrease operative as well as early postoperative risks. Better information and coordination regarding potential donors is necessary in Switzerland to obtain better results in organ transplantation.
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PMID:[Liver transplantation. Preliminary results in the district University Hospital of Geneva]. 237 94

The frequency of occurrence of alpha-1-antitrypsin (A1AT) deficiency among total of 3228 Polish children with chronic liver diseases and chronic disease of respiratory tract was determined. It was observed that among children with chronic liver diseases which disclosed more frequent defect (concentration of A1AT below 150 mg/dl was found in 10.3% of children), the highest occurrence of deficiency was in children with neonatal hepatitis (23.1%). The deficiency was connected with the presence of ZZ and MZ phenotypes of A1AT.
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PMID:Inherited defect of alpha-1-antitrypsin associated with chronic liver and respiratory tract diseases in children. 248 74

Although hepatitis B virus (HBV) has been closely associated with the development of hepatocellular carcinoma (HCC), no serologic markers of HBV can be found in up to 11% of HCC patients in developing countries and up to 68% of HCC patients in industrialized countries. Despite the absence of HBV serologic markers in these HCC patients, HBV DNA sequences have been found to be integrated into HCC DNA in 13-100% of these patients, indicating a possible role of HBV in the etiology of their HCC. Although six patients with chronic non-A, non-B hepatitis virus infection who were followed have been documented to develop HCC, it is not known whether the non-A, non-B hepatitis viruses cause or contribute to the development of HCC in some HCC patients without HBV serologic markers. Ethanol, cigarette smoking, oral contraceptives, and aflatoxin also have been suggested as possible etiologies and should be studied further. Suggested etiologies that are not supported by the published data include alpha-1-antitrypsin deficiency and schistosomiasis.
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PMID:Hepatocellular carcinoma: possible etiologies in patients without serologic evidence of hepatitis B virus infection. 253 73

Low alpha-1-antitrypsin (AAT) levels are known to be associated with liver disease. As AAT is also synthesised in the liver, we investigated whether liver disease itself may result in low AAT levels. AAT was measured in plasma from 100 patients with various liver diseases including hepatitis, cirrhosis, jaundice and liver failure. Twenty-eight patients had increased AAT values (greater than 3.1 g/L), 70 had normal AAT values (between 1.5 and 3.1 g/L) and 2 had decreased AAT levels (less than 1.5 g/L). The 2 patients with low AAT levels were found to be of the PiMZ phenotype. There was no significant correlation between any of the standard 'liver function tests' and the AAT level. Our findings suggest that in liver disease AAT levels are usually normal or increased. Low levels are uncommon and the possibility of an abnormal AAT phenotype being associated with the liver disease should be examined.
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PMID:Alpha-1-antitrypsin in liver disease. 278 65

The reactivity of alpha-1-antitrypsin (AAT) with Lens culinaris agglutinin (LCA) was studied by crossed immuno-affinity electrophoresis of the sera of 246 subjects from 6 groups (acute virus hepatitis, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma (HCC), carcinoma metastatic to the liver and normal controls). Two species of AAT (LCA-reactive and -nonreactive species) were detected on crossed immuno-affinity electrophoresis in a gel containing LCA. The percentages of LCA-reactive species of AAT in neoplastic diseases of the liver were significantly higher than those in benign liver diseases and normal controls. There was no correlation between the percentage of LCA-reactive species of AAT and serum AAT concentration in any group. Furthermore, in studying 15 pairs of serum samples before and after the subsequent development of HCC, the percentage of LCA-reactive species of AAT after HCC occurrence was significantly higher than that before, although there was no statistically significant difference between the serum AAT concentration before and after development of the disease. The latter 15 patients were all of the normal protease inhibitor phenotype (PiMM) and no change in phenotype was observed before and after the development of HCC. The results indicate that measurement of the reactivity of AAT with LCA can be a useful marker for the diagnosis of HCC and carcinoma metastatic to the liver, especially when serum concentrations of alpha-foetoprotein or other tumour markers are within the normal ranges.
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PMID:The reactivity of alpha-1-antitrypsin with Lens culinaris agglutinin and its usefulness in the diagnosis of neoplastic diseases of the liver. 282 74

Fifty-six patients with moderate to severe neonatal hepatitis were followed for 12 to 78 months. Two died from causes other than hepatitis itself and were free from liver disease at the time of death. Of the remaining 54 patients, seven died of hepatitis, two are living with chronic liver disease and psychomotor retardation, and 45 are living without liver disease. High peak bilirubin levels and liver histologic findings of periportal fibrosis, moderate to severe portal inflammation, and/or diffuse giant cell transformation appear to be major factors predictive for poor outcome. Cytomegalovirus (CMV) infection was a common associated infection. Evidence of CMV infection was found in 22 (49%) of the 45 patients studied. Three of them died, and one is still living with cirrhosis of the liver. Metabolic disorders such as alpha-1-antitrypsin deficiency, galactosemia, and aminoaciduria and/or aminoacidemia were carefully screened but were not found in these cases. A fatal case had a sibling who had died of a similar disease course. Chinese infants may have metabolic and familial cholestasis diseases requiring further investigation.
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PMID:Neonatal hepatitis: a follow-up study. 282 43

Human cirrhotic livers exhibited a strong resistance to metastasis and demonstrated high levels of both soluble and 3 M NaCl extractable metalloproteinase inhibitor(s) directed against tumor type I and type IV collagenases. This inhibitory activity was detected in human cirrhosis from diverse causes, including alpha-1-antitrypsin deficiency, alcoholic liver disease, postviral hepatitis, and biliary cirrhosis, but was nearly undetectable in normal liver. The inhibitory activity was able to be purified by carboxymethyl cellulose chromatography and gel filtration, had a molecular weight of approximately 40,000, and was relatively heat stable. Such metalloproteinase inhibitory activity was also present in conditioned media of human myofibroblast primary cultures obtained from cirrhotic liver explants but absent in conditioned media of primary normal liver explants. Purified fractions of the metalloproteinase inhibitor activity obtained from both myofibroblast conditioned media and extracts of cirrhotic liver blocked invasion but not attachment of MCF-7 cells on human amnion in vitro. The results further support the role of myofibroblasts in inhibiting tumor invasion and metastasis and provide one possible mechanism by which cirrhotic livers resist metastasis.
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PMID:High metalloproteinase inhibitor content of human cirrhosis and its possible conference of metastasis resistance. 283 Apr 5

Twelve of sixteen consecutive needle biopsies of liver with either acute or chronic hepatitis showed positive immunohistochemical staining for alpha-1-antitrypsin (AAT). Only two of the positive biopsies contained numerous, large periodic acid-Schiff positive, diastase resistant (PAS-D) globules in periportal hepatocytes; both patients were Pi MZ but only one had a low serum AAT concentration. The other 15 patients had normal or elevated serum AAT. The accumulation of AAT in hepatocytes, demonstrated by sensitive immunohistochemical staining, may indicate increased synthesis and/or impaired secretion of AAT occurring in association with various types of hepatitis.
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PMID:Detection of alpha-1-antitrypsin in hepatocytes in acute and chronic hepatitis. 332 44

Fourteen cases of alpha-1-antitrypsin deficiency are presented. All of them had a PIZZ phenotype except two in which a PIMZ phenotype was found. It must be pointed out that histological findings show a great variability among the different patients most of which did not have intracellular PAS-positive amylase inclusions in liver biopsy specimens. Clinical course did not correlate with either the age of onset of the disease or the phenotype found, thus indicating that other additional factors are involved in determining prognosis. We insist on the importance of a careful study of all neonatal hepatitis syndromes in order to rule out a alpha-1-antitrypsin deficiency.
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PMID:[Hepatic lesions caused by alpha 1-antitrypsin deficiency in childhood. Review of 14 cases]. 348 28

The weights of the spleens of series of patients with various disorders of children dating from birth or early infancy and causing splenomegaly, with or without cirrhosis of the liver, were analyzed. The linear regression equation for spleen weight versus age in months for each disease was derived, and the rate constants from these equations were adjusted for the age range of the patients in each group. The original data of Coppoletta and Wolbach were used for normal values. The rates of splenic growth of appropriate entities for which the regression equation could be computed fell into three groups, with adjusted rate constants (growth of spleen in grams per month) of 6.53-6.95 (biliary atresia, thalassemia, and cirrhosis following neonatal hepatitis), 2.30-2.62 (cirrhosis of alpha-1-antitrypsin deficiency, infantile polycystic disease, and spherocytosis), and 1.06-1.11 (cystic fibrosis and idiopathic thrombocytopenic purpura). These classes of splenic growth rates are approximately 10, 3.7, and 1.6 times the normal growth rate (0.67 g/mo). Rate constants could not be computed for the categories cirrhosis following viral hepatitis and hemolytic anemia other than spherocytosis and sickle cell anemia, and the numbers of patients with splenic vein obstruction, cirrhosis with the cholestatic syndrome of parenteral alimentation, hypoplastic anemia with hemosiderosis, tyrosinemia, Byler's disease, congenital hepatic fibrosis, and Wilson's disease were too few for analysis. The significance of the finding of classes or "quantum groups" of splenic growth rates in disorders of children, dating from birth or early infancy and causing splenomegaly, is uncertain. Comparable data on adequate series of patients with other appropriate disorders will be necessary.
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PMID:Splenic growth rates in cirrhotic and other splenomegalic diseases of childhood. 384 62


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