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M Frezza

Publications and source records attributed to M Frezza.

At least 55 records · Page 3Linked to original sources
PubMedDate not supplied

Reversal of intrahepatic cholestasis of pregnancy in women after high dose S-adenosyl-L-methionine administration.

Previous investigations have indicated that S-adenosyl-L-methionine (SAMe) leads to reversal of estrogen-induced bile flow impairment in rats. This randomized, single-blind clinical trial was performed to determine whether SAMe reverses intrahepatic cholestasis of pregnancy (ICP) which occurs in hypersensitive women associated with increased estrogen levels in late pregnancy. Eighteen women with ICP were randomly divided into three groups of six and treated for 20 days as follows: Group I received 200 mg per day of i.v. SAMe; Group II received 800 mg per day of i.v. SAMe; Group III served as control. At the beginning of the study, clinical and biochemical parameters were similar among groups. After 10 and 20 days of treatment with the higher dose of SAMe, the mean values of serum transaminases, conjugated bilirubin and total bile acids fell significantly in respect to initial levels; opposite results were found in the other two treatment groups. The final values of these selected parameters were lower in the group of subjects treated with 800 mg per day SAMe than in the other two groups of women. Pruritus graded on a 0 to 4+ scale significantly was reduced only in patients treated with the higher dose of SAMe. These results indicate a trend toward remission of ICP in women treated with 800 mg per day SAMe and suggest that SAMe administration may be a new therapeutic modality for ICP.

Adult↗
PubMedDate not supplied

[S-adenosyl-L-methionine (SAMe) and its use in hepatology].

S-adenosyl-L-methionine (SAMe), a molecule naturally present in several body tissues and fluids, is produced, by SAMe synthetase, from ATP and methionine. SAMe has a fundamental role, as methyl group donor, in transmethylation reactions in which the synthesis of membrane phospholipids (especially phosphatidylcholine) is mandatory for the maintenance of membrane fluidity. Another metabolic pathway involving SAMe, transsulphuration, is initiated with the release of -CH3 from the molecule and the formation of S-Adenosyl-homocysteine and then homocysteine and cysteine, a precursor of glutathione the main cellular antioxidant, responsible of detoxification of various compounds and xenobiotics. At last SAMe is implicated in aminopropylation process for the polyamine synthesis. The development of stable double salt of p-toluene sulphonic acid and sulphuric acid of SAMe enables the clinical use of the drug, as a therapeutical agent, for the treatment of a number of liver dysfunctions. In various animal and human models, including controlled trials, it has been demonstrated that SAMe can ameliorate some biochemical parameters and pruritus in cholestasis induced by a range of compounds (i.e. oestrogens, lithocolate, etc) and in intrahepatic cholestasis superimposed to chronic liver disease. Concerning alcohol toxicity, SAMe prevents, in ethanol fed baboons, depletion of glutathione levels, normalizes the mitochondrial enzymes and improves the histological hepatic lesions. In human healthy volunteers it has been recently demonstrated that SAMe, after ethanol ingestion, significantly lowers plasma concentration of ethanol and acetaldehyde as well. Finally, SAMe has been proposed, instead of N-acetylcysteine, as precursor of glutathione, in patients who present late after ingestion of an overdose of paracetamol.

Animals↗