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

After a brief survey of the factors that play a role in the etiopathogenesis of human hepatocellular carcinomas, a detailed description is given of the macroscopic and microscopic features of human liver cancers as well as their association with cirrhosis. The ultrastructural features of liver cancers of various degrees of differentiation are described. The mode of spread, metastasis formation of primary liver cancers, and most frequent causes of death of liver cancer patients are reviewed.
 ...
PMID:Pathology of primary liver cancer. 22 1

Serum glutamic oxaloacetic transaminase (GOT), mitochondrial GOT (GOTm), glutamic-pyruvic transaminase (GPT) and glutamate dehydrogenase activities were determined in 43 healthy controls and in 280 cases of liver diseases. A simplified column chromatographic method coupled with UV assay was employed for separation of GOTm. The activity was measured by following decrease in abosrbance of NADH at 340 nm. The lowest activity of GOTm determined with a coefficient of variation below 10% was 6 mIU/ml. High GOTm activities were found in acute hepatitis (acute stage), subacute hepatitis and primary biliary cirrhosis and were generally associated with high total GOT (GOTt) activities. The activity ratio of GOTm/GOTt varied depending on the stage and severity of liver diseases. The GOTm/GOTt ratio was decreased in acute, fulminant and subacute hepatitides. No significant reduction in the ratio was found in bile duct obstruction, alcoholic liver injury or metastatic liver cancer. Although relatively high GOTm/GOTt ratios were found in some patients with severe hepatic injury, they had no definite association with poor prognosis. These results indicate that the marked elevation in GOTt over GPT in advanced chronic hepatitis, liver cirrhosis and primary hepatoma was mainly due to preferential leakage of cytoplasmic GOT (GOTs).
 ...
PMID:The mechanism of the release of hepatic enzymes in various liver diseases. 1. Alterations in cytoplasmic and mitochondrial enzyme activities in serum. 22 31

The number of rosette forming T cells was significantly reduced in patients with acute viral hepatitis, cirrhosis of the liver and liver cancer. The frequency of T cells in various hepatic disorders correlated well with the impairment of delayed hypersensitivity response to DNCB.
 ...
PMID:Rosette forming T lymphocytes in healthy subjects and patients with liver disease. 41 38

Serum immunoglobulins were determined in 39 healthy subjects and 55 patients with a variety of acute and chronic liver diseases. Elevation of IgG and IgA was frequently observed in healthy subjects and patients with acute viral hepatitis, liver cancer and miscellaneous liver disorders. IgG and IgM were elevated in cirrhosis of the liver.
 ...
PMID:Immunoglobulins in liver disease. 41 44

Delayed cutaneous hypersensitivity response using DNCB was studied in 51 apparently healthy Pakistanis and 60 patents with acute and chronic liver diseases. A Positive response was observed in all the healthy subjects, 22 out of 29 cases with acute viral hepatitis, 8 out of 22 patients with post-necrotic cirrhosis, one out of three cases of liver cancer and all the cases of alcoholic cirrhosis. It was postulated that hyperactive cell mediated immune response and a heavy exposure to hepatitis virus may be resonsible for the observed pattern of liver disease in Pakistan.
 ...
PMID:DNCB sensitivity in healthy Pakistani subjects and patients with liver disease. 65 81

Serum concentrations of paracetamol were followed after oral administration of the drug to 21 patients with liver cirrhosis, 4 patients with secondary liver cancer, and 15 hospitalized patients without clinical evidence of liver disease. The cirrhotic patients had 50 per cent longer half-lives of the drug. They also had significantly higher values of AUC during the first 360 minutes, in spite of almost identical means values of Cmax and tCmax. Significant differences in paracetamol elimination between cirrhotics with and without ascites, or between cirrhotic with and without porto-caval shunt could not be demonstrated.
 ...
PMID:Elimination of paracetamol in chronic liver disease. 69 4

Hepatitis type B is hyperendemic in Greenland with serologic evidence of infection in 54% of adults and a hepatitis B surface antigen (HBsAg) carrier rate of 7--25%. The impact of this infection rate on the occurrence of cirrhosis and primary liver cancer (PLC) was studied. Mortality rates for cirrhosis were obtained from official mortality statistics, 1951--1975. PLC was identified by a study of all biopsy and necropsy material taken in the study area during the same period. Neither cirrhosis nor PLC was found to be a more prevalent cause of death in this population than in Northern Europe where hepatitis B is at least 10-fold less prevalent. It is concluded that hepatitis B infection per se does not contribute significantly to the development of cirrhosis or to PLC, at least in the Eskimo population of Greenland.
 ...
PMID:Occurrence of cirrhosis and primary liver cancer in an Eskimo population hyperendemically infected with hepatitis B virus. 70 73

Sera of 184 patients were examined to determine the incidence of hepatitis B surface antigen (HBsAg). Ninety-two patients had primary liver cancer (PLC) and there were 92 matched controls. Thirty-one of the 92 patients with PLC and 8 of the 92 patients with no clinical evidence of liver disease had radio-immunoassay-positive tests for HBsAg. The difference was significant (P less than 0,01). In 56 of the patients with PLC it was possible to assess the nature of associated liver disease histologically. HBsAg was found in the sera of 66,6% of patients with postcollapse cirrhosis and in 22,2% of patients with chronic Budd-Chiari syndrome. It is likely that the role played by hepatitis B infection in the pathogenesis of PLC varies according to local circumstances in different geographical areas.
 ...
PMID:Hepatitis B surface antigen and primary liver cancer. 71 32

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
 ...
PMID:Precursor lesions for liver cancer in humans. 77 94

The seasonal variations in circulating 25-hydroxycholecalciferol (25-HCC) were studied in 102 alcoholics with fatty liver disease without histologic signs of cirrhosis and in 35 patients with alcoholic cirrhosis. The mean levels were compared with those of normal persons. Alcoholics had generally lower 25-HCC values than the controls, particularly in the summer. This was primarily explained by insufficient diet and reduced exposure to sunshine. The ability of the liver to hydroxylate in the 25-position was studied in three groups of alcoholics with 1) fatty liver disease without cirrhosis, 2) compensated cirrhosis, 3) severely incompensated liver cirrhosis. All three groups exhibited a significant increase in serum 25-HCC following the peroral administration of cholecalciferol at a dose of 1 200 U daily for 7 days. Similar rises were seen 7 days after a single injection of 10 000 U cholecalciferol. This indicates a normal intestinal absorption of vitamin D, even in advanced alcoholic liver disease, and is inconsistent with a severely damaged 25-hydroxylation capacity in these patients. Osteomalacia due to impaired liver hydroxylation of vitamin D can hardly explain the increased fracture rate and the decreased bone mass, which have been described in alcoholics.
 ...
PMID:The hepatic conversion of vitamin D in alcoholics with varying degrees of liver affection. 91 Jun 39


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>