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Eubacterium lentum

Masuda N, H Oda, S Hirano, M Masuda, H Tanaka (1984) 7a-dehydroxylation of bile acids by resting cells of a Eubacterium lentum-like intestinal anaerobe, strain c-25. Appl Environ Microbiol AT. 735-739. [Pg.348]

When azithromycin is used concomitantly with digoxin, serum digoxin concentrations need to be monitored (47). While data on the effects of azithromycin on the intestinal metabolism of digoxin have not been reported so far, it is likely that it will affect Eubacterium lentum, like other macrolides. [Pg.392]

In 10% of patients taking digoxin, there is inactivation of up to 40% of the drug before absorption, by intestinal Eubacterium lentum. This can be reversed by antibiotics (334,335). The lack of effects of some beta-lactam antibiotics on serum digoxin concentrations in one study (336) might have been due to the small sample size or resistance of the bacteria. [Pg.491]

The interaction between macrohdes and digoxin is not a consequence of altered cytochrome P450 activity. Digoxin is metabolized in the gastrointestinal tract by Eubacterium lentum in the bowel flora of about 10% of patients (106). The direct antibacterial effect of macrohdes reduces digoxin metabolism and increases its systemic availabihty (134). The resultant increased digoxin plasma concentrations are associated with severe nausea, vomiting, and dysrhythmias (105,145,146). [Pg.2187]

Eubacterium lentum ATCC 25559 linolenic - trans-vaf w r acid (92%)... [Pg.1082]

Eubacterium lentum converts cholesterol (1.5-2 mg/mL) into 5/i-H-coprostanol in 90% yield 112. Another metabolite, the 5/ -estrane-3a,17/ -diol was produced with Clostridium para-putrificum in 70% yield. [Pg.1089]

Studies of the concomitant use of azithromycin with carbamazepine, terfenadine, and zidovudine have not reported drug interactions [131-133]. With the potential exception of antacids, no drug interactions have been reported with azithromycin, which does not appear to be metabolized by the cytochrome P-450 system [4, 134], Both azithromycin and clarithromycin have been associated with digoxin toxicity. The postulated mechanism is by eradication of Eubacterium lentum, an anaerobic gram-positive bacteria responsible for the metabolism of digoxin in some patients [43]. [Pg.353]

Digoxin is nearly completely absorbed from the gut. In some patients, absorption may be deaeased due to digoxin inactivation by gut bacteria (i.e., Eubacterium lentum) Digoxin absorption is reduced by concomitant administration of antacids, cholestyramine, kaolin/pectin, tetracycline, and neomycin. Radiation malabsorption and gastrointestinal motility drugs such as metoclopramide can also reduce absorption. ... [Pg.159]

Eradicate gut bacteria Eubacterium lentum) responsible for inactivation of digoxin in select patients (increased absorption)... [Pg.162]

Menaquinone-n (MK ), or vitamin K2( ), stands for 2-methyl-3-multiprenyl-1,4-naphthoquinone, where n indicates the amount of isoprene units in the side chain, a number naturally between 4 and 13. Sometimes one (or more) of the double bonds in the side chain is saturated. Physical and chemical properties of menaquinones are similar to those of VKl, with the exception of the lipohilic character, due to different design of the side chain. MK s are formed by bacteria (e.g., Escherichia coli. Staphylococcus aureus, Eubacterium lentum etc.) of the intestine, the most common configuration is -trans. Other stores of MK s were found to be animal liver (mainly MK7-13) and bone (5). [Pg.242]

Vasta V, Yanez-Ruiz DR, Mele M, Serra A, Luciano G, Lanza M, Biondi L, Priolo A (2010) Bacterial and protozoa communities and fatty acid profile in the rumen of sheep fed a diet containing added tannins. Appl Environ Microbiol 76 2549-2555 Verhulst A, Parmentier G, Janssen G, Asselberghs S, Eyssen H (1986) Biotransformation of unsaturated long-chain fatty acids hy Eubacterium lentum. Appl Environ Microbiol 51 532-538... [Pg.283]


See other pages where Eubacterium lentum is mentioned: [Pg.8]    [Pg.1011]    [Pg.287]    [Pg.39]    [Pg.154]    [Pg.231]    [Pg.1011]    [Pg.1011]    [Pg.335]    [Pg.335]    [Pg.913]    [Pg.929]    [Pg.941]    [Pg.298]    [Pg.281]    [Pg.269]    [Pg.170]    [Pg.82]    [Pg.102]   
See also in sourсe #XX -- [ Pg.37 ]




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