Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Fourteen cases of Mirizzi's syndrome are presented here. Clinical presentation was pain (14), jaundice (14), fever (10) and peritonitis (1). A clinical diagnosis of choledocholithiasis was considered in all the patients. Pre-operative diagnosis of Mirizzi's syndrome was made in five patients on the basis of cholangiogram and the remaining cases were diagnosed at surgery. The stage (type) of Mirizzi's syndrome was based on the extent of erosion of the common bile duct. Four patients had type I, seven type II and three type III lesions. Associated choledocholithiasis was present in five and acute free perforation of the gall-bladder in one. The operative procedures performed were partial cholecystectomy for type I, partial cholecystectomy, choledochoplasty and T-tube choledochostomy for type II and bilioenteric anastomosis for type III lesions. Two patients had retained common bile duct stones. Mean follow up was 14 months (range 1-27 months). One patient with secondary biliary cirrhosis continues to have persistently elevated serum alkaline phosphatase levels without any demonstrable biliary obstruction. Diagnostic and operative strategies are discussed and a follow up protocol for such patients is suggested.
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PMID:Mirizzi's syndrome: identification and management strategy. 827 24

Advanced cirrhosis is known to be associated with extrahepatic organ dysfunction, but the mechanism for this cirrhosis complication is largely unknown. We measured tissue albumin leakage in rats with biliary cirrhosis or acute cholestasis and tested the hypothesis that arachidonic acid metabolites contribute to the vascular permeability change. Six weeks after bile duct ligation, rats with biliary cirrhosis exhibited increased extravascular leakage of 125I-albumin in lung (p < 0.001) and kidney (p < 0.01) but not in heart or brain. In contrast, in cholestatic rats 10 days after bile duct ligation, only the kidney albumin leak was significantly increased (p < 0.01). Tissue thromboxane B2 levels, measured with an enzyme immunoassay, were increased in lung, kidney and liver of cirrhotic and cholestatic rats. To determine whether thromboxane A2 contributes to the vascular permeability defects in cirrhosis, we pretreated cirrhotic rats with the thromboxane synthase inhibitor dazoxiben (10 mg/kg intraperitoneally every 8 hr) for 20 hr before assessment of vascular permeability. Dazoxiben blocked the increase in thromboxane B2 level in lung but not in kidney and lowered the lung but not the kidney albumin leak index. In cholestatic rats given a higher dose of dazoxiben (40 mg/kg intraperitoneally every 8 hr) for 20 hr, the kidney thromboxane B2 level but not albumin leak was significantly lowered. We conclude that chronic biliary obstruction in rats leads to increased vascular permeability in selected extrahepatic organs and that thromboxane A2 contributes to the vascular permeability increase in the lung. Whether thromboxane A2 plays a role in renal albumin leakage will require further study.
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PMID:Tissue eicosanoids and vascular permeability in rats with chronic biliary obstruction. 832 2

Succinylated wheat germ agglutinin, specified by the amino sugar beta(4)-N-acetylglucosamine, bound frequently to the endothelial cells of the hepatic arterial branches and small vessels of the peribiliary capillary plexus, while it did not bind to the endothelial cells of venous vessels such as portal vein branches and hepatic venous radicles, nor to lymphatic vessels. Sinusoidal endothelial cells were also negative for succinylated wheat germ agglutinin. Proliferating small vessels in the enlarged portal tracts and fibrous septa in patients with extrahepatic biliary obstruction or chronic active hepatitis with or without cirrhosis tended to be positive for succinylated wheat germ agglutinin. Such findings have not been previously reported, to the best of our knowledge. Thus, succinylated wheat germ agglutinin may be a new and useful histochemical tool in routinely processed tissue sections to discriminate intrahepatic vessels into several categories, particularly into two categories (arterial and other vessels), in normal as well as diseased livers.
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PMID:Succinylated wheat germ agglutinin lectin binding in intrahepatic vessels. A new histochemical tool. 834 44

Erythrocyte and hepatocyte plasma membranes derived from CCl4-cirrhotic and bile duct ligated rats were studied. Six groups of animals were used: Group 1 received CCl4 for 8 weeks. Animals in group 2 received CCl4 for 12 weeks. Group 3 consisted in animals that received CCl4 for 8 weeks and then only vehicle for 4 weeks more. Group 4 was the control which received only vehicle. In group 5, obstructive jaundice was induced by bile duct ligation (BDL); animals in group 6 were operated without ligation of the bile duct (sham operated). The activity of Na+/K+ and Ca2+ dependent ATPases, as well as the cholesterol/phospholipid ratio (CH/PL) were determined in both, erythrocyte and hepatocyte plasma membranes. In the CCl4 groups, Na+/K+ and Ca(2+)-ATPases activity was decreased about 60-70% while the CH/PL ratio was increased significatively in both, erythrocyte and hepatocyte plasma membranes. Discontinuation of CCl4 treatment reverted the enzymatic and lipidic alterations to normal in both cell types. ATPases activity and CH/PL ratio in erythrocyte resembled to those of hepatocytes in BDL rats. A strong correlation (p < 0.005) was found when erythrocyte ATPases activity and CH/PL ratio were compared with those of hepatocytes. Moreover, histopathological analysis of liver sections correlated well with both, erythrocyte and hepatocyte biochemical findings. We concluded that determination of ATPases activity and CH/PL ratio in erythrocyte membranes could be a simple, safe and useful marker of cell liver damage in CCl4-induced liver cirrhosis and biliary obstruction in the rat.
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PMID:Erythrocyte alterations correlate with CCl4 and biliary obstruction-induced liver damage in the rat. 838 3

Primary sclerosing cholangitis (PSC) is an inflammatory disease of unknown etiology. It affects the biliary system and is characterized by fibrosis and progressive obliteration of extrahepatic and intrahepatic bile ducts. Its frequent coexistence with antibody-mediated diseases, certain human leukocyte antigens, and altered lymphocyte mechanisms suggests a strong autoimmune and genetic etiology. Other conditions such as recurrent cholangitis, acquired immunodeficiency syndrome, previous bile duct surgery, bile duct anomalies, or biliary stone disease may result in similar clinical patterns and radiologic profiles. PSC can be asymptomatic and slowly progressive over years, or it may develop rapidly with an inexorable progression to cirrhosis and portal hypertension. Clinical and biochemical abnormalities may suggest PSC, but it is the characteristic radiological pattern that secures the diagnosis. Once viewed as a rare entity, the widespread use of radiological and endoscopic methods have increased physician awareness. There is no successful medical treatment for PSC. While traditional surgical approaches have been directed at the relief of cholangitis and biliary obstruction, liver transplantation has emerged as definitive therapy for patients with PSC complicated by cirrhosis or recurrent bouts of cholangitis.
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PMID:Primary sclerosing cholangitis. 847 44

Drug-induced hepatotoxicity is a major cause of iatrogenic diseases. More than 900 compounds, including herbal medicines are involved and can reproduce the full spectrum of liver injuries. Acute hepatitis are the most frequently observed. Three types are described: acute hepatocellular hepatitis which are frequently similar to viral hepatitis, and can lead to fulminant liver failure and death within a few days, or, more insidiously, to cirrhosis; acute cholestatic hepatitis, which exhibits a better prognosis, may be misleading by mimicking biliary obstruction; mixed-pattern hepatitis, which associates features of hepatocellular and cholestatic hepatitis. Acute hepatitis generally exhibits no specific patterns. Then, the diagnosis is difficult and relies upon the elimination of other causes and a compatible or a suggestive time-relationship between drug ingestion and the onset of hepatitis as well as between drug withdrawal and recovery. Sometimes, drug hepatotoxicity is suggested by the association of hepatitis to hypersensitivity manifestations (hypereosinophilia), to some histopathological features (eosinophilic infiltration, microvesicular steatosis, giant hepatocytes) or, more uncommonly, to specific autoantibodies (anti-mitochondrial type 6, anti-LKM2, anti-LM antibodies). Cross hepatotoxicity may occur between drugs having related chemical structures.
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PMID:[Drug-induced hepatitis: epidemiologic, clinical, diagnostic and physiopathologic aspects in 1995]. 852 55

Interferons have been used to treat chronic hepatitis owing to their antiviral properties. However, now interferons are recognized to inhibit collagen production. Because fibrosis has been associated with liver damage and dysfunction, the effects of interferon-alpha 2b on biliary obstruction-induced cirrhosis were investigated. Obstructive jaundice was induced in male Wistar rats (ca. 200 g) by double ligation and division of the common bile duct. Control rats were sham operated. Interferon-alpha 2b (IFN-alpha; 1000 000 IU per rat) was administered subcutaneously daily after surgery. The animals were sacrificed after 4 weeks of bile duct ligation (BDL) or sham operation. Bilirubins and serum enzyme activities of alkaline phosphatase and gamma-glutamyl transpeptidase (determined as markers of liver damage) increased several-fold after BDL. Erythrocyte and hepatocyte plasma membrane Na+/K+- and Ca2+-ATPase activities decreased significantly in the BDL group. Administration of IFN-alpha to BDL rats resulted in a partial normalization of serum markers of liver damage. The normal activity of both ATPases on erythrocyte and hepatocyte plasma membranes was completely preserved by IFN-alpha. It is concluded that interferons possess interesting hepatoprotective effects not related to their antiviral properties but probably associated with their antifibrogenic effect.
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PMID:Interferon-alpha preserves erythrocyte and hepatocyte ATPase activities from liver damage induced by prolonged bile duct ligation in the rat. 860 32

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

To clarify the effects of obstructive jaundice on the liver, sequential changes of hepatic energy charge, the concentrations of adenine nucleotides and malondialdehyde, DNA synthesis rate, and histology of the liver were examined on the day before and Days 1, 2, 4, 7, and 14 after biliary obstruction in rats and compared with those of sham-operated controls. Foci of necrotic hepatocytes were present on Days 1 and 2 and mitoses of the hepatocytes were frequently observed with a peak on Day 2 in the jaundiced liver. Marked proliferation of bile ductules were subsequently observed on Days 7 and 14, resembling biliary cirrhosis. The DNA synthesis rate was significantly activated after bile duct obstruction with its peak on Day 2, more than nine times higher than the control value and returned to the control level on Day 14. Hepatic ATP concentration and energy charge gradually declined with prolonged jaundice and significantly lower levels persisted after Day 7 compared with the controls. The malondialdehyde level in the jaundiced liver gradually increased and became significantly higher on Day 14. We conclude that obstructive jaundice decreases hepatic energy charge and increases the lipoperoxide level. In the initial stage of obstructive jaundice, the hepatocytes proliferate associated with activated DNA synthesis probably to compensate hepatic damage; however, prolonged obstructive jaundice induces functional hepatic injury possibly necessitating biliary drainage.
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PMID:Sequential changes of energy charge, lipoperoxide level, and DNA synthesis rate of the liver following biliary obstruction in rats. 865 33

MUC1 apomucin is a specific target tumor antigen recognized by cytotoxic T cells in a major histocompatibility complex (MHC) unrestricted fashion in patients with pancreatic and breast cancer. This T-cell-mediated immune mechanism against MUC1 apomucin expressing cells has not been evaluated in nonneoplastic immune-mediated diseases. Therefore, we immunohistochemically surveyed the expression of MUC1 apomucin on biliary epithelial cells of small bile ducts in various hepatobiliary diseases, including primary biliary cirrhosis (PBC). MUC1 apomucin was detected using the monoclonal antibody DF3 and the streptavidin-biotin complex, in livers from 31 patients with PBC, 67 with chronic viral hepatitis (CH) with or without cirrhosis, 31 with extrahepatic biliary obstruction (EBO), 30 with hepatolithiasis, and from 23 normal individuals. MUC1 apomucin was infrequently and focally expressed in the biliary epithelial cells of the small bile ducts in 3 of 23 normal livers. In contrast, MUC1 apomucin was frequently and strongly expressed on the luminal surface of biliary epithelia] cells of small bile duct, in 22 of 31 patients with PBC, and in 50 of 67 patients with CH. In particular, high levels of MUC1 apomucin were expressed in bile ducts showing chronic nonsuppurative destructive cholangitis (CNSDC) in PBC and hepatitic duct injuries in CH. In EBO and hepatolithiasis, MUC1 apomucin was focally and weakly expressed in 29% and 30% of livers examined, respectively. More MUC1 apomucin was expressed in PBC and CH than in EBO, hepatolithiasis, and normal liver (P < .01, respectively). Frequent and high luminal expression of MUC1 apomucin on biliary epithelial cells in damaged small bile ducts in PBC and CH may be related to T-cell-mediated immunologic mechanisms in these diseases, probably by an MHC-unrestricted recognition process.
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PMID:Frequent expression of MUC1 apomucin on biliary epithelial cells of damaged small bile ducts in primary biliary cirrhosis and chronic viral hepatitis: an immunohistochemical study. 867 44


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