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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertyraminemia is common in hepatic cirrhosis and correlates in severity with encephalopathy. The mechanism of cirrhotic hypertyraminemia has not been established. The alternative possibilities are increased production from tyrosine and impaired degradation by monoamine oxidase. This investigation determined the pharmacokinetics of tyramine after an intravenous bolus injections of [3H]-tyramine (180--200 muCi 12 Ci/mmol sp act) in 13 cirrhotics and 9 controls. In normals, [3H]tyramine levels initially declined rapidly (alpha-phase) followed by a slower decline (beta-phase) with an average t 1/2 of 20.8 min. Average normal metabolic clearance rate and production rate were 13.2 liters/min and 15.4 microgram/min, respectively. In cirrhotic patients, the plasma disappearance curve for [3H]tyramine was qualitatively similar to that of the control subjects with no apparent different in beta-t 1/2 (17.2 min). The hypertyraminemia of cirrhosis resulted primarily from overproduction of tyramine, as the production rate (32.0 microgram/min) in these patients was significantly greater (P less than 0.05) than in controls, whereas the metabolic clearance rate remained normal (average 12.2 liters/min). A difference in ratio of tyramine metabolic products was noted as well. Cirrhotics had a high ratio of plasma 4-hydroxyphenylethanol:4-hydroxyphenylacetic acid (60:40 vs. 30:70) as compared with normals. Although the tyramine clearance rates are similar in normals and cirrhotics, different mechanisms may be responsible for catabolism.
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PMID:Tyramine kinetics and metabolism in cirrhosis. 45 60

A modified norharmane method was used for estimation of tryptamine in human urine at normal state. Tryptamine excretion did not depend on diuresis. Administration of neomycin did not affect the tryptamine excretion, which is inconsistent with the hypothesis on bacterial origin of the amine. Dynamics of tryptamine excretion was studied after administration of tryptophane, inhibitors of monoamine oxidase and their combinations. Sydnophen and sydnocarb caused hypotryptaminuria. Marked hypertryptaminuria was observed in severe chronic hepatitis and liver cirrhosis.
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PMID:[Tryptamine metabolic study in man]. 47 76

Because it has been suggested that an accumulation of false neurochemical transmitters plays a part in the cardiovascular and neurological complications of cirrhosis it appeared worthwhile to study the level of monoamine oxidase in the liver and platelets of cirrhotic patients. In fact a decrease of such activities might explain the increase of false neurotransmitters observed in cirrhotic patients. Other enzyme were also tested: the plasma benzylamine oxidase activity and the liver mixed function oxidases. 13 cases of severe cirrhosis (B, C according to Child classification) and 10 cases of less severe cirrhosis (A according to Child classification) were studied in comparison to patients affected by cholelithiasis. A defect in the level of monoamine oxidase activity of platelets and liver was observed in some cirrhotic patients together with a decrease of the level of the liver mixed function oxidases.
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PMID:Platelet monoamine oxidase, plasma benzylamine oxidase and liver mixed function oxidase in cirrhotic patients. 86 53

The basal acid output (BAO), post-pentagastrin acid output (MAO), fasting and post-prandial gastrin levels in 40 patients with proven cirrhosis of the liver were compared with those in 20 normal controls. The mean BAO and MAO were significantly lower than normal, the mean fasting gastrin level was significantly higher than normal, and the postprandial gastrin response was significantly increased and prolonged. These differences were still significant even when the patients were divided into cryptogenic and alcoholic subgroups. A significant inverse relationship between MAO and the integrated gastrin response to meal was observed both in the normal controls and in the cirrhotic patients. The MAO and integrated gastrin response of the cirrhotic patients did not correlate with the degree of liver function impairment. In five cirrhotic patients fasting and postprandial gastrin levels were unchanged after splenorenal shunt operation. A more consistent abnormality of the gastric mucosa as assessed by endoscopy and biopsies appeared to be mucosal congestion with occasional atrophic gastritis. the severity of mucosal abnormality, however, was unrelated to the degree of hypoacidity. these results indicate, firstly, that the hypergastrinaemia in cirrhotic patients is a reflection of gastric hypoacidity and bears no direct relationship to hepatic dysfunction. Secondly, the gastric hypoacidity does not accrue solely from mucosal abnormality. It is suggested that this hypoacidity may result from the presence of excessive amounts of circulating acid-inhibiting intestinal peptides, which the diseased liver fails to metabolise.
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PMID:Hypergastrinaemia in cirrhosis of liver. 97 11

In an attempt to study the collagen formation in the liver occurring in association with obstructive jaundice, the authors carried out an experiment with liver slices from common bile duct-ligated rats. Hepatic collagen was fractionated into the neutral soluble, acid soluble and insoluble fractions, and the hydroxyproline synthesis rate of each fraction was measured using 14C-proline. Determination was also made for hexosamine content in the same liver tissue. The hydroxyproline content of hepatic collagen increased as biliary obstruction was prolonged, particularly from the 4th week, which is the transitional period of liver histology into biliary cirrhosis. The hexosamine content of hepatic collagen showed a similar tendency. The neutral soluble, acid soluble and insoluble collagen fractions all increased as biliary obstruction was prolonged. The collagenosynthetic activity of the neutral soluble fraction, attained a peak in 1 to 2 weeks of biliary obstruction, which indicates that collagen fibers are formed actively in the early stage of jaundice, although there is only a slight increase in the absolute amount of fibers developed then. Serum monoamine oxidase level tended to be parallel to collagenosynthetic activity but not to collagen content.
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PMID:Biochemical study of fibrosis in the rat liver in biliary obstruction. 115 83

Mitochondrial and cytosolic functions were studied in vivo and in perfused livers from rats with secondary biliary cirrhosis induced by bile duct ligation for 5 wk and in sham-operated controls. The livers were stereologically analyzed, and mitochondrial and cytosolic functions were related to liver structure. Oxygen consumption by perfused livers expressed per stereologically determined mitochondrial volume was decreased by 49% in bile duct-ligated rats compared with control rats. Glucose production (expressed per mitochondrial volume) was reduced by more than 90% in bile duct ligation, whereas urea production was not affected. Lactate production, a cytosolic function, was increased fivefold in bile duct ligation, and both the lactate/pyruvate and the beta-hydroxybutyrate/aceto-acetate ratios were increased in the liver perfusate of bile duct-ligated rats. In comparison with control rats, the stereologically determined mitochondrial volume fraction per hepatocyte was increased by 28% in bile duct-ligated rats. Activities of mitochondrial enzymes expressed per area of mitochondrial membrane or per mitochondrial volume were either unchanged (ATPase, cytochrome c oxidase and glutamate dehydrogenase) or decreased (monoamine oxidase) in bile duct ligation. Thus in comparison with control rats, mitochondrial metabolism is impaired in perfused livers from bile duct-ligated rats; increased mitochondrial volume per hepatocyte may represent a strategy to maintain hepatic energy metabolism in rats with secondary biliary cirrhosis.
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PMID:Stereological and functional analysis of liver mitochondria from rats with secondary biliary cirrhosis: impaired mitochondrial metabolism and increased mitochondrial content per hepatocyte. 159 55

Recent evidence suggests that serotonergic mechanisms within the cardiovascular system are activated and may be important in the development of the hyperkinetic circulation and the maintenance of portal hypertension in cirrhotic patients. The in vivo pressor and positive chronotropic response together with the in vitro contractile responses of aortic rings and portal veins to serotonin were studied in three different rat models of cirrhosis, portal hypertension and jaundice: the portal vein-ligated rat, the carbon tetrachloride-induced cirrhotic rat, the chronic bile duct-ligated cirrhotic rat and the 3-day noncirrhotic, nonportal hypertensive-jaundiced rat. In addition, the activity of the enzyme monoamine oxidase type A was determined in lung homogenates prepared from the four groups of sham and treated animals. In the four different groups of sham-treated or operated pithed rats, serotonin caused a dose-dependent increase in mean arterial blood pressure without any effect on the heart rate. The pressor responses to serotonin in the three models of portal hypertension were significantly attenuated from their respective sham group. In the 3-day noncirrhotic, nonportal hypertensive-jaundiced rats, the pressor response was no different than that seen in the sham-operated rats. No evidence of consistent potentiated or blunted in vitro reactivity to serotonin of arterial rings and portal veins from the four groups of rats was seen. Portal hypertension, cirrhosis and hyperbilirubinemia had no effect on the activity of monoamine oxidase type A. These data demonstrate that portal hypertension is associated with an attenuated pressor response to serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular responses to serotonin in experimental liver disease. 195 74

A rapid method for determining urinary indole-3-acetic acid (IAA) is introduced as the tumor-marker for the screening and diagnostic purpose of cancer patients by means of high performance liquid chromatography (HPLC). Its clinical significance is discussed along with a review of literatures. The IAA concentration and creatinine level of optionally collected urine samples were measured and used for the calculation of IAA amount per unit creatinine (microgram IAA/mg creatinine) in urine. Thus, an amount of 24-hours urinary IAA could be calculated without collecting a whole day's urine supply. Analysis of urinary IAA was performed within 10 minutes by HPLC. Urinary IAA level is usually high in the patients with the upper G-I tract cancers such as gastric cancer, esophageal cancer and hepato-biliary tract cancer, and also malignant hematopoietic disorders. But it is also high in non-cancer patients such as liver cirrhosis, diabetes mellitus and cholelithiasis occasionally. The patients with high urinary IAA level also showed high urinary levels of 5-hydroxy indoleacetic acid (5-HIAA) and monoamine oxidase activity (MAO). It was characteristic that hepatocellular carcinoma showed slight elevation of urinary IAA with normal levels of 5-HIAA and MAO. It is conclusive that the positive rate of elevated urinary IAA level was high in the patients with gastric cancer with ulcer-forming type in its morphological classification, and its level tends to elevate as the disease progresses. Therefore, the measurement of urinary IAA level in an optionally collected urine sample, as the tumor-marker, can be useful to check the progression and regression of gastric cancer.
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PMID:[A rapid method for determining urinary indoleacetic acid concentration and its clinical significance as the tumor-marker in the diagnosis of malignant diseases]. 620 79

Aim of this study was to evaluate the diagnostic value of serum MAO activity (sMAO) in chronic liver disease. sMAO has been assayed by benzylamine colorimetric method. No statistically significant differences of sMAO values have been found between controls and acute viral hepatitis or various diseases patients. Differences instead between controls and patients sMAO values (chronic persistent hepatitis, chronic active hepatitis and liver cirrhosis) were statistically significant (p less than 0.005).
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PMID:[Serum monoamine oxidase (MAO) in the differential diagnosis of chronic liver disease. I]. 652 86

The simultaneous determination of the catalytic activities in serum of monoamine oxidase (EC 1.4.3.4) and N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) was performed in patients with various non-liver diseases, acute hepatitis and fibroproliferative liver disorders (cirrhosis and fibrosis) and the predictive values of the positive (both activities are pathologically elevated) and negative test results (normal activity of monoamine oxidase and/or N-acetyl-beta-D-glucosaminidase) were estimated. It was found that the incidence of the positive result is extremely low (0.024, 5/207) in patients suffering from a great variety of non-liver and liver diseases (except cirrhosis) but rather great in liver cirrhotic subjects (0.44, 18/41). A fraction of only 0.07 of liver fibrotic patients had a positive test result. Based on these data the estimated predictive value of the positive result for liver cirrhosis at a prevalence of 0.03 is 0.47. This value increases strongly with higher prevalence of cirrhosis (population preselected for chronic liver diseases). The negative predictive value for cirrhosis and the positive value for fibrosis are low. Thus, the probability of the presence of cirrhosis in patients with suspected chronic liver diseases is great in cases of abnormally high activities of both monoamine oxidase and N-acetyl-beta-D-glucosaminidase. Negative test results (normal catalytic activities of one or both enzymes), however, do not prove the absence of liver cirrhosis and/or liver fibrosis.
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PMID:The diagnostic potential of the combined determination of serum monoamine oxidase and N-acetyl-beta-D-glucosaminidase for fibroproliferative liver diseases. 685 16


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