Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic hepatitis presents as an acute hepatitis in an alcoholic. No specific laboratory tests for alcoholic hepatitis exist. Therefore, the diagnosis must be based on the clinical presentation, histology and exclusion of other causes of a similar clinical picture such as viruses and drugs. Patients with elevated bilirubin, encephalopathy and coagulopathy have a poor prognosis. Steroids, infusion of insulin and glucagon, supplementation of amino-acids and other experimental therapies do not appear to be helpful with the exception of steroids which may benefit the sickest patients. Long-term prognosis depends on the extent of cirrhotic changes present after the acute episode and on the drinking habits of the patient.
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PMID:[Alcoholic hepatitis]. 162 Dec 33

Polyamines have been known to play an important role in hepatic regeneration. In the present study, we measured the amount of urinary polyamine excretion in various liver diseases using a simple enzymatic method. Urinary polyamine excretion was elevated above the normal range in 21 out of 47 cases with fulminant hepatic failure, acute hepatitis, chronic active hepatitis, and liver cirrhosis. No change, however, was observed in 11 patients with chronic inactive hepatitis. In fulminant hepatic failure, two patients with urinary polyamine concentrations above 100 mumoles/g.cr. recovered, while two patients with concentrations of 56.2 and 26.7 mumoles/g.cr., died. In acute hepatitis, urinary polyamine excretion was significantly less in the recovery stage compared with the acute stage. When insulin and glucagon infusion therapy was performed in patients with liver cirrhosis without ascites, urinary polyamine excretion was significantly elevated after three days. These results suggest that measuring the amount of polyamine in urine is clinically useful for monitoring hepatic regeneration.
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PMID:Urinary polyamine excretion measured by a simple enzymatic method is clinically useful as an expression of hepatic regeneration in liver diseases. 208 20

We examined the level of plasma amino acids, glucose, immunoreactive insulin (IRI) and immunoreactive glucagon (IRG) of patients in the fasted state with acute hepatitis in the actual acute stage (AHa), acute hepatitis in the convalescent stage (AHc), chronic active hepatitis (CAH), chronic persistent hepatitis (CPH) and liver cirrhosis (LC). In AHa patients, the plasma glucose (FPG), plasma alanine (Ala), tryptophan (Trp) and histidine (His) levels were significantly lower and plasma cystine (Cys) level significantly higher than the control levels. This however, was not the case in the other patients. The glutamic acid (Glu) concentration was significantly higher in AHa (p less than 0.02), CAH (p less than 0.001) and CPH (p less than 0.001) and the tyrosine (Tyr) concentration was significantly higher in AHa (p less than 0.02), CPH (p less than 0.001), CAH (p less than 0.001) and LC (p less than 0.001) than they were in the controls. The lysine (Lys) concentration was significantly raised in the AHa (p less than 0.02) and CPH (p less than 0.05) cases. The IRG level was significantly higher in AHa (p less than 0.001), in AHc (p less than 0.01) and LC (p less than 0.01). Valine (Val) showed a significant decrease in concentration in AHa (p less than 0.01) and LC (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Profiles of plasma amino acids in fasted patients with various liver diseases. 208 40

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

A cooperative study was conducted to determine the efficacy of one week of treatment with infusion of 1 mg glucagon and 10 units insulin twice daily in severe acute hepatitis. Ninty-eight patients with either prothrombin time less than 60% or thrombotest or hepaplastin test less than 50% of normal were randomly assigned to hormone or placebo treatment. SGOT and SGPT values dropped after treatment with a gradual decrease or increase in total serum bilirubin or cholesterol levels similarly in both groups receiving hormone or placebo. Deranged prothrombin time improved more rapidly in the hormone group than in the placebo group. Glucagon and insulin infusion may stimulate recovery of the liver from injury.
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PMID:A multi-centre double-blind controlled trial of glucagon and insulin therapy for severe acute hepatitis. 266 9

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

The response of plasma cyclic AMP to glucagon was investigated in 18 patients with acute liver injury to determine its value as a marker for the severity of the hepatic damage. We also investigated the interrelationship between plasma cyclic AMP response and the hyperglucagonemia often seen in this disease. Plasma cyclic AMP response to glucagon was reduced significantly in patients with acute hepatitis, particularly in severe cases with bridging hepatic necrosis. There was a significant negative correlation between log (peak % cAMP) and prothrombin time (r = -0.715, p less than 0.01), and also total bilirubin (r = -0.819, p less than 0.01). In fatal cases, the early phase of plasma cyclic AMP response after glucagon stimulation was blunted. In patients with acute liver injury, basal IRG levels were significantly high and a significant negative correlation was found between log (peak % cAMP) and basal IRG levels (r = -0.816, p less than 0.01). Our results suggest that the response of plasma cyclic AMP to exogenous glucagon could be useful in evaluating the severity of acute liver injury. The lower cyclic AMP response may be attributed to reduced hepatic reserve and endogenous hyperglucagonemia.
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PMID:Impaired plasma cyclic AMP response to exogenous glucagon in acute liver injury. 609 May 30

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

A rare case of severe acute hepatitis A complicated by pure red cell aplasia (PRCA) is reported. A 60-year-old man with jaundice and hepatomegaly was diagnosed as having acute hepatitis A by positive IgM anti-hepatitis A antibody (anti-HAV). Severe anemia rapidly developed 3 weeks after admission, and the patient was diagnosed with PRCA by both bone marrow smears and erythrocyte survival study. The anemia was transient and bone marrow recovered within 1 week. However, concomitant with bone marrow recovery, the hepatitis worsened. He became drowsy and disoriented and severe jaundice, ascites, prolonged prothrombin time, increased transaminase levels, and abnormal electroencephalogram (EEG) were exhibited. Plasma exchange transfusion and glucagon-insulin (GI) therapy improved the consciousness level, but bilirubin, transaminase levels, and IgM anti-HAV titer remained high. Intravenous administration of lipophilized prostaglandin E1 (lipo-PGE1) was added to the GI therapy. Bilirubin and transaminase levels were normalized in the 8th week after the initiation of this combination therapy (17 weeks after admission). The combined use of lipo-PGE1 with plasma exchange and GI therapy appeared to be useful for the prolonged severe hepatitis in this patient.
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PMID:Severe acute hepatitis A associated with acute pure red cell aplasia. 884 89