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)

The influence of the spleen on the blood has been assessed in a series of 187 consecutive patients with chronic liver disease. Patients were described as having 'hypersplenism' if the white blood count and/or platelet count were below 4.0 X 10(9)/1 and 100 X 10(9)/1 respectively at the time of biopsy diagnosis and on at least one subsequent occasion. Using this definition 17 per cent of patients with alcoholic cirrhosis had hypersplenism, compared with 38 per cent with cryptogenic cirrhosis and 26 per cent with active chronic hepatitis. Studies with 51Cr labelled autogenous erythrocytes in 36 of the patients with different types of chronic liver disease showed that the spleen rarely caused anaemia either by excessive splenic pooling or splenic haemolysis. Further studies with 51Cr labelled platelets in 20 other patients showed that the splenic platelet pool was usually considerably increased and the platelet life span reduced. Some patients showed excessive destruction of platelets in the spleen but none of these features consistently related to thrombocytopenia. Splenic enlargement per se did not cause expansion of the plasma volume in chronic liver disease. Of a total of 17 patients who underwent surgical operations for reduction of portal pressure five had hypersplenism but in these the haematological state was not significantly improved at one month. However, none of the survivors of these operations subsequently developed hypersplenism. One patient with severe hypersplenism who underwent simple splenectomy was cured of leucopenia but not of thrombocytopenia.
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PMID:Splenic influences on the blood in chronic liver disease. 53 22

Total bile acid concentration was determined in systemic and portal serum and in liver tissue from patients with presumably normal liver function, and from patients with extrahepatic cholestasis. Systemic and portal serum bile acids were also determined in patients with alcoholic liver cirrhosis. In 5 patients, in whom a portal catheter was inserted through the umbilical vein, the diurnal variation in systemic and portal serum bile acid concentration was studied. In patients with presumably normal liver function the fasting systemic serum bile acid concentration was 4.8+/-0.5 mumol times 1(-1), and the portal concentration was 12.9+/-1.5 mumol times 1(-1). In cholestasis and liver cirrhosis the systemic and portal bile acid concentration was substantially elevated. The bile acid concentration gradient between systemic serum, portal serum, liver tissue, and hepatic bile was 1:3:80:2600 in the patients with normal liver function. In both the cholestatic and cirrhotic condition the systemic and portal serum bile acid concentration was equilibrated. Postprandially both the systemic and portal bile acid concentration increased, but the gradient between these concentrations was unchanged. The results are compatible with the hypothesis that portal and systemic serum bile acid concentrations are determined by the intestinal absorption rate in subjects with normal liver function and by the hepatic and renal clearance capacity in cholestatic and cirrhotic conditions.
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PMID:Bile acid concentrations in systemic and portal serum in presumably normal man and in cholestatic and cirrhotic conditions. 56 Jul 15

Serum somatomedin (SM) activity, measured as sulphation factor on chick embryo cartilage, and growth hormone (GH) levels were measured in peripheral, hepatic and renal veins of 23 patients with a alcoholic cirrhosis. SM activity (mean +/- SEM) was 0.65 +/- 0.05 U/ml in peripheral vein, 0.59 +/- 0.04 U/ml in hepatic vein, and 0.74 +/- 0.07 U/ml in renal vein. Mean GH levels were respectively 2.8, 2.5 and 3.1 ng/ml. Compared to peripheral vein, SM increase in renal vein was 19% (P less than 0.05). Serum SM activity was significantly lower in 13 patients with alcoholic hepatitis associated with cirrhosis than in other 10 patients (P less than 0.02 in hepatic blood and P less than 0.05 in peripheral blood). The decrease of SM activity seems related to cytolysis and hepato-cellular insufficiency. At last, in patients with alcoholic hepatitis, SM activity was lower in the hepatic vein than in the peripheral vein (P less than 0.05). The cause of this difference remains under discussion, no SM inhibitors being found in the serum samples used in this study.
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PMID:Serum somatomedin activity measured as sulphation factor in peripheral, hepatic and renal veins of patients with alcoholic cirrhosis. 58 Nov 14

The 14C-aminopyrine breath test was used to measure liver function in 14 normal subjects, 16 patients with alcoholic cirrhosis, 14 alcoholics without cirrhosis, and 29 patients taking a variety of drugs. The normal value for the breath test was 8.6 +/- 1.5%, whereas it was significantly lower (5.1 +/- 3.8%) in patients with alcoholic cirrhosis. Higher than normal values were found in some alcoholic patients without cirrhosis and in patients receiving enzyme-inducing drugs, such as phenobarbitone. There was a significant correlation between serum gamma-glutamyltransferase and breath test in these groups. Some patients with alcoholic cirrhosis may also be capable of enzyme induction.
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PMID:Aminopyrine breath test in alcoholic liver disease and in patients on enzyme-inducing drugs. 59 42

The increase in mortality from alcohol induced cirrhosis of the liver in Sweden, Norway, Finland and Denmark from 1961 to 1974 is compared. Mortality from alcoholic cirrhosis of the liver increased in Finland and Denmark tenfold and fivefold respectively from 1961 to 1974. The increase has been particularly marked since 1968. In Sweden a threefold increase and in Norway a doubling of mortality in males was ascribed to alcohol induced liver cirrhosis. Mortality from non-alcoholic cirrhosis of the liver remained practically unchanged during the period. Increases in mortality from liver cirrhosis due to alcohol abuse run parallel with increases in alcohol consumption; the countries with the highest mortality have the highest consumption. The distribution of consumption of beer, wine and spirit is compared in the four countries: consumption of spirits predominates in Sweden, in Finland spirits and beer, in Denmark beer and wine and in Norway spirits and beer. Doubling of alcohol consumption in a country is followed by a fourfold increase in the number of addicts, and fourfold increase in alcohol induced diseases.
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PMID:Alcoholic cirrhosis of the liver in the Scandinavian countries 1961-1974. 60 97

Different methods of performing the (14C) aminopyrine breath test have been assessed. A tracer dose of 2 muCi without a loading dose and with a single breath collection at two hours was the method selected, since it gave the best discrimination between patients with hepatocellular diseases and normal subjects (5.2 +/- 0.2%, mean +/- SEM). Reduced values occurred in patients with chronic active hepatitis (with and without cirrhosis) (1.5 +/- 0.2%), alcoholic cirrhosis (1.7 +/- 0.4%) and hepatitis (2.5 +/- 0.3%), and late primary biliary cirrhosis suggesting defective microsomal function with respect to demethylation. Normal results were common in early primary biliary cirrhosis. Two weeks of prednisolone therapy caused some improvement in the breath test in nine of 10 patients with chronic active hepatitis. It is concluded that the (14C) aminopyrine breath test is a simple test for detecting hepatocellular dysfunction, but has no obvious diagnostic advantage over the determination of serum aspartate transaminase and two hour post-prandial bile-acids.
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PMID:Assessment of the (14C) aminopyrine breath test in liver disease. 62 4

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

A clinical, biochemical, and pathological study was performed in 38 chronic HBsAg carriers. The study group is a part of 393 carriers found among 117 705 voluntary blood donors at the National Blood Bank, Hospital del Salvador, Santiago, Chile. None of the 38 carriers had a past history of illicit drug abuse, hepatitis, or work involving a high risk of hepatitis B virus infection. Ten individuals had a normal liver biopsy, 17 reactive non-specific hepatitis, one fatty changes, four chr onic persistent hepatitis, one aggressive hepatitis, two post-necrotic cirrhosis, and three alcoholic cirrhosis. There was not a close correlation between liver function test and liver histology. The most significant laboratory finding was the postivity of alpha fetoprotein in two cases. During the follow-up the two alpha fetoprotein patients presented a hepatocarcinoma 12 and 14 months after admission to the study.
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PMID:Clinical and pathological study of asymptomatic HBsAg carriers in Chile. 68 May 91

Approaches for the diagnosis of alcoholic cirrhosis of the liver at the dissecting table are given on the basis of the analysis of autopsy materials and liver biopsies. The etiological verification of cirrhosis is based on the peculiar morphological lesions of the liver and other organs. The liver is enlarged, its surface micronodal; histologically, an attack of acute alcoholic hepatitis is found not infrequently: necroses of hepatocytes, predominantly neutrophilic infiltration of the stroma and necrotic zones, alcoholic hyalin. Due to autolysis, alcoholic hyalin in the autopsy material changes somehow and is hardly detectable. A combination of alcoholic cirrhosis of the liver with alcoholic cardiopathy and/or chronic calcifying pancreatitis is typical.
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PMID:[Diagnosis of alcoholic liver cirrhosis during autopsy]. 72 69


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