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)

To assess the diagnostic value of radioimmunoassay determination of serum levels of glycocholic acid in alcohol-induced chronic diffuse hepatic lesions, this technique was compared by sensitivity and informative content with conventional hepatic tests. Hepatocytic function was measured in combined examination of 83 patients and 30 controls. It is shown that serum glycocholic acid concentration permits detection of early alcohol defects of the liver, excretory dysfunction in particular, control of cholestatic changes, of transformation of hepatic steatosis into hepatitis or cirrhosis, evaluation of cholestasis. The above radioimmunoassay is a useful prognostic tool in decompensated alcohol cirrhosis of the liver.
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PMID:[Clinical value of determining serum levels of glycocholic acid in alcoholic lesions of the liver]. 146 Aug 24

Changes of the number and properties of the epidermal growth factor (EGF) receptor occur during liver regeneration and may be of importance in the maintenance of hepatocellular mass in liver cirrhosis. We therefore studied the changes in the number and distribution of EGF receptor in the development of liver cirrhosis induced by bile duct ligation. Receptor binding assays demonstrated a marked decrease in the binding capacity of crude plasma membrane fractions from 45 +/- SD 16 to 19 +/- 10 fmol/mg protein (p < 0.001) in control and bile duct ligated livers, respectively while the Kd increased after 3 days of bile duct ligation from 0.5 +/- 0.2 to 1.4 +/- 0.6 nmol/l. Total receptor concentration in the same membrane fractions, as assessed by Western blot analysis, was not changed. The expression of EGF receptor mRNA was reduced to about one third of control levels after 28 days of bile obstruction. Immunohistochemistry, performed using monoclonal antibodies against EGF receptor, showed a strong labeling of cytoplasm (87 +/- 3% positive) and plasma membranes (84 +/- 24%) but no labeling of nuclei in control livers. In bile duct ligated rats, in contrast, cytoplasmic staining was decreased (15 +/- 12%) already after 3 days of bile obstruction; labeling of canalicular membranes and nuclei appeared after 14 days. The shift of EGF receptor from plasma membranes to nuclei supports the notion that EGF receptor is involved in the maintenance of hepatocellular mass in this model of liver cirrhosis. This concept is supported by the finding of decreased mRNA for EGF receptor presumably representing down-regulation as seen in regenerating rat liver.
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PMID:Epidermal growth factor receptor in chronic bile duct obstructed rats: implications for maintenance of hepatocellular mass. 146 40

Liver disease associated with cystic fibrosis (CF) is considered a secondary effect of the basic defect of the disease, leading to obstruction of bile ductules by abnormal mucoid secretions; additional factors have been involved in the pathogenesis, such as abnormalities in bile acid metabolism, nutritional deficiencies, drug hepatotoxicity, stenosis of the common bile duct by the fibrotic pancreas. Clinical presentation of liver disease in CF is rare during the first few years of life, although neonatal cholestasis can be occasionally the first manifestation of the disease. Isolated massive steatosis has been reported in less than 5% of cases as a consequence of malnutrition. Focal biliary cirrhosis is the pathognomonic hepatic lesion and is present in 25-30% of CF patients, most of whom are asymptomatic. The focally distributed lesions can extend leading to multi-lobular biliary cirrhosis with occurrence of signs and symptoms of cirrhosis and portal hypertension. Early diagnosis of CF-associated liver disease is difficult since liver function tests may be normal even in cases of overt cirrhosis: no test has proved to be sufficiently sensitive and specific and even liver biopsy is of questionable relevance due to the focal distribution of hepatic lesions. Clinical examination is of major importance, since the presence of hepatomegaly seems to correlate well with the histologic finding of fibrosis. The rationale for the use of the choleretic non-toxic bile acid ursodeoxycholic acid in CF-associated liver disease is to reduce the viscosity of bile and to replace toxic bile acids which accumulate in the hepatocyte.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver disease in cystic fibrosis. 147 Feb 80

The tumor marker CA 15.3 was studied in 85 patients with liver cirrhosis. Nine patients (10.6%) had abnormal levels of CA 15.3 with the highest values in cases of Child's C patients. However, Child's classes were not significantly associated with the level of the antigen. We found significant correlations with some laboratory tests, especially IgA. All patients with an elevated CA 15.3 value also had abnormal levels of IgA, and multivariate analysis showed that IgA was the only independent factor associated with CA 15.3. Although IgA is a marker of alcoholic liver disease, other markers of alcoholism were not associated with CA 15.3. Cytolysis and cholestasis were not significantly associated with the CA 15.3 level, but liver dysfunction seemed to be involved. Liver disease does not substantially limit the usefulness of CA 15.3 in the cancer patient who also has liver cirrhosis, since both the percentage of abnormal values and the elevation of the serum levels are moderate in cirrhotic patients.
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PMID:Breast cancer-associated antigen CA 15.3 in liver cirrhosis. 147 54

The prevalence and the pathogenesis of gallstones in patients with chronic pancreatitis have never been studied prospectively. The aim of this study was to evaluate prospectively the prevalence of gallstones with ultrasonography and to look for markers of pigment or cholesterol stone formation in gallbladder bile. Ultrasonography was performed in 39 patients and detected gallstones in 7 patients and sludge in 3. Common bile duct and intrahepatic bile duct dilatation were observed in 16 and 13 patients, respectively. Liver biopsies were obtained in 31 patients and cirrhosis was found in 4. There were calcium bilirubinate granules in 7 of the 27 bile samples examined. Cholesterol crystals were not found in any case. The nucleation time (median: 21 days) was higher in patients with chronic pancreatitis than in patients with cholesterol stones (median: 2 days) (P < 0.001) but was not different from nucleation time in patients either free of stones (median: 21 days) or with pigment stones (median: 21 days). The cholesterol saturation index was similar in patients with chronic pancreatitis and in controls. The 2 patients with chronic pancreatitis who underwent cholecystectomy had pigment stones. Calcium bilirubinate granules were more frequent in patients with intrahepatic bile ducts dilatation (P < 0.02). In conclusion, this study demonstrates a high prevalence of cholelithiasis in chronic pancreatitis patients. Pigment stone formation could be favored by cholestasis.
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PMID:[Pathogenesis of cholelithiasis in chronic pancreatitis]. 148 57

Complications of endoscopic retrograde cholangiography specific to patients with primary sclerosing cholangitis have not yet been reported. We observed transient rises of serum bilirubin after diagnostic endoscopic retrograde cholangiography in five of 15 patients and persistent rises in three of 15 patients with primary sclerosing cholangitis examined consecutively by endoscopic retrograde cholangiography from 1985 to 1990. Deterioration of cholestasis was particularly associated with advanced disease. Seven of eight patients with deterioration after endoscopic retrograde cholangiography had septal fibrosis (stage III) or cirrhosis (stage IV) and a priori elevated serum bilirubin levels. In contrast, all patients with no deterioration of cholestasis following endoscopic retrograde cholangiography had early histological changes (stage I-II), and all but one patient had normal serum bilirubin levels. We conclude that the potentially harmful effects on biliary excretion must be taken into account when the use of endoscopic retrograde cholangiography is being considered in patients with advanced primary sclerosing cholangitis.
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PMID:Deterioration of cholestasis after endoscopic retrograde cholangiography in advanced primary sclerosing cholangitis. 150 31

In 35 dogs with spontaneous hepatobiliary liver disease the kinetics and the sources of bilirubin were quantified. The disorders were extrahepatic bile duct obstruction (n = 4), fulminant hepatitis (n = 2), (sub)acute hepatitis (n = 5), chronic active hepatitis (CAH) with cirrhosis (n = 6), hepatic lymphosarcoma (n = 5), centrizonal necrosis secondary to haemolytic anaemia (n = 6) and other (n = 2). The plasma disappearance of [3H]bilirubin was analyzed with a two-compartment model in all dogs. The ratio early labeled/late labeled bilirubin was determined by measuring the incorporation of [14C]glycine into erythrocyte haem and faecal stercobilin. By introducing this relation in the model analysis the bilirubin production rates from erythrocyte destruction (PE), ineffective erythropoiesis (PI) and hepatic haemoprotein (PL) could be quantified. Total bilirubin turnover was increased in both primary haemolytic disease and most cases of hepatobiliary disease. Erythrocyte survival was reduced in all cases but one. The bilirubin clearance was impaired to 30-50% of the normal value in most cases of hepatobiliary disease and also in primary haemolysis. In dogs with fulminant hepatitis, and cirrhosis with or without CAH, the clearance rates were reduced to values below 15% of normal. In these dogs both an impaired clearance and an increased production were important determinants of hyperbilirubinaemia. In other cases plasma bilirubin was primarily determined by increased production. These clearances and production rates were similar in haemolysis and in many cases of primary hepatobiliary disease. The hepatic haemoprotein turnover was quite variable in all subgroups, ranging from 1-74% of the total bilirubin turnover.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origins and kinetics of bilirubin in dogs with hepatobiliary and haemolytic diseases. 150 35

To base the clinico-pathogenetic nonuniformity of cholestasis in different liver diseases, 135 patients distributed into groups were examined. Group I was made up of 48 patients with chronic persistent hepatitis, group II of 34 patients with chronic active hepatitis, group III of 29 patients with liver cirrhosis, and group IV of 24 patients with primary and metastatic liver carcinoma. The data obtained suggest the existence of different forms of cholestasis: multicomponent cholestasis, partial bilirubin cholestasis, partial choleacid cholestasis. In the group I patients, the incidence of cholestasis was 8.3%, in group II 2.9%, in group III 3.4%. The incidence of partial choleacid cholestasis was 4.2% in group I, 2.9% in group II, and 6.9% in group III. The presence of partial cholestasis may be caused by the impairment of the assumed "personal" carrier for different bile components.
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PMID:[The clinico-pathogenetic variants of cholestasis in different liver diseases]. 150 86

Severe liver disease complicates pregnancy in only 0.1% of the cases. Viral hepatitis is the most common cause (40%). (Liver cirrhosis usually results in amenorrhea). Liver disease unique to pregnancy comprises "intrahepatic cholestasis of pregnancy" (Increased fetal risk), "acute fatty liver of pregnancy" (AFLP) and "HELLP-syndrome", both with high maternal and fetal risk when untreated. AFLP and HELLP-syndrome are diseases of the third trimester and show similar clinical signs of jaundice, coagulopathy and elevated liver enzymes. The immediate termination of pregnancy preferably by Caesarean section has been shown to improve both, maternal and fetal outcome. Imaging methods like ultrasound are invaluable in the differential diagnosis and detection of complications like subcapsular hematoma in the liver patients with HELLP-syndrome. Fulminant hepatic failure requires intensive care, liver transplantation is an additional therapeutic option. Recurrent AFLP has been reported recently.
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PMID:[Acute hepatopathies in pregnancy: diagnosis and therapy]. 152 90

We studied hypoxic pulmonary vasoconstriction (HPV) and pulmonary gas exchange in unanesthetized rats with biliary cirrhosis induced by chronic bile duct ligation (BDL) (5 to 6 wk) and compared pulmonary vascular reactivity in perfused lungs isolated from BDL and control rats. Awake, catheter-implanted, cirrhotic rats exhibited increased cardiac output, normal systemic and pulmonary arterial pressures, and decreased total systemic (TSR) and pulmonary (TPR) vascular resistances in comparison with those in sham-operated control rats. HPV was markedly depressed in cirrhotic rats (percent increase in TPR while breathing 8% O2: 42.3 +/- 13.7% in control and 0.9 +/- 3.6% in cirrhotic rats, p less than 0.05), and this was associated with an increased AaPO2 (control rats, 15.7 +/- 1.1 mm Hg; cirrhotic rats, 23.1 +/- 1.9 mm Hg; p less than 0.05). In contrast, the pulmonary pressor response to angiotensin II was intact, and the depression of HPV in cirrhotic rats was ameliorated after angiotensin II infusion. These changes in cirrhotic rats were not due to the accompanying cholestasis since noncirrhotic rats with severe cholestasis had intact HPV and normal AaPO2. Lungs isolated from cirrhotic rats and perfused with blood from normal rats exhibited two patterns of response to hypoxia. In one group, HPV was blunted compared with that in control rats (change in pulmonary arterial perfusion pressure after 3% O2: control rats, 23.2 +/- 2.8 mm Hg; cirrhotic rats, 4.8 +/- 1.4 mm Hg; p less than 0.01). Similar to the result in intact rat, angiotensin-II-induced vasoconstriction was preserved in lungs from cirrhotic rats, and HPV increased significantly after angiotensin II infusion (to 17.3 +/- 4.8 mm Hg). In the second group, baseline pulmonary arterial pressure progressively increased during normoxia, and this increase was attenuated by hypoxic ventilation (hypoxic vasodilation).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary circulatory dysfunction in rats with biliary cirrhosis. An animal model of the hepatopulmonary syndrome. 155 5


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