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)

Three patients with symptomatic, noncirrhotic primary biliary cirrhosis who had no evidence of esophageal varices on esophagogastroduodenoscopy and who were treated with ursodeoxycholic acid, 15 mg.kg-1.day-1, for a period of 1-2 years are reported. Initially, all three patients showed improvement in symptoms of fatigue and pruritus, and there was marked improvement or normalization in serum levels of bilirubin, alkaline phosphatase, and alanine aminotransferase. However, after 1-2 years, all three patients progressed histologically to cirrhosis on follow-up liver biopsy, and all had esophageal variceal bleeding documented by esophagogastroduodenoscopy. These three patients represent examples of ursodeoxycholic acid treatment failure despite improvements in symptoms and biochemical liver test results.
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PMID:Progression of primary biliary cirrhosis with ursodeoxycholic acid therapy. 829 25

In a 4-year review of 509 patients with chronic pancreatitis, the incidence of clinically manifest fixed common bile duct (CBD) stenosis was 9% (45 patients). In 76% this was alcohol related, and pancreatic calcification was present in 51%. All patients presented with unrelenting jaundice and five (11%) had cholangitis. The mean serum bilirubin (165 +/- 108, normal 0-17 mumol/l), alkaline phosphatase (1790 +/- 1143, normal 73-207 U/l) and gamma glutamyl transferase (798 +/- 660, normal 7-64 U/l) were markedly raised. Diabetes occurred in 8 (18%). A biliary drainage operation was performed in 43 patients and 11 had concomitant pancreaticojejunostomy. Endoscopic retrograde cholangiopancreatography (ECRP) provided valuable information preoperatively in outlining both biliary and pancreatic disease in selecting patients for dual ductal drainage. Minor complications not related to biliary anastomosis occurred in 14%. Four patients died (9%), two from pseudocyst-related haemorrhage. Jaundice was successfully relieved in all and did not recur during follow-up. No secondary biliary cirrhosis was encountered, but varying degrees of portal fibrosis were present in 75% of liver biopsies. The commonest biliary pathogen was E. coli. It is recommended that a biliary bypass operation be performed when the diagnosis is radiologically confirmed and no improvement occurs within 1 month.
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PMID:Chronic pancreatitis with biliary obstruction. 156 30

It has been reported that hepatoma (HCC) cells produce abnormal proteins such as erytropietin, fibrinogen, prothrombin, and, recently, antithrombin III (AT III). In a preliminary report, we reported increased AT III levels in patients bearing HCC independent of their clinical liver status. The present study was performed to assess antithrombin III levels and other serological data present in patients with cirrhosis and in patients with cirrhosis and clinical findings of neoplastic disease. In 70 well-matched patients (47 with cirrhosis and 23 with cirrhosis and proven HCC) serum total cholesterol, albumin, prothrombin, alkaline phosphatase, AFP, aminotransferases, and AT III were determined. Together with AFP and alkaline phosphatase, patients with HCC had higher values of AT III (88 +/- 7%) and total cholesterol (184 +/- 17 mg/100 ml), as compared with cirrhotic patients (AT III 56 +/- 3.6%; total cholesterol 113 +/- 5 mg/100 ml) (P less than 0.001). No difference was observed between these two groups for albumin, prothrombin, and aminotransferases. In HCC patients, AT III levels were related to the total cholesterol level (R2 = 0.317), whereas in the cirrhotic patients it correlated with the prothrombin level (R2 = 0.274). These data suggest that in HCC patients a greater rate of synthesis of AT III occurs, whereas in cirrhotic patients lower levels of AT III occur due to impaired synthesis or increased catabolism of the protein. The serial determination of AT III in cirrhotic patients as a means of detecting neoplastic transformation is suggested.
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PMID:Hepatocarcinoma in cirrhosis. Is antithrombin III a neoplastic marker? 164 42

In the last decade, the primary, biliary liver cirrhosis was diagnosed in 17 female patients aged between 33 and 72 years. The most frequent complaint were itching and jaundice. Hepatomegaly and itching predominated in the clinical signs Laboratory tests have shown and increase in alkaline phosphatase activity, gamma-glutamyltranspeptidase, and alanine-aminotransferase activities, accelerated ESR and decrease in blood serum albumins. Immunological abnormalities were found in 15 patients, including 12 with antimitochondrial antibodies. Liver biopsy was carried out in all patients enabling to diagnose the primary cirrhosis in 14 of them. Duration of the disease was between 1 and 9 years. Immunosuppressive treatment was carried out in 10 patients, and symptomatic treatment in the remaining 7 patients. No difference in the effect of therapy on actual health state of patients was seen.
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PMID:[Primary biliary liver cirrhosis in patients treated at Szczecin hospitals in 1978-1988]. 166 45

Serum Mn-superoxide dismutase (Mn-SOD) was determined in patients with various liver diseases including 31 patients with primary biliary cirrhosis (PBC), 46 with hepatocellular carcinoma (HCC), 17 with liver cirrhosis (LC), 23 with chronic hepatitis (CH) and 12 patients with obstructive jaundice with an enzyme-linked immunosorbent assay using a specific monoclonal antibody. The serum level in patients with PBC (407 +/- 35 ng/ml, mean +/- SEM; n = 31) was significantly increased (p less than 0.01) compared with those of other liver diseases. Mn-SOD level did not correlate with total bilirubin level, gamma-glutamyl transpeptidase activity, alkaline phosphatase activity, alanine aminotransferase activity, IgM, or with ceruloplasmin level in the sera of the patients. When the patients with PBC were histologically subdivided into four groups according to Scheuer's classification (Scheuer PJ. Primary biliary cirrhosis. In: Scheuer PJ, ed. Liver biopsy interpretation. 3rd ed. London: Bailliere Tindall, 1980:47-56), a high level of serum Mn-SOD was noticed in the early stage as well as in the advanced stage of the disease. Immunoblot analysis confirmed the reactivity and specificity of the monoclonal antibody to the enzyme protein in the patients' sera. Immunostaining of a liver biopsy specimen from the patients with PBC revealed increased expression of the enzyme protein in damaged epithelial cells of interlobular bile ducts, bile ductules, and degenerated hepatocytes. These data suggested that free radicals including superoxide anion are possibly involved in the pathogenesis of the disease and Mn-SOD may play some role in a protection against the superoxide anion.
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PMID:Elevated level of serum Mn-superoxide dismutase in patients with primary biliary cirrhosis: possible involvement of free radicals in the pathogenesis in primary biliary cirrhosis. 168 6

We investigated by enzyme electrophoresis after prolonged neuraminidase treatment the activity of "intestinal variant" (alpha 2-globulin mobility) alkaline phosphatase (EC 3.1.3.1; ALP) in the plasma of 189 patients selected for disorders (diabetes mellitus, liver cirrhosis, and chronic renal failure) with a known high frequency of increased plasma intestinal (beta-globulin mobility) ALP activity. The overall frequency of the variant ALP was 23.8%, whereas in the samples showing intestinal ALP it was 45.0%. The variant ALP was not observed in the absence of intestinal ALP, nor in patients of blood group A. Its frequency did not differ significantly between the different patient groups. Quantification of the variant ALP by densitometry was unsatisfactory but the quantity could be estimated by subtracting the intestinal ALP activity measured by electrophoresis from the activity determined by immunoassay with monoclonal antibody that reacts with both the intestinal and the variant forms. This indicated median activity of 12 U/L for the variant, approximately equal to that of the concomitant intestinal ALP. From the effects of papain and bromelain treatments, we suggest that "intestinal variant" represents intestinal ALP with attached membrane-binding domain.
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PMID:Intestinal variant alkaline phosphatase in plasma in disease. 170 Jul 41

The liver is an estrogen responsive organ. Clinically, estrogens may play a role in the induction of liver tumors and, experimentally, estrogens are involved in the control of hepatocyte proliferation. The results of a prospective controlled clinical trial using an anti-estrogen, tamoxifen, in patients with unresectable hepatocellular carcinoma (HCC) are presented below. Thirty-eight consecutive cirrhotics with HCC were allocated to either 30 mg/day tamoxifen or no treatment. The two groups of patients were matched for mean age, male/female ratio, Child-Pugh risk group, approximate tumor volume (US and/or CT scan) and etiology of the underlying cirrhosis. The drug appeared to have no side effects. Survival was significantly prolonged in tamoxifen-treated patients with 22% (vs. 5%) survival at 12 months. No differences were observed between males and females or alcoholic and non-alcoholic cirrhosis. In 53% of tamoxifen-treated patients the levels of alpha-fetoprotein dropped and, in this subgroup, survival was further prolonged. Tumor volume, lactate dehydrogenase (LDH) and alkaline phosphatase slowly increased, suggesting a slower, but continuous, progression of the disease. In conclusion, anti-estrogen treatment appears effective in the palliation of unresectable or otherwise untreatable HCC. A reduction in alpha-fetoprotein levels appears to be a favorable prognostic index.
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PMID:Unresectable hepatocellular carcinoma: a prospective controlled trial with tamoxifen. 170 74

(1) Liver cirrhosis was induced in male rats by treatment with carbon tetrachloride and phenobarbitone for 130-142 days. Detailed histological examination showed all livers from rats treated with carbon tetrachloride had annular fibrosis, necrosis, loss of normal hepatic architecture and other features that were consistent with an established micronodular cirrhosis. (2) Plasma biochemical analysis showed a significant reduction in total protein concentration (13%), which was due entirely to a reduction in plasma albumin (29%). There were also large increases in the plasma activities of alkaline phosphatase (110%) and aspartate aminotransferase (159%), when compared to phenobarbitone-treated controls. Plasma cholesterol was also increased (67%), but other plasma analytes were not significantly altered. (3) The soleus (Type I), plantaris (Type II) and gastrocnemius (Types I and II) muscles were dissected and examined for possible differential effects. There were minor reductions in all three muscle weights, but these changes did not reach statistical significance. The protein, RNA and DNA concentrations, total muscle content and content relative to body weight in cirrhotic rats were also not significantly altered in any of the muscles. Cirrhosis did not cause any perturbations in derived parameters, i.e. amount of synthetic apparatus per cell, RNA/DNA ratio, apparent cell size, protein/DNA ratio and the capacity for protein synthesis or RNA/protein ratio. (4) The gastrocnemius was fractionated into soluble, stromal and myofibrillar proteins. The concentrations and contents of all three proteins were unaltered in cirrhotic animals, compared to controls. (5) It is concluded that in this experimental model of cirrhosis there were no effects on those skeletal muscle variables which are strikingly altered by chronic alcohol feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver histology, blood biochemistry and RNA, DNA and subcellular protein composition of various skeletal muscles of rats with experimental cirrhosis: implications for alcoholic muscle disease. 170 23

Serum CA 19-9 and alpha-fetoprotein (AFP) levels were determined in 211 patients with liver cirrhosis and 27 with primary hepatocellular carcinoma (HCC) associated with liver cirrhosis. This was done to determine the usefulness of CA 19-9 level with respect to AFP level in distinguishing between these two illnesses, and to assess the influence of some clinical and biochemical variables on these tests in patients with liver cirrhosis with or without primary HCC. Pathologic AFP values were found in 23 of 27 (sensitivity, 85%) patients with HCC; CA 19-9 levels increased in only 12 of 27 (sensitivity, 44%) HCC patients, the values being comparable with those of patients with liver cirrhosis. In liver cirrhosis a substantial number of false-positive values was found for both markers, although they were higher for CA 19-9 (50 of 211 versus 39 of 211). In liver cirrhosis correlations were found between AFP level and alanine amino-transferase level; and between CA 19-9 level and (1) total bilirubin value, (2) alkaline phosphatase level, and (3) pseudocholinesterase level. The authors conclude that CA 19-9 level is a poor biochemical marker, inferior to AFP level, in the detection of a carcinomatous transformation of liver cirrhosis. The finding of false-positive AFP values in liver cirrhosis seems mainly attributable to cellular proliferation and necrosis. Cholestasis seems to greatly affect serum CA 19-9 level variations, probably by reducing its liver metabolism.
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PMID:Serum CA 19-9 and alpha-fetoprotein levels in primary hepatocellular carcinoma and liver cirrhosis. 138 Dec 71

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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PMID:Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989). 174 13


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