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Biomedical subjects

G Ideo

Publications and source records attributed to G Ideo.

At least 73 records · Page 4Linked to original sources
PubMed1976

[Controlled clinical trial of 2-mercapto-propionyl-glycine in chronic hepatopathies].

A controlled clinical trial comparing 2-Mercapto-Priopionyl-Glycine (2-MPG) plus B12 vitamin with B12 vitamin alone in chronic liver disease has been conducted in seven hospitals in Italy. Patients were divided into two groups on the basis of liver histology; group I included 26 patients showing histological evidence for chronic persistent hepatitis (C.P.H.) (according to De Groote et al.) whereas group II consisted of 54 patients with chronic aggressive hepatitis (C.A.H.) or compensated liver cirrhosis. Patients of each group were randomly allocated to 2-MPG plus B12 vitamin, or to placebo plus B12 vitamin, in a double-blind way. The drug (or placebo) was diluted in 500 ml of 10% Levulose, and administered intravenously; 1000 gamma of B12 vitamin were added to each bottle. Patients in the 2-MPG group received 2.5 gms of the drug daily; the treatment lasted for 30 days. The following parameters were checked in all patients on admission, and repeated at the end of treatment: Serum bilirubin, serum Cholesterol, A.P., BSP retention, Prothrombin time, S-GOT, S-GPT, Gamma-GT, Total serum Protein, serum electrophoresis, Immunoglobulins. Patients given 2-MPG showed significant decreases of serum transaminases, and improvement of BSP retention.

Amino Acids, Sulfur↗
PubMed1976

Paracetamol metabolism in the rat: relationship to covalent binding and hepatic damage.

1. The degree of liver damage observed 48 h after administration of 14C ring-labelled paracetamol (3-23 mmol/kg) to rats was proportional to the amount of a highly reactive metabolite retained in the liver, bound covalently to hepatocellular proteins. 2. With increasing doses of paracetamol, urinary excretion of the glucuronide and sulphate conjugates reached a plateau, whereas the output of cysteine and mercapturic acid conjugates increased markedly. 3. The degree of covalent binding at 48 h was proportional to the rate of urinary elimination of these two latter conjugates in the first 24 h after dosing.

Acetaminophen↗
PubMed1975

[S-Adenosylmethionine: plasma levels in hepatic cirrhosis and preliminary results of its clinical use in hepatology. Double-blind study].

Since S-adenosylmethionine (SAMe) plasma levels are highly reduced in cirrhotic patients, this, showing that a more or less overt deficiency of SAMe-dependent biological transmethylations does exist in the hepatocyte pathology, mostley affecting the albuminopoyesis. Treatment with 15 mg SAMe i.v. or i.m. administered four times a day for 30 days' period, induced in 15 patients with hepatic cirrhosis a statistically significant improvement of the afore mentioned livel cell function, albuminopoyesis: a significant improvement was also observed in the other biohumoral parameters considered to test hepatic function. Administration of equimolecular (with respect to SAMe) doses of L-methionine and ATP to a group of 15 cirrhotic patients under clinical conditions similar to those of the group previously studied, induced none of the modifications observed in the latter. This proved that the therapeutic effects are due only to S-adenosylmethionine.

Adolescent↗
PubMed1975

[Double-blind polycentric study of the action of S-adenosylmethionine in hepatic cirrhosis].

Two comparable groups of patients with hepatic cirrhosis of different genesis in a compensation phase have been treated for 30 days with S-adenosylmethionine and vitamine B-12 (28 cases) or with vitamine B-12 alone (25 cases). The drugs were given by slow intravenous route at the daily dose of 150 mg of SAMe and 2000 gamma of vit. B-12 or of 2000 gamma of vit. B-12 alone, in two adminstrations. An evaluation of the results was carried out mostly on the laboratory data testing the liver function. Only the group of patients who had received SAMe showed significant modifications of all the parameters considered. This is confirming SAMe ability to restore hepatocyte activity bringing also to normal the protein synthesis.

Aged↗
PubMed1975

Hepatic glutathione depletion and impaired bromosulphthalein clearance early after paracetamol overdose in man and the rat.

1. Plasma clearance of bromosulphthalein was impaired in patients within 8 h, and in rats within 2 h , of paracetamol overdose, before biochemical signs of liver damage had appeared. 2. Paracetamol and bromosulphthalein competed for uptake into the liver and excretion into the bile. Impaired hepatic uptake of bromosulphthalein could also be demonstrated in man at doses of the drug within the therapeutic range. 3. In patients studied a smaller proportion of bromosulphthalein was retained in the plasma as the glutathione conjugate after an overdose than after therapeutic doses. This effect could be reproduced in the rat and shown to be due to depletion of hepatic glutathione and to impairment in the activity of the enzyme glutathione-S-aryl transferase. 4. These studies provide further evidence that depletion of hepatic glutathione occurs after paracetamol overdose in man, as in the experimental animal, allowing the subsequent accumulation and binding of a toxic metabolite of the drug within liver cells. Impaired enzymic conjugation of the toxic metabolite with hepatic reduced glutathione may also be important in this situation.

Acetaminophen↗
PubMed1975

Early inhibition of hepatic bilirubin conjugation after paracetamol (acetaminophen) administration in the rat.

Administration of paracetamol (acetaminophen) 13.3 mmol kg-1 body weight to rats led 2 h later to an impaired capacity to conjugate an intravenous load of bilirubin, in the absence of biochemical signs of liver damage and before the reactive metabolite of the drug had become bound within the liver. In addition, paracetamol inhibited the excretion into the bile of conjugated bilirubin, although the plasma levels of the uncomjugated pigment only were elevated. This study provides additional evidence that hepatic glucuronide conjugation is impaired early after paracetamol overdose, and that this precedes the accumulation and binding of the hepatotoxic metabolite of the drug within the liver cells.

Acetaminophen↗