Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and histopathological evolution of 7 children with severe chronic active hepatitis and 8 with moderate chronic active hepatitis were studied. The majority (11-15) of the children had a clear past history of acute viral hepatitis. The cases of chronic active hepatitis with a moderate activity had a favorable evolution, but not the cases of severe chronic active hepatitis. Four of them developed into liver cirrhosis, in two the morphological alteration did not improve, and only one case showed a chronic presistent hepatitis.
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PMID:Clinical and histopathological evolution of active chronic hepatitis. 9 21

The determination of enzyme activity in serum for the diagnosis of chronic hepatitis has become increasingly popular. According to the author's experience serum aminotransferase is raised in about 100% of cases of chronic active hepatitis and also in active cirrhosis, but in only about 70--80% of persisting hepatitis or in moderately active chronic hepatitis. They are frequently normal in inactive cirrhosis. After aminotransferases the alkaline phosphatase is of great importance for the differential diagnosis of icterus. If aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase are determined at the same time, every cholestatic icterus can be diagnosed with certainty.
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PMID:[Clinical enzyme diagnosis in chronic hepatitis. Possibilities and limitations (author's transl)]. 10 40

Two women, aged 41 and 51 years, developed jaundice, encephalopathy, and hypoprothrombinemia during rapid weight loss four and 12 months after jejunoileal bypass for refractory obesity. Both were treated for liver failure and received a prolonged course of nutrition parenterally and orally. Serial liver biopsy specimens demonstrated extensive alcoholic-like hepatitis and cirrhosis that improved with nutritional repletion and reanastomosis. Postoperative biopsy specimens later demonstrated minimal portal fibrosis in one patient and inactive mild cirrhosis in the other. Although previous reports indicate that patients usually die when they develop liver failure of this severity after jejunoileal bypass, prolonged intensive nutritional repletion was associated with sufficient clinical and histologic improvement in these two patients so that intestinal reanastomosis could be performed safely.
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PMID:Liver failure with steatonecrosis after jejunoileal bypass: recovery with parenteral nutriton and reanastomosis. 10 83

Retrospective evaluations were made of abdominal echograms in 61 patients who underwent liver biopsy within 3 weeks after ultrasound study. Without knowledge of clinical or biopsy data, determinations were made by two independent observers of: (1) liver size, (2) beam penetration, (3) echogenicity, (4) vascularity, (5) ancillary abnormality, and (6) diagnostic impression. Using these parameters, the presence of generalized parenchymal disease was identified in 81% of reviews of patients with cirrhosis. Thus, in patients with known cirrhosis, there was a 19% false negative rate. In normal patients, 76% were correctly called normal by the reviewers. However, in 24% generalized parenchymal disease was suggested (24% false positive). Patients with fatty liver could not be reliably distinguished from patients with cirrhosis, nor could patients with hepatitis be easily separated from those with normal livers. In all of these determinations, the combination of several features provided more diagnostic accuracy than any single echographic finding.
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PMID:Accuracy of ultrasonography in diagnosis of hepatocellular disease. 11 64

Liver dysfunction was observed in 33% of patients treated by hemodialysis and kidney transplantation. Fifty-eight percent of these cases of hepatitis occurred in patients with past or present HBs antigenemia, and 77% of HBsAg-positive patients showed evidence of LD. However, during the course of a program conducted from 1969 to 1976 and involving 267 patients, the decrease in the prevalence of HBs antigenemia observed during the last two years did not lead to any reduction in LD incidence. In a small number of patients, potentially hepatotoxic drugs could be incriminated, but in our experience azathioprine never appeared to be involved. In a few patients, LD was due to granulomatous disease of the liver, such as tuberculosis and schistosomiasis. Twenty-one (7%) of the 267 patients at risk developed chronic hepatitis, which contributed to death in nine patients. In 12 cases (three deaths), this form of hepatitis occurred in HBsAg-positive patients, and in nine cases (six deaths), in HBsAg-negative patients. In three of these latter individuals, cytomegalovirus could be incriminated. Routine monthly screening for CMV in kidney recipients confirmed the high incidence of this viral infection in such patients. Studies on murine CMV infection have demonstrated that this infection can be enhanced by histoincompatible graft or by cyclophosphamide in a model that is very close to the kidney recipient. As in mice, CMV infection in kidney recipients apparently results from reactivation of a latent infection. It seems to play a major role in the LD observed and could apparently lead to chronic hepatitis and even to cirrhosis of the liver. Finally, the occurrence of LD in HBsAg-, anti-HBs- and antiCMV-negative patients would suggest the responsibility of other viruses for the pathogenesis of liver disease in patients treated by hemodialysis and kidney transplantation. Besides Epstein-Barr virus, other viruses, such as hepatitis C virus, should be thoroughly scrutinized.
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PMID:Liver disease in patients undergoing hemodialysis and kidney transplantation. 11 44

The carcinogenicity of aflatoxin B1 (AFB1) has been under evaluation in nonhuman primates for the past 13 years. A total of 47 Old World monkeys, chiefly rhesus and cynomolgus, have received AFB1 i.p. (0.125 to 0.25 mg/kg) and/or p.o. (0.1 to 0.8 mg/kg) for 2 months or longer, and 12 are currently alive and without evidence of tumor. Thirteen of the 35 monkeys necropsied to date (37%) developed one or more malignant neoplasms, yielding an overall tumor incidence of 28%. Five of the neoplasms were primary liver tumors (2 hepatocellular carcinomas and 3 hemangioendothelial sarcomas), and 2 cases of osteogenic sarcoma were found. Other tumors diagnosed were 6 carcinomas of the gall bladder or bile duct, 3 tumors of the pancreas or its ducts, and one papillary Grade I carcinoma of the urinary bladder. The tumors developed in animals receiving an average total AFB1 dose of 709 mg (range, 99 to 1354 mg) for an average of 114 months (range, 47 to 147 months). Fifteen of the 22 necropsied monkeys (68%) without tumor showed histological evidence of liver damage, including toxic hepatitis, cirrhosis, and hyperplastic liver nodules. These animals had received an average total AFB1 dose of 363 mg (range, 0.35 to 1368 mg) for an average of 55 months (range, 2 to 141 months). Our results indicate that AFB1 is a potent hepatotoxin and carcinogen in nonhuman primates and further support the hypothesis that humans exposed to this substance may be at risk of developing cancer.
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PMID:Induction of osteogenic sarcomas and tumors of the hepatobiliary system in nonhuman primates with aflatoxin B1. 11 76

A new precipitating antigen-antibody system possibly was demonstrated by immuno-diffusion in the serum of patients suffering from non A-non B hepatitis. The antigen appears during the first four weeks of transaminases elevation. In acute cases was transient antigenemia (average 3 weeks). Antibodies appeared rapidly after the disappearance of antigen. The same antigen was also detected, by immunodiffusion and by immunofluorescence, in the liver nuclei of infected hepatocytes. This antigen specific appears for non A-non B hepatitis since it is neither found in the serum of normal subjects nor in that of patients with cirrhosis toxic or viral that hepatitis A or B. The hypothesis of a virus associated antigen is the most likely explanation.
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PMID:[Demonstration of a serum and liver antigen in acute or chronic non A-non B viral hepatitis]. 12 Sep 41

Purified and concentrated preparations of Australia antigen had no stimulating effect on leukocytes of human subjects under study when tested either on DNA-polymerase activity, 3H-thymidine uptake or chromosomal alterations. Moreover, in patients with chronic hepatitis and cirrhosis of the liver no correlation between antigenemia and chromosome aberrations in blood leukocyte cultures could be detected. On the other hand, a serum obtained from a virus hepatitis patient with Australia antigen in the blood was found to stimulate leukocyte cultures from one patient with Down's syndrome and antigenemia, one mentally retarded patient and three normal donors. This stimulating agent is obviously not associated with Australia antigen.
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PMID:Investigation of the nature of Australia antigen. I: The absence of biological activity of Australia antigen in human blood leukocyte culture. 12 42

The results of liver scans performed with 99mTc-sulphur colloid in 169 patients suffering from diffuse liver diseases and in 48 normal controls were evaluated. The patients with reactive hepatitis, acute hepatitis, chronic persistent hepatitis, fatty liver and fibrosis of the liver show only minimal deviations from the scintigraphic pattern. On the contrary, highly increased colloid uptake in the spleen is found in cases of chronic aggressive hepatitis, whilst the intrahepatic distribution of the colloid is approximately normal. In cases of liver cirrhosis, increased colloid uptake is found in the left lobe of the liver as well as in the spleen and in the bone marrow. Either normal findings or cirrhosis-like changes of the colloid distribution are observed in patients with alcoholic hepatitis.
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PMID:[Liver scanning in diffuse liver disease (author's transl)]. 12 69

The results of subtyping the B antigen in 551 sera from patients with viral hepatitis, chronic evolutive hepatitis and cirrhosis, chronic carriers, donors and healthy subjects, were confirmed as positive HBAg by diffusion in agar, counterelectrophoresis and radioimmunology, and characterized by the d-y and w-r determinants by rheophoresis. The high incidence of the y determinant in all nine counties investigated probably reflects the prevalence of this serotype in Romania, recalling the distribution of subtypes observed in the south of Europe.
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PMID:[Distribution of subtypes of viral hepatitis B antigen in areas of Rumania]. 13 42


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