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 correlation of collagen metabolism to liver contents of cyclic AMP and GMP as well as blood level of hormones was investigated in 105 patients with chronic hepatitis and liver cirrhosis. In patients with active hepatitis and cirrhosis showing the highest intensity of collagen metabolism there appeared elevated levels of cyclic AMP, somatotropic hormone and insulin against low levels of hydrocortisone and thyroxin. The relations between characteristics of plasma protein-bound oxyproline (PBOP), circadian oxyprolinuria and regulatory mechanisms under study suggest a competitive control of hepatic connective tissue metabolism maintained by hormones via cyclase systems. In high levels of blood PBOP and low ones of hydrocortisone, glucocorticoids unlike D-penicillamine promoted inhibition of liver collagen synthesis.
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PMID:[Various characteristics of collagen metabolism in patients with chronic diseases of the liver]. 262 62

To clarify the factor(s) responsible for changes in the plasma cyclic GMP concentration in liver diseases, we measured the plasma levels of cyclic GMP, along with cyclic AMP, in various clinical stages of chronic liver diseases and acute hepatitis. The level of cyclic GMP was found to increase significantly in the early stage of acute hepatitis, in the decompensated stage of liver cirrhosis, and in malignant diseases. In the former two states, it is postulated that decreased hepatic mass is responsible for the changes in the plasma cyclic GMP concentration. The retention rate of indocyanin green (ICGR15) was highly correlated with the plasma cyclic GMP level. The result suggests that the determination of plasma cyclic GMP is useful as an index of the reserve function of the liver in disease states.
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PMID:Deranged metabolism of cyclic nucleotides in liver diseases. 299 Nov 1

Levels of plasma cyclic AMP, serum immunoreactive insulin (IRI), serum c-peptide immunoreactivity (CPR) and blood sugar (BS) were determined 0, 15, 30, 45 and 60 min after a glucagon injection (0.01 mg per kg body weight) in normal controls, patients with acute hepatitis and liver cirrhosis. Plasma cyclic AMP responses to glucagon in liver disease patients varied widely in peak value, and only in patients with fulminant hepatitis and decompensated liver cirrhosis with poor prognosis was the response suppressed. The peak response of BS was found significantly later in liver cirrhosis patients than in normal controls. IRI and CPR responses to glucagon were lower in acute hepatitis patients than in normal controls and liver cirrhosis patients. IRI levels and their sum were also lower in acute hepatitis patients, although CPR levels were not significantly different. Thus, the ratio of the sum of CPR from 0 to 60 min to that of IRI was significantly higher in acute hepatitis, indicating impaired pancreatic secretion of insulin to glucagon stimulation as well as increased uptake of insulin by the liver in acute hepatitis.
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PMID:Responses of plasma cyclic AMP, serum immunoreactive insulin, C-peptide immunoreactivity and blood sugar levels to glucagon in patients with liver diseases. 300 Jan 42

A laboratory study including estimation of 25 OH vitamin D, terminal parathormone (PTH) C and N fractions, urinary cyclic AMP (AMP cU) and ionised calcium, was carried out in 25 patients, 10 cases of alcoholic cirrhosis without decompensation (group 1) and 15 cases of decompensated cirrhosis (group 2) in order to seek evidence in favour of hyperparathyroidism secondary to cirrhosis. The results show: 1) The existence of hypovitaminosis D which seems to be independent of the liver failure. 2) A very definite increase in terminal PTH N in group 2 compared with group 1 (p < 0.01), without any increase in terminal C fraction. 3) An insignificant increase in urinary cyclic AMP in group 2 compared with group 1. 4) A low serum ionised calcium in group 2 compared with 14 controls (p < 0.05). The terminal N PTH was correlated significantly with urinary cyclic AMP and ionised calcium. The evidence is in favour of secondary hyperparathyroidism where the ionised calcium plays a role, but one wonders whether other factors do not intervene, e.g. serum iron, owing to the discovery of a significant link between serum iron and terminal N PTH levels.
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PMID:[Hyperparathyroidism secondary to cirrhosis. Arguments supplied by ionized calcium, urinary cyclic AMP and blood N-terminal parathyroid hormone]. 625 46

The increase in plasma cyclic adenosine-3':5'-monophosphate (cAMP) was measured after intravenous injection of 1 mg of glucagon in 26 normal subjects, 36 patients with hyperthyroidism, 35 patients with hypothyroidism and 24 patients with euthyroid goitre. While patients with euthyroid goitre responded normally, the plasma cyclic AMP response in patients with hyperthyroidism was considerably increased and in those with hypothyroidism decreased. 4 patients with cirrhosis of the liver had reduced responses and 1 patient with extrahepatic obstructive jaundice an enhanced response. This test seems to be a valuable additional parameter for the description of the thyroid-dependent metabolic situation. However, because of its unspecificity it cannot replace the measurement of serum T3, T4 and thyrotropin (TSH) response to thyroliberin (TRH).
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PMID:[The effect of thyroid function on the increase of plasma cyclic AMP following glucagon injection (author's transl)]. 625 72

Urinary excretion of cyclic GMP (cGMP) and the plasma level of cyclic AMP (cAMP) were determined in patients with liver diseases. The urinary excretion of cGMP, expressed on the basis of creatinine excreted per day, was at significantly higher levels not only in primary hepatoma but also in liver cirrhosis, while the plasma level of cAMP was higher only in liver cirrhosis. Thus, the ratio of urinary cGMP excretion to plasma cAMP level in primary hepatoma was significantly higher than that in liver cirrhosis. In cirrhotic patients studied by catheterization, the level of cGMP in the hepatic vein was significantly lower than that in the superior mesenteric or portal vein, indicating the uptake of cGMP by the liver. Since cGMP excretion correlated with KICG both in liver cirrhosis and primary hepatoma, the increased cGMP excretion appeared to be explained by a reduced uptake of cGMP by the liver.
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PMID:Increased excretion of urinary cyclic GMP in primary hepatoma and preneoplastic liver. 629 71

Following an intravenous bolus of 1 mg glucagon plasma level time profiles of glucagon, cyclic AMP and glucose were monitored for two hours in 6 healthy adult volunteers, 6 patients with decompensated cirrhosis, 6 patients with acute viral hepatitis and at recovery, 6 patients with extrahepatic and 4 patients with intrahepatic cholestasis. Elimination half-livers of glucagon (controls = 22.5 +/- 5.6 min) were significantly prolonged in patients with cirrhosis (52.2 +/- 30.8 min) amd acute hepatitis (58.6 +/- 26.3 min). The glucagon - induced rise in cyclic AMP was similar in all subjects but independent of the phase of the hepatitis (acute or recovery) maximal cyclic AMP values were significantly higher in those patients compared to controls. In contrast glucose response was much lower (p less than 0.001) in patients with hepatitis (acute and recovery). All measured parameters, demonstrated considerable individual variations and a large overlap between the different groups of subjects. Therefore it is concluded that these observations negate the diagnostic and functional usefulness of the glucagon test as a predictive liver function index.
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PMID:Glucagon-induced alterations of plasma levels of cyclic AMP and glucose in patients with liver disease. 632 1

Ample data exist indicating that alcoholism profoundly affects the hemostatic mechanism. In alcoholic patients without cirrhosis, the primary effect is on the blood platelet. Both quantitative and qualitative abnormalities appear during ethanol ingestion. Alcohol-related thrombocytopenia appears to be due to a combination of events: an increased rate of platelet destruction leading to decreased platelet survival and ineffective thrombopoiesis resulting in decreased effective platelet production. The qualitative abnormalities are also multiple and include decreased platelet aggregation, release, and procoagulant activity and decreased storage pool nucleotides, cyclic AMP, and MAO activity. The functional and metabolic abnormalities are associated with striking disturbances in ultrastructural morphology. These defects cause prolongation of the bleeding time and place affected patients at risk for hemorrhagic complications. The relationship between the quantitative abnormalities and the occurrence of thrombocytopenia is obscure, although their severity appears to increase in parallel. The various defects are readily corrected after cessation of drinking. Hence, their long-term significance, absent development of cirrhosis, is questionable. In alcoholic patients with cirrhosis, both platelet abnormalities and coagulation defects may be present. Which predominates in severity varies with each individual. Due to the chronicity of the underlying clinical state, the duration of the defects is more likely to be prolonged if not permanent. In addition, owing to the mechanism of their development, treatment or correction of the defects is difficult and of transitory benefit.
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PMID:Effect of alcoholism on hemostasis. 699 Apr 98

Transient granulocytopenia and lymphopenia may occur in acute alcoholics without splenomegaly, cirrhosis, infection, and megaloblastic anemia due to folate deficiency. The bone marrow in granulocytopenic patients is frequently hypocellular with few mature granulocytes, and the functional marrow granulocyte reserve is reduced. These findings suggest a depressed granulopoietic activity in these patients. The mechanism by which alcohol suppresses granulopoiesis remains unclear. Direct toxicity of alcohol on granulopoietic stem cells and increased individual susceptibility to the toxic effect of alcohol may be important factors. Alcohol also causes functional impairment of granulocytes (adherence, motility, and chemotaxis), macrophages (motility and phagocytosis), and lymphocytes (blastogenic transformation and development of delayed dermal hypersensitivity reaction), probably by perturbation of the cell membrane resulting in an increased intracellular cyclic AMP level.
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PMID:Effects of alcohol on granulocytes and lymphocytes. 737 52

Hepatitis B virus infection is responsible for both morbidity and mortality in kidney transplant recipients. Adenine arabinoside 5'-monophosphate (ARA-AMP), a synthetic purine nucleotide with anti-viral activity, leads to a sustained interruption of HBV replication in approximately 40% of immunocompetent patients. We report the results of a pilot study using ARA-AMP to treat HBV-related chronic active hepatitis in kidney transplant recipients. Ten patients (2 females and 8 males, mean age 44 years, mean time post-transplantation 163 months) received a 28-day course of ARA-AMP intramuscularly: 5 mg/kg twice daily for the first 5 days during hospitalization and subsequently 5 mg/kg once daily at home for the remaining 23 days. Mean follow-up was 18 months, ranging from 7 to 28 months. All patients but one had biopsy-proven chronic hepatitis, including five cases of cirrhosis. All patients had been chronic HBs Ag carriers for more than 1 year and had active replication as assessed by the presence of serum HBV DNA (mean titre, 270 pg/ml, ranging from 12 to 997 pg/ml, Genostics method). HBe Ag was present in 7 of the 10 patients. Pretreatment creatinine was normal. In four of the 10 patients, HBV DNA became undetectable respectively 1, 1, 5, and 11 months after beginning ARA-AMP. In five patients, HBV DNA decreased during ARA-AMP therapy but subsequently increased although no change was noted during the follow-up period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effectiveness of adenine arabinoside 5'-monophosphate in kidney transplant recipients with chronic active hepatitis B. 752 77


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