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 effect of liver disease on glucagon metabolism was examined in nine patients with chronic liver disease who were studied both before and after the creation of a surgical portasystemic shunt. Hepatocellular function did not deteriorate after shunt surgery. However, hepatic perfusion with splanchnic venous blood, as determined by scintisplenoportography, decreased after shunt surgery in six subjects but appeared unaltered in three. Basal plasma immunoreactive glucagon (IRG) levels in the pre-shunt cirrhotic group were significantly greater (p <0.005) than in control subjects and further increased (p <0.05) after shunt surgery. Moreover, the increase in basal IRG after shunt was evident only in patients in whom portasystemic shunting was demonstrably increased by surgery. Despite the higher basal IRG levels postoperatively, shunt surgery in the cirrhotics did not alter basal glucose and insulin levels or the glucose and insulin response to a glucose or protein load. Circulating IRG was heterogeneous in the pre-shunt cirrhotic patients: the 9000 molecular weight fraction comprised 27+/-4%, the 3500 mol. wt. fraction 71+/-4%, and the > 40 000 mol. wt. fraction was minimal. After shunt surgery, the relative proportion of the 9000 mol. wt. fraction of IRG (13+/-3%) decreased significantly (p <0.05) and this fall was associated with a corresponding increase in the 3,500 mol. wt. fraction (84+/-4%). It is concluded that, in cirrhosis, hyperglucagonaemia is: (1) dependent on the degree of portasystemic shunting rather than impaired hepatocellular function; (2) predominantly due to increased circulating 3500 molecular weight glucagon; and (3) not a major factor in the pathogenesis of carbohydrate intolerance in liver disease.
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PMID:Effect of portasystemic venous shunt surgery on hyperglucagonaemia in cirrhosis: paired studies of pre- and post-shunted subjects. 53 93

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

Twenty-one of 30 patients with essential mixed cryoglobulinemia (EMC) had evidence of liver involvement. The liver disease was characterized by the absence of clinical symptoms, hepatosplenomegaly, mild elevation of enzymes, abnormal BSP retention and low albumin levels. Histology, available in 12 patients, showed either chronic persistent or chronic active hepatitis or liver cirrhosis; 44% of the patients had HBsAg or HBsAb in sera and/or cryoglobulins, confirming the high frequency of exposure to hepatitis B virus (HBV) infection in EMC. However, liver lesions were similar in all patients, regardless of HBV exposure. Since other factors usually associated with chronic liver diseases were absent or apparently irrelevant, it is temptative to speculate that a 'cryoglobulinemic hepatitis' may exist as a distinct syndrome. The characteristic complement profile of the patients with EMC (low CH50 and C4, normal C3PA), not related to albumin levels, can help to differentiate this disease from chronic liver disease without cryoglobulins.
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PMID:Liver involvement in essential mixed cryoglobulinemia. 54 44

The possible role of Coxiella burneti as a cause of chronic liver disease in man was investigated in Cyprus. Serology, using the complement fixation test and phase 1 and phase 2 antigens, was performed on 16 patients with cryptogenic cirrhosis and two patients with chronic active hepatitis. Antibody studies were also done on 106 adult Cypriot villagers and on 13 shepherds from flocks infected with C. burneti, to provide a base line for comparative purposes. No evidence was found to implicate the organism as a cause of chronic liver disease. As the number of patients investigated was small it was not possible to exclude C. burneti as an occasional pathogen, and guiding principles were formulated for future investigations.
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PMID:Investigation of Coxiella burneti infection as a possible cause of chronic liver disease in man. 55 68

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

Techniques of hepatic vein catheterization, hepatic venous pressure measurement, and occlusion phlebography using a balloon catheter are described. Hepatic venous pressure measurements (n=95) and hepatic occlusion phlebography were combined in 32 cases. In patients with liver cirrhosis (n=63) a significant elevation of hepatic venous pressure gradients was found. A decrease of the pressure gradient was seen after portacaval and splenorenal shunt operations. Hepatic occlusion phlebography showed alterations of hepatic veins only in patients with cirrhosis. A rough correlation between pressure gradients and the extent of changes in the liver veins was found. Hepatic occlusion phlebography, in patients who had undergone shunt procedure, demonstrated various collaterals. Combined hepatic vein pressure measurements and hepatic occlusion phlebography using a balloon catheter are proposed as a very suitable method for the evaluation of chronic liver disease and portal hypertension.
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PMID:Clinical value of hepatic vein catheterization. Improved pracability by balloon catheter technique. 61 18

In order to evaluate the role of hepatitis B virus (HBV) in the etiology of chronic liver diseases, paired sera of 143 patients with biopsy-documented chronic hepatitis were tested for HBsAg and anti-HBs by radioimmunoassay method. HBsAg was detected in 67.3% of patients with a preceding verified eipsode of acute hepatitis, and in 26.7% of patients with a cryptogenic form of chronic hepatitis. HBsAg was not found in any of patients with alcoholic chronic hepatitis and in only two of 18 patients with other forms of chronic liver disease. No significant difference in the incidence of anti-HBs was observed in all groups of patients. According to previous studies our results confirm the higher prevalence of HBV infection in etiology of chronic persistent and aggressive hepatitis and indicate that this prevalence may be observed especially in Middle and South Italy. The presence of HBsAg in the serum of 37.2% of our patients with cirrhosis compared with 9% of reported cases in North Italy suggest that HBV plays an important role in the etiology of cirrhosis of the liver in our area.
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PMID:[Epidemiologic study of chronic hepatitis in relation to heptatis B virus infections (author's transl)]. 61 63

In rats after portacaval anastomosis (an animal model of chronic liver disease), transport of tryptophan and other members of the large neutral amino acid group from blood to brain was markedly enhanced. Increased transport activity was apparently restricted to the neutral amino acid transport system, since brain uptake of glucose, inulin, and tyramine was unaffected while blood-brain arginine transport was significantly reduced. These results strikingly confirm the hypothesis that carrier-mediated blood-brain transport is the limiting factor determining the availability of the neutral amino acids to the brain. The encephalopathy associated with cirrhosis may be the result of abnormal neurotransmitter metabolism and neurotransmission secondary to increased neutral amino acid transport activity and an increased brain content of members of the neutral amino acid group.
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PMID:Blood-brain neutral amino acid transport activity is increased after portacaval anastomosis. 66 19

Serum aspartate aminotransferase (AST) concentrations are commonly determined to detect hepatocellular damage. However, discrepancies between serum AST values and histological signs of active liver damage sometimes occur in patients with cirrhosis. The enzyme AST requires pyridoxal-5-phosphate (PLP) (active vitamin B6) as a co-enzyme to express its activity. Since approximately 90% of patients with severe cirrhosis are vitamin B6-deficient, it has been suggested that vitamin B6 supplements given to these patients might cause an elevation of falsely low serum AST concentrations. Treatment of 8 vitamin B6-deficient cirrhotic patients with pyridoxine hydrochloride (50 mg intravenously twice daily for 1 week) increased their serum AST concentrations from 121 +/- 18 (mean +/- SEM) to 136 +/- 26 lU/l, while treatment of a second group of 9 patients with the active co-enzyme PLP increased AST concentrations from 118 +/- 17 to 146 +/- 20 lU/l. Neither of these increases was statistically significant. Plasma PLP increased from 2,4 +/- 0,7 to 18,5 +/- 7,6 ng/ml after pyridoxine, and from 3,3 +/- 0,7 to 27,0 +/- 6,2 ng/ml after PLP supplementation. It is concluded that B6 deficiency is unlikely to be an important determinant of serum AST concentrations in patients with chronic liver disease.
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PMID:Vitamin B6 and aspartate aminotransferase activity in chronic liver disease. 67 85

D-Galactose metabolism and demethylation of aminopyrine by healthy controls and patients with chronic active hepatitis (CAH) and cirrhosis (Ci), were assessed by a breath analysis technique measuring 14CO2 exhalation after oral ingestion of 14C-D-galactose or 14C-aminopyrine. Patients with CAH and Ci exhibited decreased 14CO2-exhalation rates following 14C-D-galactose or 14C-aminopyrine. D-Galactose oxidation capacity of the liver can be assessed by a breath analysis technique in analogy to the demethylating function for aminopyrine. The ordinary oral D-galactose tolerance test seems, however, superior in comparison to the 14C-D-galactose tolerance test, in discriminating between healthy controls and patients with chronic liver disease.
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PMID:14C-D-galactose breath test for evaluation of liver function in patients with chronic liver disease. 68 Apr 18


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