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Macrolide antibiotics selective toxicity

Macrolides, both erythromycin and others, inhibit the synthesis of bacterial proteins. The primary mechanisms of protein synthesis are identical in humans and bacteria. However, there is a significant difference that allows a specific antibiotic to exhibit selective toxicity with respect to bacteria. [Pg.467]

In contrast, decreases in theophylline metabolism by selective inhibitors of CYP1A2, such as fluvoxamine and some quinolone antibiotics, or by selective and potent inhibitors of CYP3A4, such as the macrolide antibiotics, have resulted in serious theophylline toxicity (22). It is postulated that taken over time, the macrolide antibiotics act as mechanism-based inhibitors of CYP isoforms other than just CYP3A4. Some nonselective inhibitors of P450s, such as cimetidine, some p-blockers and calcium channel blockers, and others (19,22), also appear to inhibit the metabolism of theophylline enough to cause toxicity. [Pg.690]


See other pages where Macrolide antibiotics selective toxicity is mentioned: [Pg.471]    [Pg.1419]    [Pg.301]    [Pg.92]    [Pg.385]    [Pg.259]    [Pg.159]    [Pg.148]   
See also in sourсe #XX -- [ Pg.5 , Pg.261 , Pg.262 ]




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