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)

In the course of 4 years, among 11,738 admissions there were 245 (2.08%) patients with cholestasis (106 women and 139 men). Intrahepatic cholestasis (i.c.) was detected in 46.5%, and extrahepatic (e.c.) in 53.5%. The most frequent cause of i.c. were alcoholic and nonalcoholic chr. liver disease (fatty liver, chr. hepatitis, cirrhosis) (37% and 30%), acute viral hepatitis (15%) and toxic liver injury (14%) respectively. The causes of e.c. were: choledocholithiasis (44%), cancer of the pancreatic head (15%), cancer of gallbladder and extrahepatic ducts (12%) and cancer of liver (10%). The causes of c. were benigne, in 78.2%, while malignant neoplasms were present in 21.8%. Out of the multitude of laboratory tests two appeared particularly significant: glut, transpeptidase was pathologic in 81% of alcoholic liver disease, in 62% of the cases with obstructive jaundice and in 27.7% of malignant neoplasms. LX-lipoprotein examined in 52 patients was positive in 24% of i.c., and 60% of e.c. Proliferation of bile ducts was the most frequent finding in surgical liver biopsies in choledocholithiasis cases.
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PMID:Differential diagnosis, laboratory tests and histology in 245 patients with cholestasis. 52 15

Twelve of 43 patients with chronic active hepatitis (CAH) (28%) manifested clinical and laboratory features of cholestasis. The criteria for selection of these patients included at least two of the following: chronic or recurrent pruritus, serum alkaline phosphatase levels of 300 mU./ml. and cholesterol of 300 mg./dl. or more. When compared with 31 control cases these patients were found to have a preponderance of Ashkenazi Jews of Roumanian origin, a higher prevalence of joint and thyroid involvement and higher serum Ig-M Levels. Mortality was similar in both groups but patients with cholestatic features tended to die earlier in the course of the disease. Retrospectively, it was found that they had been treated more intensively, attained complete remissions less frequently and developed cirrhosis more readily. There were no significant differences in the frequency of HBsAg and anti-HBs, the mode of onset, the frequency of hepatosplenomegaly and jaundice, the hematologic findings and the prevalence of autoantibodies. Like acute cholangiolitic viral hepatitis, CAH with cholestatic features emerges as a more serious disease than the classical form of CAH.
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PMID:Chronic active hepatitis with cholestatic features. I. A clinical and immunological study. 53 97

The value of serum bile acids (SBA) in the diagnosis of hepatobiliary disease has been investigated. A modified GLC method was used, with an overall coefficient of variation of +/- 11% in the control range. Serum was obtained after a 12 hour fast, and two hours after a fatty meal from 73 patients and 14 control subjects. In controls the total fasting SBA of 2.17 +/- 0.86 mumol/l increased significantly (p less than 0.001) to 3.81 +/- 1.14 mumol/l after a meal. All icteric patients had raised SBA, but in 23 anicteric patients there was no significant difference in the detection of chronic liver disease by fasting SBA, postprandial SBA, AST, or gamma GTP. Compared with controls, serum in patients contained proportionately less deoxycholic acid (p less than 0.001), there was proportionately more cholic acid in extrahepatic obstruction (p less than 0.001), and proportionately more chenodeoxycholic acid in patients with cirrhosis, viral hepatitis, and neoplasia (p less than 0.001). In control subjects, the fasting cholic:chenodeoxycholic acid ratio ranged from 0.5-1.0, and differed significantly (p less than 0.001) from patients with extrahepatic obstruction 0.96-3.6, and cirrhosis 0.1-0.5. It is concluded that serum bile acids measured by sensitive methods can provide useful diagnostic information.
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PMID:Serum bile acids in the diagnosis of hepatobiliary disease. 59 Aug 51

In a series of 221 patients with various liver diseases studied in Iraq using counterimmunoelectrophoresis and passive haemagglutination techniques, HBsAg was detected in 40.8 per cent of cases with acute viral hepatitis, in 40 per cent in cryptogenic cirrhosis, in 50 per cent in chronic hepatitis, in 100 per cent in active cirrhosis and 71.4 per cent in hepatoma. In acute hepatitis the antigenaemia was highest early in the course of the disease. The duration of antigenaemia ranged from three to 16 weeks. In 3.4 per cent of cases the antigenaemia persisted for more than 35 weeks. In 31.3 per cent of acute hepatitis there was no evidence of parenteral infection.
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PMID:Hepatitis B surface antigen in various liver diseases in Iraq. 60 44

We have studied the cytotoxicity against rabbit liver cells of lymphocytes from the peripheral blood of 71 patients with various liver diseases. The group with chronic active hepatitis and three patients with acute alcoholic hepatitis showed significantly higher mean values of lymphocytotoxicity (P less than 0.001) compared with the other patients with chronic persistent hepatitis, post-necrotic fibrosis and cirrhosis. Wilson's disease, and prolonged viral hepatitis. The mean cytotoxicity of these last groups did not differ significantly from controls. In four out of six patients with chronic active hepatitis a significant decrease of lymphocytotoxicity was found after immunosuppressive therapy with oral prednisolone. A good correlation between the lymphocytotoxicity test and histological signs of activity suggests that a cell-mediated immune aggression is present in this disease.
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PMID:Lymphocytotoxicity test against rabbit hepatocytes in chronic liver diseases. 63 39

Arterial and venous plasma concentrations of total immunoreactive angiotensin II (AT II), its bioactive hepta-octapeptide fraction and its inactive hexapeptide were measured in normal subjects (n=16), in patients with acute viral hepatitis (n=12), and in treated (n=16) and untreated (n=17) patients with cirrhosis of the liver and ascites. Independent of normal or increased values of total immunoreactive AT II, the ratio between the hepta-octapeptides and the hexapeptide remained unchanged. This might indicate continuous octapeptide generation and balanced metabolite turnover throughout the systemic circulation. Moreover, a significant arterio-venous peptide gradient was lacking. It has to be concluded that total venous plasma AT II sufficiently reflects both the arterial hormone concentration and its major fraction of hepta-octapeptides in arterial (79%) and venous (76%) blood.
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PMID:Total immunoreactive angiotensin ii, its hepta-octapeptide fraction, and its hexapeptide in patients with liver disease. 64 13

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.
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PMID:DNCB sensitivity in healthy Pakistani subjects and patients with liver disease. 65 81

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.
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PMID:[1-14C]Ethanol breath test in alcoholic liver disease. 65 31

The labeled bile salt tolerance test is the measure of the decrease in plasmatic radioactivity after intravenous injection of carboxyl-14C-labeled chenic acid. The label is distributed in the blood, taken up by hepatocytes and then secreted in the bile. The decrease in plasmatic radioactivity during the 4 h following the injection follows a bi-exponential curve. It has been studied in 6 normal subjects, 4 patients equipped with "T tube", 3 cases of acute viral hepatitis, 4 cases of hepatic steatosis, and 6 cases of hepatic cirrhosis. The first slope (b1) represents the hepatic uptake of the label. It is lowered in cases of viral hepatitis and in cirrhosis. The second slope (b2) represents hepato-biliary secretion of the label. It is lowered in patients equipped with a "T tube". From 100 min after the injection, the plasma concentration of radioactivity remains constant. This is the residual value (R), and it is very low in normal subjects. It is increased in cases of acute viral hepatitis and cirrhosis, indicating displacement of a fraction of the bile salt pool into peripheral blood. After a standard meal, the R value is not modified in the normal subject. In cases of steatosis and cirrhosis, a temporary peak may be seen, indicating recirculation of the label towards the periphery due to a porto-systemic shunt or a hepatocyte lesion.
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PMID:[Clinical application of the radiolabeled bile salt tolerance test]. 67 9

There is an increased incidence of unwanted sedation associated with chlordiazepoxide usage in the elderly and in patients with liver disease. To determine whether pharmacokinetic alterations could account in part for these observations we studied the disposition and elimination of intravenously administered chlordiazepoxide in 27 healthy controls aged 16 to 86 years, 8 patients with cirrhosis, and 5 patients with acute viral hepatitis. Both increasing age and parenchymal liver disease led to similar changes in chlordiazepoxide pharmacokinetics. Over the age range 20 to 80 years, elimination half-life (t1/2(beta)) increased from 7 to 40 hr (r, 0.67; P less than 0.001) attributable to a decrease in plasma clearance from 30 ml per min to 10 ml per min (r, -0.71; P less than 0.001) and an increase in volume of distribution from 0.26 to 0.38 liters per kg (r, 0.60; P less than 0.05). Similarly, a decrease in plasma clearance in cirrhosis (7.7 +/- 2.1 compared to 15.3 +/- 4.4 ml per min, P less than 0.01) and acute viral hepatitis (6.1 +/- 4.3 compared to 18.1 +/- 7.1 ml per min, P less than 0.01) relative to age-matched controls and an increase in the volume of distribution resulted in a prolongation of the elimination half-life in both forms of liver disease. Impaired elimination of chlordiazepoxide may account in part for the increased incidence of oversedation seen in the elderly and in patients with liver disease.
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PMID:Effect of age and parenchymal liver disease on the disposition and elimination of chlordiazepoxide (librium). 68 May 5


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